As a reversible post-transcriptional modification, N6-methyladeno sine is the most common form of RNA modification in eukaryotic mRNA. Cancer stem cells (CSCs), which are a subpopulation of cells with self-renewal ability and differentiation potential, have been regarded to be one of the roots of tumor occurrence, recurrence, and metastasis. Currently, numerous studies have demonstrated that m6A RNA modification is critically implicated in the regulation of CSCs stemness or the CSC-like traits of cancer cells. This review summarized the effects of m6A RNA modification-related enzymes and underlying mechanisms contributing to CSCs or cancer cell stemness, which may provide novel targets and research directions for the specifical elimination of CSCs or cancer cells with stemness.

Metastasis is the major cause of cancer-related mortality. Metastasis is a process through which cancer spreads from its initial location to other sections of the body. Cancer cells' epithelial-mesenchymal transition (EMT), anoikis resistance, cell migration, and angiogenesis are all well-known steps in this process. Investigating the molecular processes that govern cancer metastatic progression may lead to more effective diagnostic and treatment strategies. Long non-coding RNAs (lncRNAs) have recently discovered to have a vital more than 200 nucleotides. A rising body of research indicates that lncRNAs have a role in a wide range of biological processes and diseases, including cancer. The usage of LncRNA in cancer metastasis has been widely researched. However, according to current studies, lncRNA is mostly associated with the EMT process. This review focuses on the processes behind lncRNA involvement in cancer metastasis.

Parkinson’s Disease (PD) is a prevalent progressive neurodegenerative condition affecting millions globally. Research has found that individuals with PD have a reduced risk of certain cancers, such as colon, lung, and rectal cancers, but an increased risk of brain cancer. Therefore, there is an urgent need for the development of advanced PD diagnostic methods and for investigating the relationships between risk factors, such as lifestyle due to handedness associated with various types of cancers. Recent ad- vancements in magnetic resonance imaging have enhanced PD diagnosis, reducing misdiagnosis and facilitating more accurate disease progression monitoring. Nevertheless, challenges exist, particularly in the distinction of PD between left-handed and right-handed patients over time. This survey provides an overview of contemporary deep learning-based imag- ing analysis methodologies, encompassing both non-longitudinal and lon- gitudinal contexts. We also explore existing limitations and prospects for refinement to gain deeper insights. These insights are poised to inform the development of personalized treatment strategies for PD patients while elucidating the current disparities between deep learning models and their efficacious implementation in clinical practice.

The paramount prerequisite for effective anti-cancer drugs is their ability to eradicate malignant cells while sparing non-cancer cells. The divergence in properties between malignant and non-cancer cells establishes a "therapeutic window," a critical consideration for achieving desirable treatment outcomes. Central to this is the imperative of a cancer drug's "selectivity and specificity." Taxanes, a pivotal class of successful anti-cancer drugs, continue to serve as the linchpin of cancer treatment due to their efficacy across a spectrum of cancer types. Operating as broad-spectrum chemotherapeutic agents, taxanes exert cytotoxic effects on proliferative cancer cells by binding to and stabilizing microtubules, disrupting mitosis, inducing mitotic catastrophe, and resulting in cell death. The distinct proliferative nature of cancer cells, as opposed to less proliferative non-cancer cells, affords taxanes a measure of specificity and selectivity. Nevertheless, sporadic yet recurring evidence suggests that taxanes also operate through non-mitotic mechanisms. Taxanes' binding and stabilization of microtubules lead to micronucleation and subsequent cell death, impacting both mitotic and non-mitotic cells. Recent discoveries indicate that the flexible and weakened nuclear envelope of malignant cells renders them sensitive to taxane-mediated micronucleation and cell death during various phases of the cell cycle. Conversely, non-cancerous cells typically exhibit a more robust and sturdy nuclear envelope, rendering them more tolerant to taxane-induced nuclear envelope fragmentation and subsequent micronucleation and cell death. The expression levels of nuclear envelope structural proteins, particularly Lamin A/C, emerge as indicators of taxane sensitivity. This evolving understanding underscores that nuclear envelope malleability, in conjunction with a high proliferation rate, is a pivotal determinant of taxane specificity and selectivity against malignant cells. These insights necessitate reconsidering oncological strategies to augment taxane efficacy, overcome resistance, and mitigate side effects.

Breast cancer, as a malignant tumor with easy metastasis and poor prognosis, threatens the health of women around the world. Increasing studies have shown that the Bcl-2 family of apoptosis-related proteins is often expressed abnormally in breast cancer. The Bcl-2 homology 3 (BH3) mimetic peptide can bind and neutralize Bcl-2, preventing its binding to the apoptosis "effector" proteins Bak and Bax, thereby promoting the apoptosis process. However, there is a lack of effective intracellular delivery system for BH3 to exert its biological activity. Therefore, this study utilized an activatable supercharged polypeptide (ASCP) tumor-targeted delivery platform based on pH and protease response to achieve the targeted release of BH3 at the tumor site. Ultimately, intracellular delivery of BH3 was achieved and induced apoptosis of breast tumor cells, preventing the development of breast cancer.

The latent transforming growth factor-beta (TGF-β) binding protein 1 (LTBP1) has been implicated in various cellular processes, but its role in triple-negative breast cancer (TNBC) remains unclear. In this study, we investigated the impact of LTBP1 on TNBC progression and its underlying mechanisms. Analysis of online datasets revealed elevated LTBP1 mRNA expression in breast cancer tissues compared to normal adjacent tissues. Kaplan-Meier Plotter analysis indicated that high LTBP1 expression was negatively correlated with relapse-free survival (RFS), distant-metastasis free survival (DMFS), and overall survival (OS) of breast cancer patients. Additionally, LTBP1 mRNA levels were associated with chemotherapy resistance. Functional assays in TNBC cells demonstrated that LTBP1 knockdown suppressed cell proliferation, induced apoptosis, and attenuated migration and invasion. In vivo studies confirmed that LTBP1 knockdown inhibited tumor growth in a xenograft mouse model. Mechanistically, LTBP1 positively correlated with genes involved in signaling regulation and organelle organization, with significant associations to GTPase binding and the RhoA/ROCK pathway. LTBP1 knockdown reduced RhoA activity and phosphorylation of Myosin Light Chain 2 (MLC2), suggesting inhibition of the RhoA/ROCK signaling pathway. Moreover, activation of the RhoA/ROCK pathway partially rescued the effects of LTBP1 knockdown on TNBC cell proliferation, apoptosis, migration, and invasion. In conclusion, our findings suggest that LTBP1 promotes TNBC progression through activation of the RhoA/ROCK signaling pathway, highlighting its potential as a therapeutic target for TNBC.

Although docetaxel treatment yields a high survival rate for prostate cancer (PCa), resistance eventually develops in many patients. Understanding the underlying mechanisms of docetaxel resistance is essential for improving treatment strategies. Cytokines, which play a role in cell signaling and immune responses, have been implicated in drug resistance mechanisms. The study revealed that interleukin-8 (IL-8) was consistently overexpressed in both docetaxel-resistant PCa cell lines. Thus, the expression levels of cytokines released from docetaxel-sensitive (PC-3- and DU-145) and resistant (PC-3/R-DU-145/R) PCa cells were compared. IL-8 was found to be commonly expressed in resistant cell lines. This finding led to the hypothesis that IL-8 could play a key role in mediating PCa cell resistance to docetaxel. IL-8 siRNA treatment increased docetaxel sensitivity in both resistant cells. To demonstrate the mechanism of IL-8-related resistance, MDR1 expression was evaluated. After IL-8 siRNA treatment MDR1 expression was reduced in both resistant cells suggesting that IL-8 regulates the docetaxel resistance of PCa cells via modulation of multidrug resistance 1 (MDR1). By expanding the knowledge of the cytokines and their effect mechanisms, novel approaches can be developed for the treatment of docetaxel-resistant prostate cancer. Further investigations into the role of IL-8 in docetaxel resistance could offer valuable insights into the development of effective treatment strategies for PCa patients.

Lung cancer is the leading cause of cancer-related deaths. Non-small cell lung cancer (NSCLC) accounts for about 85% of all lung cancers, and lung adenocarcinoma is the most common NSCLC. Most patients with lung cancer eventually lead to local and metastatic recurrence, including many patients who have completely removed the primary tumor during surgery and have no noticeable metastasis. There are two different deoxynucleotide triphosphate (dNTP) libraries in eukaryotic cells. The de novo synthesis of dNTPs in the cytoplasm is coordinated with the cell cycle and reaches a peak in the S phase, thereby providing deoxynucleotides for the replication of genomic DNA. In contrast, the mitochondrial pool of dNTPs is maintained through the mitochondrial deoxynucleoside rescue pathway throughout the cell cycle and is essential for mtDNA replication. Mitochondria are vital cell powers in assimilation and catabolism. Oxidative phosphorylation (OXPHOS) of mitochondria is essential for the self-renewal of cancer stem-like cells in lung cancer, glioblastoma and leukemia. Thymidine kinase 2 (TK2) and deoxyguanosine kinase (DGUOK) are two mitochondrial deoxynucleoside kinases, which are responsible for the transport of pyrimidine and purine deoxynucleoside in mitochondria. Apoptosis and autophagy are important processes that regulate cell proliferation and death in normal cells and cancer cells. Inducing cancer cell apoptosis and autophagy is an effective means to treat malignant tumors. This review discusses the research progress of the relationship between mitochondrial deoxyguanosine kinase and lung adenocarcinoma cell apoptosis and autophagy.

With the improvement of people's living standards and the increasing emphasis on health, new and higher demands are also placed on the medical industry. The diagnosis and treatment methods combining artificial intelligence and medicine are bound to receive more and more attention and promotion. At present, drug design is stepping into the era of artificial intelligence, and academia and industry are actively applying artificial intelligence technology to all aspects of drug research and development, including drug screening, molecular characterization, drug activity and druggability optimization, chemical reaction design, etc. Relying on the big data information of millions of patients, the artificial intelligence system can quickly and accurately mine and screen out suitable drugs. Through computer simulations, artificial intelligence can make predictions about drug activity, safety, and side effects, and find the best drug that matches the disease. This technology will shorten the drug development cycle, reduce the cost of new drugs and improve the success rate of new drug development.

Ferroptosis, a recently identified form of programmed cell death, is characterized by the accumulation of lipid peroxidation, reactive oxygen species, and elevated free iron levels, involving the regulation of glutathione metabolism, iron metabolism, lipid metabolism, and oxidative stress biology. Tumor metastasis, a critical hallmark of malignancy and a key contributor to cancer recurrence and mortality, has been extensively linked to iron dysregulation, highlighting the potential of agents inducing iron-mediated cell death as promising strategies for preventing and treating metastasis. This review offers a comprehensive understanding the regulatory mechanisms underlying ferroptosis and its crucial role in the three distinct stages of metastasis: invasion, circulation, and colonization.

Cancer, a pervasive threat to human health, presents formidable challenges to traditional treatment approaches. Tumor immunotherapy has emerged as a promising strategy for combating malignancies by bolstering the body's immune response to thwart tumor metastasis and recurrence. Nonetheless, the intricacies of tumors, patient heterogeneity, and the presence of tumor-immunosuppressive microenvironments have limited the overall efficacy of immunotherapy, achieving only approximately a 20% success rate. In recent years, nanomaterials have garnered increasing attention in the realm of tumor immunotherapy due to their inherent advantages, such as excellent biocompatibility, precise targeting, and controlled drug release. Nanomaterials empower immunostimulatory molecules and therapeutic agents with the ability to specifically target tumors, amplify drug accumulation at tumor sites, facilitate local immune modulation, alleviate immunosuppressive microenvironments, and thereby enhance the effectiveness of tumor immunotherapy. This review provides an overview of the current state of immunotherapy and offers insights into the ongoing research progress surrounding various nanomaterials aimed at augmenting the efficacy of immunotherapy.

Background: Hepatocellular carcinoma (HCC) stands out as one of the most lethal cancers globally, given its complexity, recurrence following surgical resection, metastatic potential, and inherent heterogeneity. In recent years, researchers have systematically elucidated the significance of long non-coding RNA (lncRNA) in the initiation and progression of HCC. The introduction of The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases has significantly enhanced the prognostic assessment of HCC. However, the association between HCC and cell senescence has been infrequently explored in the literature. Method: We downloaded liver hepatocellular carcinoma (LIHC)-related messenger RNA and lncRNA expression levels from TCGA. Correlation analysis, Cox regression, and least absolute shrinkage and selection operator (LASSO) regression analysis were employed to validate the lncRNA risk model associated with cellular aging. Comparing the infiltration of diverse immune cells enabled the identification of distinct differences in the immunological microenvironments of the two risk groups. Subsequently, we conducted a real-time polymerase chain reaction (qPCR) experiment to confirm the accuracy of the selected lncRNAs. Results: A predictive framework for HCC was constructed based on the expression levels of five lncRNAs. Multivariate and univariate Cox regression analyses revealed that lncRNA signatures associated with senescence were independently correlated with an increased risk of HCC. Additionally, the nomogram also provides a more refined and sensitive model. Further investigation into the variations in immune cells and functions between the high-risk and low-risk groups was conducted. Subsequently, a qPCR experiment results revealed underexpression of AC068756.1, AC090578.1, AC145343.1, and LINC0022 in Huh7 and LM3 cells. In contrast, AP003392.4 did not exhibit a significant difference between Huh7 and control cells. Conclusion: The prognostic features and nomogram, consisting of five aging-related lncRNAs (AC068756.1, AC090578.1, AC145343.1, AP003392.4, and LINC00221), may be useful in predicting the overall survival of HCC.