Tumor nanovaccines have attracted great interest recently, due to a variety of advantages including high stability, efficient antigen packing and delivery, and the capacity to elicit sustained anti-tumor immune responses. Despite these advantages, existing nanovaccines are constrained by intricate manufacturing procedures and high production costs, prompting a need to develop simpler and more cost-effective solutions. In this study, we introduce a novel STING-activating tumor nanovaccine, designated OVA/Tp@Mn-DNA. The preparation of OVA/Tp@Mn-DNA nanovaccine is a straightforward process involving the self-assembly of Mn2+ and DNA molecules into nanospheres, which are then crosslinked with both antigenic peptides and antigen-presenting cells (APC)-targeting peptides. Our findings reveal that the OVA/Tp@Mn-DNA nanovaccine facilitates the delivery of antigens to APCs, activates STING signaling pathway effectively and triggering robust cellular immune responses. Results from xenograft mouse tumor model demonstrate a remarkable therapeutic potential of OVA/Tp@Mn-DNA in combating tumors. Collectively, our work presents a new strategy offering OVA/Tp@Mn-DNA as an uncomplicated and economical nanovaccine for potent tumor immunotherapy.

Nasopharyngeal carcinoma (NPC) is characterized by high metastatic potential and therapeutic resistance, necessitating the development of novel and safe therapeutic strategies. Hyperactivation of the PI3K/AKT signaling pathway, often driven by the oncogenic microRNA-21 (miR-21) and the subsequent suppression of PTEN, plays a key role in NPC progression. Chelerythrine (CHE), a natural plant-derived alkaloid, exhibits potent anti-tumor activities; however, its precise regulatory mechanisms and translational potential in NPC remain elusive. Network pharmacology was employed to predict the core downstream cascades of CHE against NPC. In vitro, CCK-8, real-time cellular analysis (RTCA), flow cytometry, wound healing, and Transwell assays were utilized to evaluate the specific cytotoxicity and anti-malignant effects of CHE in normal nasopharyngeal epithelial cells (NP69) and NPC cells (5–8 F and 6-10B). RT-qPCR was used to quantify the expression of primary (pri-miR-21), precursor (pre-miR-21), and mature miR-21. In vivo, a BALB/c nude mouse xenograft model was established to systematically assess the tumor-suppressive efficacy and macroscopic/histological biosafety of CHE. Furthermore, definitive rescue experiments were conducted using a specific PI3K activator and lentivirus-mediated miR-21 modification cell lines. Network pharmacology highlighted the PI3K/AKT pathway as the key effector cascade of CHE. Functionally, CHE exhibited a highly favorable safety profile in NP69 cells and in vivo major organs, while significantly inhibiting NPC cell proliferation, migration, and invasion, and inducing apoptosis. Mechanistically, CHE synchronously suppressed the expression of pri-miR-21 and pre-miR-21, indicating a transcriptional downregulation of miR-21. This upstream suppression led to the restoration of the tumor suppressor PTEN, subsequent inactivation of the PI3K/AKT pathway, and reversal of the epithelial-mesenchymal transition (EMT) phenotype. Importantly, co-treatment with a PI3K activator or lentiviral overexpression of miR-21 significantly counteracted the tumor-suppressive effects of CHE, whereas miR-21 knockdown synergistically potentiated its efficacy. Collectively, our findings indicate that CHE is a safe and effective therapeutic candidate for NPC. It exerts its anti-tumor and anti-metastatic effects by transcriptionally downregulating miR-21, thereby relieving PTEN suppression and systematically inactivating the PI3K/AKT signaling axis.

METHODS:Molecular docking was employed to analyze the binding affinity between the active components of YQJDF and AKT1. MTT assay, real-time cell analysis (RTCA), wound healing assay and Matrigel invasion chamber assay were used to evaluate the effect of YQJDF extract on proliferation, migration and invasion abilities of human NPC cell lines 5-8F and 6-10B, and the changes in cellular protein expression levels were detected using Western blotting. In a BALB/c nude mouse model bearing NPC cell xenografts, tumor growth were observed following treatment with daily gavage with normal saline or YQJDF extract (15.357 g/kg) for 18 consecutive days or with intraperitoneal injections of 5-Fu every other day. The changes in the expressions of AKT1/GLUT1 signaling axis proteins in the xenografts were examined using Western blotting. RESULTS:In the NPC cell lines, treatment with YQJDF extract significantly inhibited cell proliferation, migration, and invasion, and downregulated the expressions of p-AKT, GLUT1, XIAP, N-cadherin, and vimentin. The application of GLUT1 or AKT1 activators partially reversed the inhibitory effects of YQJDF on the NPC cells. In the tumor-bearing mouse models, treatment with YQJDF extract obviously suppressed tumor growth and down-regulated the expression of AKT, p-AKT and GLUT1 in the tumor tissues. CONCLUSIONS:YQJDF inhibits proliferation, invasion, and migration of NPC cells by inhibiting the AKT1/GLUT1 signaling pathway.

The intratumoral microbiome, comprising diverse bacteria, fungi, and viruses residing within tumor tissues, is increasingly recognized as a multidimensional oncogenic modulator, acting akin to a “microbial conductor” orchestrating key cancer hallmarks. Its compositon exhibits substantial heterogeneity across individuals and is closely associated with the host immunity, the tumor microenvironment (TME), and therapeutic efficacy. Specific microbial species can “conduct” pro-tumorigenic processes by producing carcinogenic metabolites, dysregulating inflammatory signaling, or facilitating immune evasion. Conversely, other microorganisms may exert anti-tumorigenic effects by stimulating anti-tumor immunity or directly inhibiting cancer cell proliferation. Furthermore, the intratumoral microbiome can influence therapeutic outcomes by modulating the metabolism of chemotherapeutic agents or altering the efficacy of immunotherapies. Therefore, a deeper understanding of the intratumoral microbiome and its complex interplay with tumors holds immense potential to unravel fundamental mechanisms of cancer development and progression, while simultaneously revealing novel avenues for precision oncology strategies. This review outlines the biological roles of the microbiota in modulating the hallmarks of cancer hallmarks, summarizes current knowledge on its multidimensional interactions driving tumor progression, and discusses the translational potential of targeting or leveraging the intratumoral microbiome based on recent advancements. Future research integrating multi-omics profiling, spatial technologies, and functional validation will be essential for resolving methodological limitations and accelerating the clinical translation of microbiome-based interventions.

Homoharringtonine is a natural alkaloid with significant pharmacological potential that has demonstrated promising efficacy in the treatment of hematological malignancies in recent years. This article systematically reviews the pharmacological mechanisms of Homoharringtonine, focusing on its key roles in inducing apoptosis, inhibiting cell cycle progression, and reducing cell migration and invasion. Additionally, HHT exhibits multiple biological activities, including immunomodulation, antiviral effects, and anti-fibrotic properties, with recent studies also revealing its potential neuroprotective functions. In clinical trials, Homoharringtonine has demonstrated promising efficacy in the treatment of hematological malignancies, particularly in various types such as acute myeloid leukemia and chronic myeloid leukemia. Despite the significant antitumor effects observed in clinical applications, its low bioavailability and potential side effects remain major challenges that limit its widespread use. This article details the latest research advancements aimed at enhancing the bioavailability of Homoharringtonine, including various drug delivery systems such as nanoparticles and liposomes, as well as chemical modification strategies. These approaches not only improve HHT’s bioavailability in vivo but also enhance its targeting ability while reducing toxicity to normal cells. Furthermore, the combination of HHT with other drugs presents broader prospects for clinical treatment. By exploring the diverse pharmacological activities of Homoharringtonine in depth, this article aims to provide a foundation for developing novel therapeutic approaches based on natural products, thereby advancing HHT’s application research in cancer treatment and other fields.

Nasopharyngeal carcinoma is a type of malignant tumour occurring in the nasopharyngeal mucosal epithelium. This carcinoma often has no obvious symptoms in the early stages and is frequently diagnosed at mid-to-advanced stages. Interleukin-6 (IL-6) is a multifunctional cytokine that can participate in the regulation of the immune system, haematopoiesis, induction of acute phase protein secretion, and cell proliferation and differentiation of. IL-6 is a core molecule in tumour inflammation and carcinoma metastasis that promotes various tumours. This article discusses the promoting effects of IL-6 in the occurrence and development of nasopharyngeal carcinoma from the perspectives of release of pro-inflammatory factors, regulation of the tumour microenvironment, enhanced migration and invasion abilities of tumour cells and distant metastasis, and improved tumour immune evasion functions. In addition, important implications of IL-6 for the diagnosis, treatment, and prognosis of nasopharyngeal carcinoma are discussed.

Colorectal cancer remains a leading cause of cancer-related mortality worldwide, emphasizing the importance of early detection through accurate polyp identification. However, colonoscopy relies heavily on precise polyp segmentation in endoscopic images, yet this task remains challenging due to morphological variability, low contrast, and imaging artifacts. In this study, we propose HSSAM-Net, a lightweight deep learning framework that integrates a Hyper-Scale Shifted Aggregation Module to capture multi-scale contextual information while preserving fine-grained details, Progressive Reuse Attention mechanism that strengthens feature propagation across the encoder-decoder pathway, and Max-Diagonal Pooling/Unpooling (MaxDP/MaxDUP) a novel dual-branch sampling scheme to improve texture representation, feature alignment to enhance feature aggregation, context learning, and boundary refinement. The proposed model is evaluated on five benchmark datasets (Kvasir, CVC-ClinicDB, ETIS, CVC-300, EndoCV2020). Experimental results show that HSSAM-Net consistently outperforms state-of-the-art methods across benchmark datasets, HSSAM-Net consistently achieves state-of-the-art accuracy (Dice: 0.949–0.952, mIoU: 0.924–0.930), while maintaining real-time efficiency at 24.1 FPS with only 0.9 M parameters. Furthermore, an analysis of trainable parameters and inference speed confirms its suitability for real-time clinical applications. Our findings demonstrate that HSSAM-Net achieves a favorable trade-off between accuracy and efficiency, advancing the development of practical and reliable computer-aided colonoscopy systems.

This review explores the dual role of miR-195 in cancer, acting as both a tumor suppressor and, in specific contexts, a tumor promoter. It highlights its molecular mechanisms, focusing on key signaling pathways such as Wnt-1/β-catenin, VEGF/VEGFR, and PI3K/AKT/mTOR, as well as its involvement in competitive gene regulation. The clinical potential of miR-195 in cancer screening, diagnosis, prognosis, and therapy is examined, particularly its ability to enhance therapeutic efficacy and reduce recurrence risk when combined with chemotherapy or immunotherapy. Despite these promising aspects, challenges such as precise regulation, efficient delivery systems, and clinical translation remain. Future research should prioritize advancing miR-195’s integration into personalized medicine, immunotherapy, and novel delivery technologies, aiming to establish it as a reliable biomarker and therapeutic target for improved cancer care.

The challenges posed by both climate change and population expansion are unlike anything agriculture has ever seen, and in order to sustain and boost agricultural output, new and creative technology must be used. Artificial intelligence (AI) is one such exponent of change that offers possible solutions in a number of agricultural production fields. Emphasis will be placed on robotic automation, machine learning applications, and the concept of precision farming. This research explores how integration in agriculture has made AI an excellent support for decision processes in crop management, providing real-time monitoring and predictive analytics. Higher agricultural yields and resilience are made possible by genetic advancements and AI in resource optimization. However, due to technological, societal, and legal obstacles, the promise for AI in agriculture has not yet materialized. Against this background, this study requires holistic policy frameworks, education, and stakeholder engagement as countermeasures to such challenges. The future potential applications of AI in agriculture continue to change the sector on behalf of improving global food security and sustainability; this concludes the study. This paper tries to bring to light the critical role that AI is most likely to play in shaping future agricultural practices based on an in-depth analysis of the current state of technology and upcoming opportunities.

Nasopharyngeal carcinoma (NPC) is a malignant neoplasm that is highly prevalent in East Asia and presents significant therapeutic challenges due to limited treatment options and severe adverse effects. Ursolic acid (UA) is a pentacyclic triterpenoid with anticancer activity in various tumors; however, its mechanism of action in NPC remains unclear. This study integrated network pharmacology with experimental validation to elucidate the molecular mechanism underlying the effect of UA against NPC. Screening of a network pharmacology database identified 39 targets common to UA and NPC, among which P53, STAT3, Bcl-2, IL1B, and CASP3 showed high node degrees in the protein–protein interaction network. Gene Ontology analysis revealed that these targets were primarily enriched in stress response and apoptosis regulation, whereas Kyoto Encyclopedia of Genes and Genomes analysis indicated significant enrichment in the P53 signaling and apoptosis pathways. UA dose-dependently inhibited the proliferation of the NPC cell lines S18 and S26 (p < 0.01), and induced apoptosis, as demonstrated by Annexin V-FITC/PI double fluorescence staining and confirmed by Hoechst 33,342 staining showing nuclear condensation. UA also caused mitochondrial membrane depolarization, as indicated by JC-1 staining. Western blot analysis showed significant upregulation of P53 and the pro-apoptotic protein BAX (p < 0.01), and downregulation of the anti-apoptotic protein Bcl-2 (p < 0.01) following UA treatment. This study is the first to show that UA induces apoptosis in NPC cells by activating the P53 signaling pathway using network pharmacology and experimental validation.

Copy number variations (CNVs) play a vital role in regulating genes expression and tumorigenesis. We explored the copy number alterations in early-stage lung adenocarcinoma using high-throughput sequencing and nucleic acid flight mass spectrometry technology, and found that 8q22.1-22.2 is frequently amplified in lung adenocarcinoma tissues. COX6C localizes on the region and its expression is notably enhanced that driven by amplification in lung adenocarcinoma. Knockdown of COX6C significantly inhibits the cell proliferation, and induces S-G2/M cell cycle arrest, mitosis deficiency and apoptosis. Moreover, COX6C depletion causes a deficiency in mitochondrial fusion, and impairment of oxidative phosphorylation. Mechanistically, COX6C-induced mitochondrial deficiency stimulates ROS accumulation and activates AMPK pathway, then leading to abnormality in spindle formation and chromosome segregation, activating spindle assemble checkpoint, causing mitotic arrest, and ultimately inducing cell apoptosis. Collectively, we suggested that copy amplification-mediated COX6C upregulation might serves as a prospective biomarker for prognosis and targeting therapy in patients with lung adenocarcinoma.

Nasopharyngeal carcinoma (NPC) is an aggressive head and neck tumor that is influenced by a variety of molecular factors during its pathogenesis. Among these, the phosphatase and tensin homolog (PTEN) plays a crucial role in regulatory networks. This article systematically reviews the multifaceted functions of PTEN in NPC, including its roles in inhibiting cell proliferation, regulating migration and invasion, promoting autophagy and apoptosis, and influencing resistance to radiotherapy. Molecular factors such as long non-coding RNA, microRNA (miRNA), and circular RNA can modulate PTEN through various pathways, thereby impacting the biological behavior of NPC. In addition, PTEN is involved in regulating the tumor microenvironment of NPC, and its interaction with the Epstein-Barr virus has also recently become a focus of research. A comprehensive understanding of the PTEN regulatory network provides a foundation for future personalized and targeted therapeutic strategies. This study expands our understanding of the pathogenesis of NPC and suggests new directions in the field of tumor biology and NPC treatment.

T follicular helper cells (Tfh) were initially identified nearly two decades ago as critically important in directing B-cell maturation and antibody generation in the germinal centers of secondary lymphoid tissues. Since then, Tfh cells have become the center of sustained investigation in oncology due to their unique, often paradoxical roles in tumour immunity. Specifically, Tfh cells in the tumour microenvironment can enhance anti-tumour immune response or promote, through the same mechanisms, tumour progression. These dual roles largely result from Tfh cells controlling unique cytokine secretions and, in turn, shifting the net effect of the Tfh-driven immune response (by directly and indirectly affecting the activities of other cytotoxic T cells and natural killer cells). The dual nature of the Tfh is the basis for our commentary, which highlights their simultaneous identity as a curse and a gift to oncology. Indeed, the curtain calls for a better understanding Tfh cell biology, so that their potential can be used to benefit oncology. We discuss how prevalent Tfh cells in tumors can be beneficial in directing potent anti-tumour immune responses. We also review how the characterization of Tfh cells in tumors has now led to their identification as candidate biomarkers of response to immunotherapy, and how they are now being evaluated as targets for new immunotherapies leading to new clinical trials. The study concludes by emphasizing how the unique biological properties of Tfh cells can be leveraged to advance cancer treatment, ultimately aiming to enhance the effectiveness of clinical oncology practices.

Curcumin (CUR) is a lipophilic natural polyphenol that can be isolated from the rhizome of turmeric. Studies have proposed that CUR possesses a variety of biological activities. Due to its anti-inflammatory and antioxidant properties, CUR shows promise in the treatment of inflammatory bowel disease, while its anti-obesity effects make it a potential therapeutic agent in the management of obesity. In addition, curcumin’s ability to prevent atherosclerosis and its cardiovascular benefits further expand its potential application in the treatment of cardiovascular disease. Nevertheless, owing to the limited bioavailability of CUR, it is difficult to validate its specific mechanism of action in the treatment of diseases. However, the restricted bioavailability of CUR makes it challenging to confirm its precise mode of action in disease treatment. Recent research indicates that the oral intake of curcumin may lead to elevated levels of residual curcumin in the gastrointestinal system, hinting at curcumin’s potential to directly influence gut microbiota. Furthermore, the ecological dysregulation of the gut microbiota has been shown to be critical in the pathogenesis of human diseases. This review summarizes the impact of gut dysbiosis on host health and the various ways in which curcumin modulates dysbiosis and ameliorates various diseases caused by it through the administration of curcumin.

Mitochondrial transcription termination factor 3 (MTERF3) negatively regulates mitochondrial DNA transcription. However, its role in hepatocellular carcinoma (HCC) progression remains elusive. Here, we investigate the expression and function of MTERF3 in HCC. MTERF3 is overexpressed in HCC tumor tissues and higher expression of MTERF3 positively correlates with poor overall survival of HCC patients. Knockdown of MTERF3 induces mitochondrial dysfunction, S-G2/M cell cycle arrest and apoptosis, resulting in cell proliferation inhibition. In contrast, overexpression of MTERF3 promotes cell cycle progression and cell proliferation. Mechanistically, mitochondrial dysfunction induced by MTERF3 knockdown promotes ROS accumulation, activating p38 MAPK signaling pathway to suppress HCC cell proliferation. In conclusion, ROS accumulation induced by MTERF3 knockdown inhibits HCC cell proliferation via p38 MAPK signaling pathway suggesting a promising target in HCC patients.

Breast cancer (BC) significantly contributes to cancer-related mortality in women, underscoring the criticality of early detection for optimal patient outcomes. Mammography is a key tool for identifying and diagnosing breast abnormalities; however, accurately distinguishing malignant mass lesions remains challenging. To address this issue, we propose a novel deep learning approach for BC screening utilizing mammography images. Our proposed model comprises three distinct stages: data collection from established benchmark sources, image segmentation employing an Atrous Convolution-based Attentive and Adaptive Trans-Res-UNet (ACA-ATRUNet) architecture, and BC identification via an Atrous Convolution-based Attentive and Adaptive Multi-scale DenseNet (ACA-AMDN) model. The hyperparameters within the ACA-ATRUNet and ACA-AMDN models are optimized using the Modified Mussel Length-based Eurasian Oystercatcher Optimization (MML-EOO) algorithm. The performance is evaluated using a variety of metrics, and a comparative analysis against conventional methods is presented. Our experimental results reveal that the proposed BC detection framework attains superior precision rates in early disease detection, demonstrating its potential to enhance mammography-based screening methodologies.

This study aimed to investigate the effect and potential mechanism of evodiamine (EVO) on proliferation and apoptosis of nasopharyngeal carcinoma (NPC) cells. EVO inhibited proliferation, blocked cell cycle progression, and induced apoptosis of NPC cells. There are 27 known anti-NPC targets of EVO, of which eight are core targets, namely SRC, ERBB2, STAT3, MAPK8, NOS3, CXCL8, APP, and HDAC1. Molecular docking analysis showed that the binding of EVO with its key targets (SRC, ERBB2) was good. EVO also reduced the expression of SRC and ERBB2, the key proteins p-MEK and p-ERK1/2 of the MAPK/ERK signaling pathway, and the downstream proteins PCNA and XIAP. EVO inhibited the growth of NPC xenografts in nude mice and reduced the expression levels of SRC, ERBB2, ERK1/2, p-ERK1/2, PCNA and XIAP in NPC tissue. When the MAPK/ERK signaling pathway was activated by epidermal growth factor (EGF), the expression levels of PCNA and XIAP increased, the cell proliferation index increased, and the apoptosis rate decreased in the EGF + EVO treatment group compared to treatment with EVO alone. These changes indicated that the inhibitory effect of EVO on proliferation and apoptosis of NPC cells was related to the down-regulation of SRC and ERBB2 expression, and further inhibition of the MAPK/ERK signaling pathway.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/locate/withdrawalpolicy).This article has been retracted at the request of the Editor-in-Chief.The authors have plagiarized Figure 2 and Table 1 of a paper that had already appeared in Trends in Cancer, Volume 9, Issue 4, P309-325, April 2023, https://doi.org/10.1016/j.trecan.2022.12.007 and used these as Figure 1 and Table 1 here. The authors have stated that this has been a mistake and apologize for it.One of the conditions of submission of a paper for publication is that authors declare explicitly that their work is original and has not appeared in a publication elsewhere. Re-use of any data should be appropriately cited. As such this article represents a severe abuse of the scientific publishing system. The scientific community takes a very strong view on this matter and apologies are offered to readers of the journal that this was not detected during the submission process.

ObjectiveThis study aims to assess the current research status, focus areas, and developmental trends in nasopharyngeal carcinoma (NPC) through a bibliometric analysis. MethodsArticles focusing on NPC published from 2000 to 2023 were retrieved from the Web of Science database. VOSviewer and CiteSpace were used for bibliometric and visual analysis. ResultsA total of 14516 related publications were retrieved. There has been a steady increase in the number of NPC-related publications from 2000 to 2023. China was the dominant country in this field with 8948 papers (61.64%), followed by the USA (2234, 15.39%). Sun Yat-sen University was the most influential institution, while Ma J was the most prolific author. Furthermore, Head And Neck-journal For The Sciences And Specialties Of The Head And Neck was the most prolific journal. International Journal of Radiation Oncology Biology Physics had the highest total citation counts. "Introduction chemotherapy", "Concurrent chemotherapy", "Epithelial-mesenchymal transition", "Cancer stem cells", "MicroRNAs", "LncRNA", "Exosomes", and "Biomarker" were the most common keywords. The reference "Chen YP, 2019, Lancet" had the highest citations and strong outbreak value. ConclusionThe past two decades have witnessed a significant increase in research on NPC. The optimization of treatment mode is the most widely studied aspect at present. The mechanism of occurrence and development and the most favorable diagnostic and therapeutic targets are the research hotspots in the future.

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. Functionally uncharacterized genes are an attractive repository to explore candidate oncogenes. It is demonstrated that C21orf58 displays an oncogenic role in promoting cell growth, tumorigenesis and sorafenib resistance of HCC cells by abnormal activation of STAT3 signaling. Mechanistically, a novel manner to regulate STAT3 signaling that adaptor C21orf58 forms a ternary complex is reveal with N-terminal domain of STAT3 and SH2 domain of JAK2, by which C21orf58 overactivates wild-type STAT3 by facilitating its phosphorylation mediated by JAK2, and hyper-activates of constitutively mutated STAT3 due to preferred binding with C21orf58 and JAK2. Moreover, it is validated that inhibition of C21orf58 with drug alminoprofen, selected by virtual screening, could effectively repress the viability and tumorigenesis of HCC cells. Therefore, it is identified that C21orf58 functions as an oncogenic adaptor, reveal a novel regulatory mechanism of JAK2/STAT3 signaling, explain the cause of abnormal activity of activated mutants of STAT3, and explore the attractive therapeutic potential by targeting C21orf58 in HCC.