Abstract Brain tumor treatment remains a significant challenge due to their high mortality and resistance to current therapies. This paper discusses the promising potential of hydrogel-based nanoparticles as innovative drug delivery systems for brain tumor therapy. Extensive characterization techniques reveal the ability of these Nano-systems to demonstrate prolonged blood circulation and targeted delivery, leading to improved survival rates. Designed with optimized physicochemical characteristics, these nanoparticles effectively cross the blood–brain barrier, circumventing a major impediment to drug delivery to the brain. By delivering drugs directly to the tumor bed, these nanoparticles enhance therapeutic outcomes and minimize adverse effects. In addition, this review investigates the techniques for characterizing, visualizing, and modifying these nanoparticles, as well as the standing challenges and promising research avenues for their clinical application. Further investigations are encouraged by this review to investigate potential advancements in hydrogel-based nanoparticle therapeutic approaches for brain tumors. This includes investigating tailored hydrogels, hybrid systems, computational modeling, and the integration of gene therapy and immunotherapy techniques. The study also addresses the need for enhanced synthesis techniques, stability, scalability, and cost-cutting measures to overcome obstacles and advance the clinical use of hydrogel-based nanoparticles in treating brain tumors. Graphical abstract

A crucial cellular mechanism that has a complex impact on the biology of cancer, particularly in solid tumors, is autophagy. This review explores how metabolic processes trigger autophagy, which helps metastatic tumor cells go dormant and recur. During metastasis, tumor cells frequently encounter severe stressors, such as low oxygen levels and nutritional deprivation, which causes them to activate autophagy as a survival tactic. This process allows cancer stem cells (CSCs) to withstand severe conditions while also preserving their features. After years of dormancy, dormant disseminated tumor cells (DTCs) may reappear as aggressive metastatic cancers. The capacity of autophagy to promote resistance to treatments and avoid immune detection is intimately related to this phenomenon. According to recent research, autophagy promotes processes, such as the epithelial-to-mesenchymal transition (EMT) and helps build a pre-metastatic niche, which makes treatment strategies more challenging. Autophagy may be a promising therapeutic target because of its dual function as a tumor suppressor in early-stage cancer and a survival promoter in advanced stages. To effectively treat metastatic diseases, it is crucial to comprehend how metabolic processes interact with autophagy and affect tumor behavior. In order to find novel therapeutic approaches that can interfere with these processes and improve patient outcomes, this study highlights the critical need for additional investigation into the mechanisms by which autophagy controls tumor dormancy and recurrence.

Over the past few decades, cancer research has increasingly focused on tumor microenvironment (TME). The TME contains diverse cellular components and secreted factors, including leukocytes, endothelial cells, cancer-associated fibroblasts, and other non-cancerous cells and extracellular matrix proteins. The interactions between tumor cells and microenvironment elements are complex and unpredictable. Nonetheless, these relationships govern and control several cancer traits, including immune response, metastasis, differentiation status, cell proliferation, and resistance to cell death. In this line, Matricellular proteins, including periostin (POSTN), are increasingly recognized for their regulatory roles in the TME and cancer progression. Periostin is involved in tumor biology through matrix remodeling, invasion, and proliferation. In this review, we focused on the role of periostin as a biomarker for cancer growth and treatment resistance and a potential prognostic and therapeutic factor in cancer patients. In addition, we will discuss the periostin's dual role as both a promoter and inhibitor of tumor growth, depending on its concentration and cellular context. Key findings indicate that low periostin levels may suppress cancer progression by preventing epithelial-to-mesenchymal transition (EMT). In contrast, high levels can enhance migration and metastasis through the activation of integrin signaling pathways. Furthermore, we will discuss the implications of targeting periostin in therapeutic strategies, particularly in light of its complex functions within the TME.

The intricate cellular process, known as the epithelial-mesenchymal transition (EMT), significantly influences solid tumors development. Changes in cell shape, metabolism, and gene expression linked to EMT facilitate tumor cell invasion, metastasis, drug resistance, and recurrence. So, a better understanding of the intricate processes underlying EMT and its role in tumor growth may lead to the development of novel therapeutic approaches for the treatment of solid tumors. This review article focuses on the signals that promote EMT and metabolism, the intracellular signaling pathways leading to EMT, and the network of interactions between EMT and cancer cell metabolism. Furthermore, the functions of EMT in treatment resistance, recurrence, and metastasis of solid cancers are covered. Lastly, treatment approaches that focus on intracellular signaling networks and metabolic alterations brought on by EMT will be discussed.

Breast cancer is the most common cancer in women, making for one-third of all malignancies in females. Between 40 and 45 percent of instances of hereditary breast cancer are caused by mutations in the breast and ovarian cancer susceptibility gene 1 (BRCA1). Breast cancer risk is raised by mutations in its Really Interesting New Gene (RING) and BRCA1 C-Terminal (BRCT) domains. Thus, the goal of this study was to identify new mutations in the BRCA1 gene's RING and BRCT domains. To examine BRCA1 mutation spectra, 107 patients were chosen who had a documented family history of ovarian or breast cancer. Direct DNA sequencing and single-stranded conformational polymorphism (PCR-SSCP), both based on the polymerase chain reaction, were used to screen for mutations in the RING and BRCT domains of the BRCA1 gene. In-silico analysis was used for the in-vitro research outcome. The study's findings indicated that the population carries several BRCA1 sequence variations, including C.55C > A, C.36A > T, C.60A > T, C.199G > C, C.164A > T, C.251A > G, C.4996T > G, C.5032A > T, C.5041A > G, and C.5291T > A. The Breast Cancer Information Core (BIC) searched and examined the mutations. Every mutation was a new mutation. Additionally, a bioinformatics investigation revealed that several variations had an impact on the pathogenicity and stability of the protein. After calculating the relative risk (RR) of research linked to danger, it was found that there was a strong correlation (RR = 1) between the newly discovered genetic mutations and an elevated risk of breast cancer. Our research emphasizes the value of mutation screening in cases of familial ovarian or breast cancer, as well as the possible ramifications of these results for genetic counseling and cancer prevention.

A seizure is the brain's uncontrolled, abnormal electrical activity, which may result in altered states of consciousness, behavior, memory, or emotion. Seizures start biologically with the activation of susceptible brain neurons, which causes synchronized discharges of larger groups of connected neurons. A few potential causes of seizures include medications, genetics, electrolyte abnormalities, sleep state, infections, brain inflammation, and injuries. Medicinal plants are a rich source of various chemical molecules with distinct structures and biological activity. Most plants contain active components, including coumarin, glycosides, alkaloids, terpenoids, flavonoids, peptidoglycans, and other elements often associated with the effects of antiseizures. Isolating and identifying biologically active compounds and molecules from nature have resulted in the development of novel treatments, which in turn have contributed to the advancement of the health and pharmaceutical sectors throughout the history of humanity. In this review, we thoroughly summarize the information on the anti-seizure activities of medicinal plants and bioactive chemicals, focusing on molecular targets and cellular signaling pathways. All available research has contributed to medicinal plants as a reasonable option for seizure prevention and treatment, as well as drug development and manufacturing. To better comprehend the underlying molecular mechanisms, more research is required. If these mechanisms are discovered, it will be easier to identify new targets and create innovative anti-seizure therapeutic drugs to enhance patient survival and life quality. This work is expected to provide insights and ideas for the further research of Bioactive compounds from medicinal plants, their qualities, and the scientific basis for their improved clinical use.

Type 1 diabetes (T1D) is a chronic autoimmune condition that affects millions of people worldwide. Insulin pumps or injections are the standard treatment options for this condition. This article provides a comprehensive overview of the several type 1 diabetes treatment options, focusing on oral insulin. The article is divided into parts that include immune-focused treatments, antigen vaccination, cell-directed interventions, cytokine-directed interventions, and non-immunomodulatory adjuvant therapy. Under the section on non-immunomodulatory adjunctive treatment, the benefits and drawbacks of medications such as metformin, amylin, sodium-glucose cotransporter inhibitors, glucagon-like peptide-1 receptor agonists (GLP-1 Ras), and verapamil are discussed. The article also discusses the advantages of oral insulin, including increased patient compliance and more dependable and regular blood sugar control. However, several variables, including the enzymatic and physical barriers of the digestive system, impair the administration of insulin via the mouth. Researchers have looked at a few ways to get over these challenges, such as changing the structure of the insulin molecule, improving absorption with the use of absorption enhancers or nanoparticles, and taking oral insulin together with other medications. Even with great advancements in the use of these treatment strategies, T1D still needs improvement in the therapeutic difficulties. Future studies in these areas should focus on creating tailored immunological treatments, looking into combination medications, and refining oral insulin formulations in an attempt to better control Type 1 Diabetes. The ultimate objective is to create accurate, customized strategies that will enhance glycemic management and the quality of life for individuals with the condition.

The resistance of cancer cells to chemotherapy, also known as chemo-resistance, poses a significant obstacle to cancer treatment and can ultimately result in patient mortality. Epithelial-mesenchymal transition (EMT) is one of the many factors and processes responsible for chemo-resistance. Studies have shown that targeting EMT can help overcome chemo-resistance, and nanotechnology and nanomedicine have emerged as promising approaches to achieve this goal. This article discusses the potential of nanotechnology in inhibiting EMT and proposes a viable strategy to combat chemo-resistance in various solid tumors, including breast cancer, lung cancer, pancreatic cancer, glioblastoma, ovarian cancer, gastric cancer, and hepatocellular carcinoma. While nanotechnology has shown promising results in targeting EMT, further research is necessary to explore its full potential in overcoming chemo-resistance and discovering more effective methods in the future.

Stem cells, particularly bulge hair follicle stem cells (HFSCs), have recently attracted significant interest due to their potential for tissue repair and regeneration. These cells, marked by their expression of Nestin (a neural stem cell marker), suggest the possibility of neural differentiation into neurons. This study investigated the use of retinoic acid (RA) and epidermal growth factor (EGF) to induce HFSC transformation into mature neurons, identified by synaptophysin expression. Rat whisker follicles were cultured in a medium suitable for HFSC survival and proliferation. Immunostaining techniques were used to identify HFSCs and assess their differentiation into neural cells. The addition of RA and EGF to the culture medium aimed to induce this differentiation. Findings demonstrate that HFSCs expressed Nestin, indicating their pluripotent nature. Treatment with RA and EGF resulted in synaptophysin expression, a marker of mature neurons, which was absent in the control group. However, this treatment group also displayed a decrease in the expression of other neural markers (βIII tubulin and NeuN). This study suggests that a combination of RA and EGF can accelerate HFSC differentiation into synaptophysin-positive cells in vitro. This research paves the way for further exploration of its potential application in neuro-regeneration. Schematic illustrates the process of isolating hair follicles from the whisker pads of 6–8-week-old rats, followed by the cultivation and neural differentiation of the isolated hair follicles. The final stage results in the generation of synaptophysin-expressing neurons. The figure created with biorender.com.

Extensive research in countries with high sociodemographic indices (SDIs) to date has shown that coronavirus disease 2019 (COVID-19) may be directly associated with more severe outcomes among patients living with haematological disorders and malignancies (HDMs). Because individuals with moderate to severe immunodeficiency are likely to undergo persistent infections, shed virus particles for prolonged periods, and lack an inflammatory or abortive phase, this represents an overall risk of morbidity and mortality from COVID-19. In cases suffering from HDMs, further investigation is needed to achieve a better understanding of triviruses and a group of related variants in patients with anemia and HDMs, as well as their treatment through vaccines, drugs, and other methods. Against this background, the present study aimed to delineate the relationship between HDMs and the novel COVID-19, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Besides, effective treatment options for HDM cases were further explored to address this epidemic and its variants. Therefore, learning about how COVID-19 manifests in these patients, along with exploiting the most appropriate treatments, may lead to the development of treatment and care strategies by clinicians and researchers to help patients recover faster.

Most medical investigations have found a reduced blood level of miR-146a in type 2 diabetes (T2D) patients, suggesting an important role for miR-146a (microRNA-146a) in the etiology of diabetes mellitus (DM) and its consequences. Furthermore, injection of miR-146a mimic has been confirmed to alleviate diabetes mellitus in diabetic animal models. In this line, deregulation of miR-146a expression has been linked to the progression of nephropathy, neuropathy, wound healing, olfactory dysfunction, cardiovascular disorders, and retinopathy in diabetic patients. In this review, besides a comprehensive review of the function of miR-146a in DM, we discussed new findings on type 1 (T1MD) and type 2 (T2DM) diabetes mellitus, highlighting the discrepancies between clinical and preclinical investigations and elucidating the biological pathways regulated through miR-146a in DM-affected tissues.

Severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) infection is a serious threat to lung cancer patients. Hereby, we hypothesize that Coronavirus disease 2019 (COVID-19) may contribute to lung cancer progression by increasing extracellular adenosine triphosphate (ATP) levels and hyperactivating the purinergic P2X purinoceptor 7 receptor (P2X7R). Hyperactivation of P2X7R by increased extracellular ATP may stimulate multiple signaling pathways and factors such as NLRP3 inflammasome; as a result, interleukin (IL)-1β, and IL-18 pro-inflammatory cytokines are released, JNK, Rho kinase, HMGB1-RAGE, PI3K/AKT, hypoxia-inducible factor-1 alpha (HIF-1α), and ERK. NLRP3 activation may play a pivotal role in fatal cytokine storm in critically ill patients with COVID-19 and tumor progression in patients with lung cancer. Consequently, inhibiting these signaling pathways may deviate immune responses toward anti-tumoral responses, and suppress lung cancer progression and cytokine storms. Therefore, targeting P2X7R by means of oxidized ATP and anti-P2X7 monoclonal antibodies may provide promising therapeutic approaches to prevent lung cancer progression in COVID-19 patients; however, no clinical trials have yet been conducted, and their clinical efficacy remains to be elucidated.

Coronavirus disease-2019 (COVID-19), as a worldwide serious issue has been shown to lead to progression and poor outcomes in cancer patients. The underlying mechanisms for SARS-CoV-2 infection's adverse effects on cancer patients have not been fully understood. We hypothesized that CD147 and Cyclophilin A (CyPA) not only can play a significant role in infection severity but also can contribute to cancer progression and chemotherapy resistance in cancer patients with COVID-19. In addition, we hypothesized that the expression of both CD147 and CyPA could be increased by Hypoxia-inducible Factor-1 alpha (HIF-1α) activation during hypoxic conditions that occurred during COVID-19. Therefore, this evidence can open a new window in the management of cancer patients during the pandemic and therapeutic approaches targeting CD147 and CyPA could be a potentially promising therapeutic approach for such patients.

Acute myeloid leukemia (AML) comprises a multifarious and heterogeneous array of illnesses characterized by the anomalous proliferation of myeloid cells in the bone marrow microenvironment (BMM). The BMM plays a pivotal role in promoting AML progression, angiogenesis, and metastasis. The immune checkpoints (ICs) and metabolic processes are the key players in this process. In this review, we delineate the metabolic and immune checkpoint characteristics of the AML BMM, with a focus on the roles of BMM cells e.g. tumor-associated macrophages, natural killer cells, dendritic cells, metabolic profiles and related signaling pathways. We also discuss the signaling pathways stimulated in AML cells by BMM factors that lead to AML progression. We then delve into the roles of immune checkpoints in AML angiogenesis, metastasis, and cell proliferation, including co-stimulatory and inhibitory ICs. Lastly, we discuss the potential therapeutic approaches and future directions for AML treatment, emphasizing the potential of targeting metabolic and immune checkpoints in AML BMM as prognostic and therapeutic targets. In conclusion, the modulation of these processes through the use of directed drugs opens up new promising avenues in combating AML. Thereby, a comprehensive elucidation of the significance of these AML BMM cells' metabolic and immune checkpoints and signaling pathways on leukemic cells can be undertaken in the future investigations. Additionally, these checkpoints and cells should be considered plausible multi-targeted therapies for AML in combination with other conventional treatments in AML.4fLEX7tLHnLn8Cp1swJnhpVideo Abstract

Despite community vaccination against coronavirus disease 2019 (COVID-19) and reduced mortality, there are still challenges in treatment options for the disease. Due to the continuous mutation of SARS-CoV-2 virus and the emergence of new strains, diversity in the use of existing antiviral drugs to combat the epidemic has become a crucial therapeutic chance. As a broad-spectrum antiparasitic and antiviral drug, ivermectin has traditionally been used to treat many types of disease, including DNA and RNA viral infections. Even so, based on currently available data, it is still controversial that ivermectin can be used as one of the effective antiviral agents to treat severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or not. The aim of this study was to provide comprehensive information on ivermectin, including its safety and efficacy, as well as its adverse effects in the treatment of COVID-19.

Phytotherapy ResearchEarly View LETTER TO THE EDITOR Kaempferol's potential effects against SARS-CoV-2 and COVID-19-associated cancer progression and chemo-resistance Hamidreza Zalpoor, Corresponding Author Hamidreza Zalpoor [email protected] orcid.org/0000-0002-8057-2804 Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran Network of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), Universal Scientific Education & Research Network (USERN), Tehran, Iran Correspondence Vahideh Tarhriz, Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Email: [email protected], [email protected] Hamidreza Zalpoor, Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Email: [email protected]Search for more papers by this authorMahsa Liaghat, Mahsa Liaghat Network of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), Universal Scientific Education & Research Network (USERN), Tehran, Iran Department of Medical Laboratory sciences, Faculty of Medical Sciences, Kazerun Branch, Islamic Azad University, Kazerun, IranSearch for more papers by this authorMaryam Bakhtiyari, Maryam Bakhtiyari Network of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), Universal Scientific Education & Research Network (USERN), Tehran, Iran Department of Medical Laboratory Sciences, Faculty of Allied Medicine, Qazvin University of Medical Sciences, Qazvin, IranSearch for more papers by this authorHooriyeh Shapourian, Hooriyeh Shapourian Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, IranSearch for more papers by this authorAbdullatif Akbari, Abdullatif Akbari Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran Network of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), Universal Scientific Education & Research Network (USERN), Tehran, IranSearch for more papers by this authorShaghayegh Shahveh, Shaghayegh Shahveh American Association of Naturopath Physician (AANP), Washington, DC, USASearch for more papers by this authorMohsen Nabi-Afjadi, Mohsen Nabi-Afjadi Department of Biochemistry, Faculty of biological science, Tarbiat Modares University, Tehran, IranSearch for more papers by this authorSohrab Minaei Beirami, Sohrab Minaei Beirami Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran Research Center for Infectious Diseases and Tropical Medicine, Tabriz University of Medical Sciences, Tabriz, IranSearch for more papers by this authorVahideh Tarhriz, Corresponding Author Vahideh Tarhriz [email protected] [email protected] orcid.org/0000-0002-3018-9313 Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran Research Center for Infectious Diseases and Tropical Medicine, Tabriz University of Medical Sciences, Tabriz, Iran Correspondence Vahideh Tarhriz, Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Email: [email protected], [email protected] Hamidreza Zalpoor, Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Email: [email protected]Search for more papers by this author Hamidreza Zalpoor, Corresponding Author Hamidreza Zalpoor [email protected] orcid.org/0000-0002-8057-2804 Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran Network of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), Universal Scientific Education & Research Network (USERN), Tehran, Iran Correspondence Vahideh Tarhriz, Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Email: [email protected], [email protected] Hamidreza Zalpoor, Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Email: [email protected]Search for more papers by this authorMahsa Liaghat, Mahsa Liaghat Network of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), Universal Scientific Education & Research Network (USERN), Tehran, Iran Department of Medical Laboratory sciences, Faculty of Medical Sciences, Kazerun Branch, Islamic Azad University, Kazerun, IranSearch for more papers by this authorMaryam Bakhtiyari, Maryam Bakhtiyari Network of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), Universal Scientific Education & Research Network (USERN), Tehran, Iran Department of Medical Laboratory Sciences, Faculty of Allied Medicine, Qazvin University of Medical Sciences, Qazvin, IranSearch for more papers by this authorHooriyeh Shapourian, Hooriyeh Shapourian Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, IranSearch for more papers by this authorAbdullatif Akbari, Abdullatif Akbari Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran Network of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), Universal Scientific Education & Research Network (USERN), Tehran, IranSearch for more papers by this authorShaghayegh Shahveh, Shaghayegh Shahveh American Association of Naturopath Physician (AANP), Washington, DC, USASearch for more papers by this authorMohsen Nabi-Afjadi, Mohsen Nabi-Afjadi Department of Biochemistry, Faculty of biological science, Tarbiat Modares University, Tehran, IranSearch for more papers by this authorSohrab Minaei Beirami, Sohrab Minaei Beirami Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran Research Center for Infectious Diseases and Tropical Medicine, Tabriz University of Medical Sciences, Tabriz, IranSearch for more papers by this authorVahideh Tarhriz, Corresponding Author Vahideh Tarhriz [email protected] [email protected] orcid.org/0000-0002-3018-9313 Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran Research Center for Infectious Diseases and Tropical Medicine, Tabriz University of Medical Sciences, Tabriz, Iran Correspondence Vahideh Tarhriz, Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Email: [email protected], [email protected] Hamidreza Zalpoor, Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Email: [email protected]Search for more papers by this author First published: 27 January 2023 https://doi.org/10.1002/ptr.7706 Funding information: Research Center for Infectious Diseases and Tropical Medicine, Tabriz University of Medical Sciences, Tabriz, Iran Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. 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Dexamethasone, a synthetic glucocorticoid drug, is widely used as an anti-inflammatory/anti-allergic agent worldwide. Several previous studies suggested that in the inflammatory or enriched free radical condition, Dexamethasone directly binds to DNA leading to DNA breakage/remodeling and subsequently cancer or other DNA breakage-related disorders. So, for the first time, we computationally and experimentally investigated the interaction of the Dexamethasone drug, alone and in combination with H2O2, ascorbic acid, iron, and copper, with a routine supercoiled plasmid DNA. In the next step, the intrinsic DNA binding constant (kd) was calculated using UV absorption titration method via Dexamethasone interaction with calf thymus DNA (ctDNA). Also, the interaction of the drug with antioxidant enzymes including catalase, superoxide dismutase, glutathione peroxidase 4, and glutathione reductase was investigated by molecular docking methods. Interestingly, our in-vitro study demonstrated that dexamethasone binds to DNA by binding energy of −5.35 kcal/mol. Our study also indicated that dexamethasone/DNA interaction leads to no DNA breakage while its combination with the mineral supplies causes DNA damage/breakage. These results are consistent with our Docking study that indicated dexamethasone strongly binds to DNA and the catalytic site of glutathione peroxidase 4, the FAD-binding site of the glutathione reductase, the active site of the superoxide dismutase, and NADPH binding residues of the catalase enzyme. Therefore, we hypothesize that Dexamethasone may indirectly cause DNA damage by inhibiting antioxidant defense enzymes and causing oxidative stress in cells.

The coenzyme ubiquinone-10 (CoQ10) is not only an important part of the electron transport chain of the mitochondrial inner membrane but also has complex biological functions beyond mitochondrial respiration. It is a natural nutrient that is not only produced by the body but is also found in foods, such as meat, eggs, fish, and vegetable oils. Because some types of cancer reduce CoQ10 blood levels, the use of CoQ10 supplements is recommended for the treatment of cancer patients. The anti-cancer effects of CoQ10 supplementation have been reported in several cancers, including colon and breast cancer. CoQ10 scavenges free radicals to reduce oxidative stress and minimize tissue damage. CoQ10 protects the body from damage caused by chemotherapy drugs by reducing the production of inflammatory cytokines and other inflammatory factors. Recent studies suggest that CoQ10 may be a supplement to pharmacotherapy for hepatocellular carcinoma. This article examines the effects of CoQ10 in hepatocellular carcinoma.

Numerous studies have revealed that cancer patients are more likely to develop severe Coronavirus disease-2019 (COVID-19), which can cause mortality, as well as cancer progression and treatment failure. Among these patients who may be particularly vulnerable to severe COVID-19 and COVID-19-associated cancer progression are those with oral squamous cell carcinoma (OSCC). In this regard, therapeutic approaches must be developed to lower the risk of cancer development, chemo-resistance, tumor recurrence, and death in OSCC patients with COVID-19. It may be helpful to comprehend the cellular and molecular mechanisms by which the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) contributes to these problems. In this line, in this review, we described the potential cellular and molecular mechanisms that SARS-CoV-2 can exert its role and based on them pharmacological targeted therapies were suggested. However, in this study, we encourage more investigations in the future to uncover other cellular and molecular mechanisms of action of SARS-CoV-2 to develop beneficial therapeutic strategies for such patients.