One of the most common treatments used for cancer is chemotherapy. Different drugs are used in chemotherapy depending on the type of cancer. In this regard, one of the most basic problems in chemotherapy is drug resistance, in which people undergoing treatment develop resistance to chemotherapy drugs over time. Therefore, the drug dose must be increased over time or the interval between treatments must be reduced, which leads to side effects and damage to normal cells and tissues. Various factors play a role in drug resistance, including ATP-binding cassette (ABC) transporters, which lead to drug resistance by transporting these drugs outside the cell. Also, various factors, including signaling pathways and heat shock proteins (HSP), can play an effective role in drug resistance by interfering with these pumps or other factors involved in drug resistance. A body of studies indicated that, one of the most important signaling pathways that involved in drug resistance is Notch pathway. This pathway plays a fundamental role in drug resistance in cancers by interfering with various mechanisms. Therefore, in this study, our goal is to investigate the role of Notch pathway mechanisms in drug resistance in different cancers.

INTRODUCTION:Cancer is a leading cause of death worldwide, with many cancers lacking effective early screening methods. Early diagnosis is critical for improving survival and quality of life, and for reducing the financial burden of late-stage treatment. Liquid biopsy has emerged as a promising, minimally invasive diagnostic strategy. METHODS:This review provides a comprehensive analysis of the current state of liquid biopsy technologies for cancer detection. It evaluates the primary analytical techniques used to detect circulating tumor biomarkers, including Circulating Tumor Cells (CTCs), cell-free DNA (cfDNA), various non-coding RNAs (ncRNA), and extracellular vesicles. RESULTS:Liquid biopsies enable molecular characterization for diagnosis, treatment classification, and monitoring. However, the analysis reveals that a significant weakness of many current techniques is insufficient sensitivity for reliably detecting early-stage cancers, when treatment is most effective. DISCUSSION AND CONCLUSION:While liquid biopsy represents a revolutionary approach to oncology, technological hurdles remain. This review addresses these challenges and provides recommendations for advancing biomarker assay sensitivity and specificity. Overcoming these limitations is essential for translating liquid biopsy into effective, widespread clinical screening for early cancer detection.

The p53 protein is one of the pivotal proteins that plays an important role in various cellular processes including apoptosis, autophagy, cell cycle, and cell death and it considered as a guardian gene. If the mutation occurs in p53, not only its tumor suppressor activity is reduced, but it also acquires oncogenic properties. Functional point of view, when DNA is damaged, p53 stops the cell cycle, meanwhile, if p53 is also damaged, the damaged DNA will multiply and the cell cycle will continue indefinitely and eventually given rise to cancer. Almost all the reactions and transmission of messages that happen in the body are controlled by signaling pathways, and if there is a disturbance in the signaling pathways, it has adverse consequences in terms of pathophysiology. p53 and signaling pathways control each other’s function bilaterally, and if there is a disturbance in the communication between these two due to mutations and various factors, it leads to many diseases and cancers. Hence, given the importance of this subject, in this article, we decided to outlines the relationship between the p53 protein and various signaling pathways that interact with p53 in various diseases.

Type I interferons (IFN-I) exert a significant influence on the immune system. Produced by certain immune cells, they affect other immune cells and mediate diverse effects, including antiviral activity, inhibition of tumor growth, and suppression of cell proliferation. IFN-I is also implicated in the development and persistence of autoimmune disorders. Research has shown that abnormal IFN-I levels and IFN-I-regulated gene expression in the blood or tissues of individuals with autoimmune diseases are associated with disease onset, clinical manifestations, and severity. Monogenic conditions known as Type I interferonopathies-caused by mutations affecting the IFN-I signaling pathway-share clinical features with systemic lupus erythematosus (SLE). Both preclinical models and clinical trials targeting the IFN-I signaling pathway have yielded promising results for the treatment of autoimmune diseases. This review provides an overview of the interplay between epigenetics, various types of RNAs, transcription factors, and IFN-I. It discusses epigenetic modifications and transcription factor dysregulation, offering insights into disease mechanisms and potential future therapeutic advancements.

The development of breast cancer (BC) is a multistep process in which different cells and genes are involved, and its prevention and treatment are challenging. If BC is detected in the early stages, it can be prevented and the survival rate is high, and vice versa. Growing studies show that in recent years, many advances have been made in the field of BC prevention and treatment. Tamoxifen (TAM) is one of the important drugs used in the treatment of BC. Research shows that stem cells and various genes have a key role in TAM drug resistance in BC. Therefore, in this study, we intend to clarify the genes that are involved in the resistance to TAM in BC and perhaps take a small step in the prevention and treatment of BC.

As a heterogeneous multifactorial disorder, PCOS still has a misty etiology. Its underlying pathophysiological causes can be further elucidated by proteomic analyses and molecular network analysis to understand the interaction pathways involved in the PCOS-associated perturbations. We conducted a proteomic study on ovulatory PCOS serum samples using nano-LCMS/MS technique. Then, we analysed the proteomic profiles of substantially dysregulated proteins by projecting them onto protein interaction mapping and molecular network analysis software tools Gene Mania and STRING. We further investigated the involvement of the affected proteins in different PCOS-associated disorders and classified them through a review of the literature along with functional annotation software tools DAVID and Panther. We found a total of 228 proteins in serum; 109 were found in both ovulatory PCOS and controls, and 42 of those showed a difference of ≥twofold (19 higher in ovulatory PCOS and 23 lower). Among them, 35 proteins exhibited an association with the pathophysiological mechanisms underlying the manifestation of ovulatory PCOS manifestation and their correlations with PCOS-concurrent disorders were revealed. There were also 87 proteins that were only found in ovulatory PCOS and 32 that were only found in controls. We further highlighted significant functional hub molecules within protein interaction networks. Our findings indicated that the ovulatory PCOS involves a wide range of functional molecule derangements, which trigger aberrant biological responses and molecular interactions leading to the emergence of complications associated with ovulatory PCOS. Further omics studies are required to explain the different physiological mechanisms of the functional molecules contributing to the pathogenicity of this heterogeneous syndrome.

The tumor microenvironment (TME) contains tumor cells, surrounding cells, and secreted factors. It provides a favorable environment for the maintenance of cancer stem cells (CSCs), the spread of cancer cells to metastatic sites, angiogenesis, and apoptosis, as well as the growth, proliferation, invasion, and drug resistance of cancer cells. Cancer cells rely on the activation of oncogenes, inactivation of tumor suppressors, and the support of a normal stroma for their growth, proliferation, and survival, all of which are provided by the TME. The TME is characterized by the presence of various cells, including cancer-associated fibroblasts (CAFs), tumor-associated macrophages (TAMs), CD8 + cytotoxic T cells (CTLs), regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), mesenchymal stem cells (MSCs), endothelial cells, adipocytes, and neuroendocrine (NE) cells. The high expression of inflammatory cytokines, angiogenic factors, and anti-apoptotic factors, as well as drug resistance mechanisms in the TME, contributes to the poor therapeutic efficacy of anticancer drugs and tumor progression. Hence, this review describes the mechanisms through which the TME is involved in apoptosis, angiogenesis, metastasis, and drug resistance in tumor cells.

Cancer is one of the common diseases that affects people in the society, the prevalence of which has decreased somewhat in recent years. Various genetic and environmental factors play a role in the development and progression of cancer. NRF2 is a transcriptional regulator that controls the expression of antioxidant response element-related genes. It plays an important role in regulating the physiological and pathophysiological consequences of oxidant exposure. NRF2 is also responsible for regulating the expression of various cellular protective genes. NRF2 activity is regulated at multiple levels including protein stability, transcription, and post-transcription. The Keap1–Cul3–Rbx1 axis is the most prominent regulator of NRF2 activity. Apoptosis is a type of programmed cell death that is initiated by two intrinsic and extrinsic pathways. Caspases play a major role in this cell death pathway. Apoptosis pathway is related to many cells signaling pathways that are interconnected. Disruption in one pathway affects the other pathway. One of these signaling pathways is the NRF2 pathway, which is associated with apoptosis, which are interconnected and play an important role in disease prevention or progression. Therefore, in this study, we decided to investigate the relationship between NRF2 and apoptosis in cancer.

The most common methods of treating cancer are surgery, chemotherapy, and radiotherapy. However, given that some cancers are not operable, the best method is chemotherapy and radiotherapy. Over time, people become resistant to chemotherapy drugs, and increasing the dose of the drug leads to damage to normal cells. In this article, various sources such as Google Scholar, PubMed, and Semantic Scholar were used, and articles between 1997 and 2025 that were relevant to our topic were selected. Various factors are involved in drug resistance. Melatonin is a hormone that has various roles in the body. One of its most important functions is regulating the circadian rhythm of sleep and its anti-inflammatory and antioxidant properties. According to studies, melatonin plays a role in the treatment of some diseases and cancers. The roles of melatonin in cancer treatment include anti-apoptotic, anti-angiogenic, and anti-migratory effects, as well as drug resistance and cell cycle regulation. As mentioned, one of the main reasons for the failure of cancer treatment is drug resistance, and the role of melatonin in drug resistance in cancers has been proven. Therefore, in this study, our goal is to investigate the mechanisms through which melatonin plays a role in drug resistance in different types of cancer.

Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor involved in the regulation of various genes, including cell protection genes and genes encoding detoxification enzymes, metabolic enzymes, drug transporters, inflammation-related proteins, and antioxidant enzymes. Nrf2 itself is regulated by mechanisms induced by Kelch-like ECH-associated protein 1 (KEAP1) in response to electrophilic and oxidative stresses. One type of cell death is pyroptosis. In this type of cell death, the cell expands, the cell membrane ruptures, and the cell contents are released, which activates immune and inflammatory responses. The activation of these inflammatory pathways triggers caspase-1 or caspase-4/5/11, which can further cleave gasdermin D (GSDMD). The N-terminal region of GSDMD, upon release, binds to membrane lipids and disrupts the cell membrane. According to the literature, Nrf2 reduces the levels of reactive oxygen species (ROS) and suppresses pyroptosis. Therefore, based on this finding and considering the importance of pyroptosis in cell death and its relationship with Nrf2, this study aimed to explore the relationship between pyroptosis and Nrf2 in different diseases.

Autism spectrum disorder (ASD) is a pervasive neurobehavioral condition characterized by disruption of behavioral and emotional patterns in individuals with this condition. Given that various environmental and genetic factors play a fundamental role in the pathophysiology of ASD, it can be said that ASD is a multifaceted disease. This study used scientific databases including Google Scholar, PubMed, Scopus, and Semantic Scholar. In this review, we aimed to select manuscripts based on our field and relevant to the topic of our article. Emerging studies have shown that many neural, anatomical, and chemical factors play a role in the development of ASD. In this regard, an increasing body of studies has pointed out the relationship between chemical factors, including hormones, which play an important role in ASD. These hormones include melatonin, serotonin, thyroid, oxytocin, vasopressin, insulin-like growth hormone (IGF-1), etc. For instance, IGF-1 levels are low in ASD individuals, or melatonin levels are reduced in ASD individuals. Therefore, with take into account these findings, in this review, we decided to check over the association of these hormones to ASD and have a concise overview of their potential as therapeutic solutions to reduce the effects of ASD.

Ferroptosis is a type of cell death that multiple mechanisms and pathways contribute to the positive and negative regulation of it. For example, increased levels of reactive oxygen species (ROS) induce ferroptosis. ferroptosis unlike apoptosis, it is not dependent on caspases, but is dependent on iron. Exosomes are membrane-bound vesicles with a size of about 30 to 150 nm, contain various cellular components, including DNA, RNA, microRNAs (miRNAs), lipids, and proteins, which are genetically similar to their cells of origin. Exosomes are found in all bodily fluids, including blood, saliva, and urine. Cells often release exosomes after their fusion with the cell membrane. They play an important role in immune regulation and cell-cell communication. miRNAs, which are noncoding RNAs with a length of about 18 to 24 nucleotides, are involved in regulating gene expression after transcription. Emerging data suggests that exosomal miRNAs are implicated in various pathophysiological mechanisms of cells, including metastasis, drug resistance, and cell death. In addition, functional studies have indicated that exosomal miRNAs can play a key role in the modulation of cell death by regulating ferroptosis. Therefore, in this review, given the importance of exosomal miRNAs in ferroptosis, we decided to elucidate the relationship between exosomal miRNAs and ferroptosis in various diseases.

Cancer, an important global health problem, is defined by aberrant cell proliferation and continues to be the main cause of death globally. The tumor microenvironment (TME) plays an essential role in the development of cancer, resistance to therapy, and regulation of the immune response. Some immune cells in the TME, like T cells, B cells, macrophages, dendritic cells, and natural killer cells, can either stop or help tumor growth, depending on how metabolic and cytokine changes happen. Cytokines function as essential signaling molecules that modulate immune cell metabolism, altering their functionality. This review focuses on how cytokine-mediated metabolic reprogramming affects the activity of immune cells inside the TME, which can either make the immune response stronger or weaker. New ways of treating cancer that focus on metabolic pathways and cytokine signaling, such as using IL (Interleukin) - 15, IL- 10, and IL- 4, show promise in boosting immune cell activity and making cancer treatments more effective. Finding these pathways could lead to new ways to treat cancer with immunotherapy that focus on metabolic competition and immune resistance in the TME.

Objective:Hepatic cells face oxidative stress-induced damage, but plant antioxidants may offer protection. This study aimed to assess Elaeagnus angustifolia L. fruit extract's potential in shielding rat livers from CCl4 damage. Materials and Methods:30 Male Wistar rats were randomly divided into five groups: normal control (received distilled water), E. angustifolia hydroalcoholic extract control, CCl4 control, E. angustifolia extract pretreatment (600 mg/kg), and silymarin pretreatment (100 mg/kg). After 14 days of oral administration of extracts, CCl4 was injected intraperitoneally. The samples were collected 48 hr later. Histological and biochemical analyses were then carried out. Results:CCl4 injection caused significant (p<0.001) changes in liver serum enzymes, lipid profile, bilirubin, total protein, serum albumin, antioxidant enzymes, malondialdehyde, Inflammatory cytokines, and liver tissue morphology. E . angustifolia extract pre-treatment significantly (p<0.05) returned changes to the normal state. Conclusion:This study's findings revealed that E. angustifolia extract pretreatment could reduce liver injury caused by CCl4 in rats.

Members of the 14-3-3 protein family are involved in various cellular processes, including migration, angiogenesis, cell cycle, apoptosis, and signal transduction. Nevertheless, the 14-3-3 family possibly plays a fundamental role in the development of diseases and cancer by regulating various biological pathways. MicroRNAs (miRNAs) are mainly transcribed by RNA polymerase II (pol II), with only a few exceptions involving RNA polymerase III (pol III). They can control cell mechanisms through different pathways. miRNAs inhibit or destroy mRNAs by binding to them. They control intracellular mechanisms by binding to molecules such as the 14-3-3ζ protein. miRNAs play a role in regulating this protein, and by inducing or suppressing it, they contribute to either the development or the prevention of the diseases. Therefore, considering the importance of the 14-3-3ζ protein in different pathways within the body, we decided to investigate the relationship between miRNAs and 14-3-3ζ and clarify their interactions, in this review.

Matrix metalloproteinase (MMPs) is a class of zinc-dependent enzymes that play an important role in the invasion and metastasis of cancer cells and have different types. MMP-2 is one of the important enzymes of this family. MicroRNAs (miRNAs) are noncoding RNAs that are involved in the regulation of gene expression of many enzymes and factors in the body. Emerging data have highlighted the relationship between MMP-2 and miRNAs. Studies have shown that miRNAs regulate MMP-2 by binding to the 3′ untranslated region (3′ UTR), which leads to a decrease or increase in MMP-2 expression and its enzymatic activity. For example, decreased expression of miR-106b leads to increased growth and invasion of breast cancer (BC) cells through increased expression of MMP-2. Therefore, understanding the regulatory mechanisms related to MMP-2 and miRNAs will provide new insights into the molecular pathways that drive BC progression and highlight potential therapeutic targets for the management of invasion and metastasis. Hence, in this study, we aimed to elucidate the relationship between MMP-2 and miRNAs in BC.

Breast cancer (BC) is the second cancer-dyeing reason among women worldwide. Surgical, radiation, and medicine-based approaches are the current methods for BC treatment; however, they did not overcome metastasis BC robustly. Finding treatments to improve the survival rate appears to be an essential attitude. Telomer is a fundamental part of the linear eukaryote chromosome. Despite the low-telomerase activity in somatic cells, it has been reported that more than 90

One of the biggest challenges of today's society is cancer, which imposes a significant financial, emotional and spiritual burden on human life. Breast cancer (BC) is one of the most common cancers that affects people in society, especially women, and due to advanced treatment strategies and primary prevention, it is still the second cause of cancer-related deaths in society. Various genetic and environmental factors are involved in the development of BC. MicroRNAs (miRNA)s are non-coding RNAs, that the degradation or inhibition of them plays an important role in the prevention or development of cancer by modulating many cellular pathways including apoptosis, drug resistance, and tumorigenesis. Drug resistance is one of the important defense mechanisms of cancer cells against anticancer drugs and is considered one of the main causes of cancer treatment failure. Different miRNAs, including mir-7, mir-21, mir-31, and mir-124 control different cell activities, including drug resistance, through different pathways, including PI3K/AKT/mTOR, TGF-β, STAT3, and NF-kB. Therefore, cell signaling pathways are one of the important factors that miRNAs control cellular activities. Hence, in this study, we decided to highlight an overview of the relationship between miRNAs and signaling pathways in the development of drug resistance in BC.

Autophagy is a significant catabolic procedure that increases in stressful conditions. This mechanism is mostly triggered after damage to the organelles, the presence of unnatural proteins, and nutrient recycling in reaction to these stresses. One of the key points in this article is that cleaning and preserving damaged organelles and accumulated molecules through autophagy in normal cells helps prevent cancer. Since dysfunction of autophagy is associated with various diseases, including cancer, it has a dual function in tumor suppression and expansion. It has newly become clear that the regulation of autophagy can be used for the treatment of breast cancer, which has a promising effect of increasing the efficiency of anticancer treatment in a tissue- and cell-type-specific manner by affecting the fundamental molecular mechanisms. Regulation of autophagy and its function in tumorigenesis is a vital part of modern anticancer techniques. This study discusses the current advances related to the mechanisms that describe essential modulators of autophagy involved in the metastasis of cancers and the development of new breast cancer treatments.

In today’s world, one of the main problems is cancer, which still has a long way to go to cure it, and it brings a lot of financial and emotional costs to the people of society and governments. Breast cancer (BC) and cervical cancer (CC), two of the most common cancers, are caused by several genetic and environmental factors in women. These two cancers’ involvement rate is higher than other cancers in women. microRNAs (miRNAs) are non-coding RNA molecules with a length of 18 to 24 nucleotides, which play an important role in post-translational changes. miRNAs themselves are divided into two categories, oncomiRs and tumor suppressors. OncomiRs have a part in tumor expansion and tumor suppressors prevent tumor development and progress. miRNAs can control cellular processes by regulating various pathways including autophagy, apoptosis, and signaling. Apoptosis is a type of programmed cell death that includes intrinsic and extrinsic pathways and is different from other cell death pathways such as necrosis and ferroptosis. Apoptosis controls the growth, differentiation, and death of cells by regulating the death of damaged and old cells, and since miRNAs are one of the factors that regulate apoptosis, and divided into two categories: pro-apoptotic and anti-apoptotic. We decided in this study to investigate the relationship between miRNAs and apoptosis in the most common women’s cancers, BC and CC.