There is a growing interest in the role of the miRNA family in human cancer. The miRNA-192 family is a group of conserved small RNAs, including miR-192, miR-194, and miR-215. Recent studies have shown that the incidence and mortality of breast cancer have been increasing epidemiologically year by year, and it is urgent to clarify the pathogenesis of breast cancer and seek new diagnostic and therapeutic methods. There is increasing evidence that miR-192 family members may be involved in the occurrence and development of breast cancer. This review describes the regulatory mechanism of the miRNA-192 family affecting the malignant behavior of breast cancer cells and evaluates the value of the miRNA-192 family as a diagnostic and prognostic biomarker for breast cancer. It is expected that summarizing and discussing the relationship between miRNA-192 family members and breast cancer, it will provide a new direction for the clinical diagnosis and treatment of breast cancer and basic medical research.

MicroRNAs (miRNAs) constitute a class of small non-coding RNAs that play a pivotal role in post-transcriptional gene regulation. The dysregulation of miRNAs has been widely implicated in the pathogenesis of diverse human cancers. Among these, miR-205 has attracted considerable attention owing to its aberrant expression patterns in multiple cancer types, where it regulates tumor initiation and progression via diverse molecular mechanisms. Apoptosis, a fundamental biological process essential for cellular homeostasis, represents a tightly regulated form of programmed cell death that significantly influences cancer development under both physiological and pathological conditions. In malignant cells, miR-205 exhibits a dual regulatory role by modulating apoptosis-related signaling pathways and their downstream target genes, thereby displaying both oncogenic and tumor-suppressive functions. This comprehensive review systematically explores recent advances in understanding the functional role of miR-205 in apoptosis regulation across a spectrum of human malignancies and highlights its potential therapeutic implications for future cancer therapies.

Breast cancer (BC), as a highly prevalent malignant tumor worldwide, is still unclear in its pathogenesis and has poor therapeutic outcomes. Alternative polyadenylation (APA) is a post-transcriptional regulatory mechanism widely found in eukaryotes. Precursor mRNA (pre-mRNA) undergoes the APA process to generate multiple mRNA isoforms with different coding regions or 3′UTRs, thereby greatly increasing the diversity and complexity of the eukaryotic transcriptome and proteome. Studies have shown that APA is involved in the progression of various diseases, including cancer, and plays a crucial role. Therefore, clarifying the biological mechanisms of APA and its regulators in breast cancer will help to comprehensively understand the pathogenesis of breast cancer and provide new ideas for its prevention and treatment.

The objective of this study was to find the key regulatory molecules in the cell senescence process through observing the expression of telomere-associated factor during the normal cell replicative senescence process. Based on the established cell replicative senescence model, reverse transcription-polymerase chain reaction and western blot analyses were used to detect telomere-associated factor expression at the mRNA and protein levels, including that of human telomere binding protein 1, tankyrase 1, telomerase RNA, telomere protection protein 1 (POT1), and p53 during the process of human embryonic lung fibroblast replicative senescence. The results showed that transcription of human telomere binding protein 1 did not change with cell senescence, whereas the protein expression of human telomere binding protein 1 increased gradually and then decreased rapidly; there was no change in the mRNA and protein expression of POT1; with the replicative senescence of human embryonic lung fibroblasts, expression of POT1 decreased gradually; TRF1 showed an increasing trend with cell senescence; and p53 protein expression did not change. Together, the results from this study suggest that human telomere binding protein 1, POT1, and TRF1 played important roles in cell senescence.

In recent years, the role of microRNAs (miRNAs) in disease has attracted considerable interest, underscoring their potential utility as diagnostic biomarkers. miR‑100, belonging to the miR‑99 family, is integral to the pathophysiological processes underlying numerous diseases. miR‑100 has been found to influence the pathogenesis of a variety of noncancerous diseases. As for cancer, this factor plays a significant role in various tumors throughout diverse systems, influencing essential processes including cell proliferation, invasion, migration and apoptosis of cancerous cells. This review examines the existing literature on miR‑100 in the context of non‑cancerous diseases and cancer, investigates its mechanisms of action across different diseases and considers its potential role as a diagnostic biomarker as well as its involvement in cancer drug resistance.

Βreast cancer (BC) is the most common malignant tumor among women. Its significant heterogeneity and complex molecular mechanisms pose major clinical challenges, including limited therapeutic efficacy and drug resistance. Recently, microRNAs (miRs) have been recognized as key post‑transcriptional regulators involved in tumorigenesis and tumor progression through multiple pathways. Among these, the miR‑200 family (miR‑200a, miR‑200b, miR‑200c, miR‑429 and miR‑141) has attracted considerable attention due to its pivotal role in BC. The present review systematically summarizes the genomic characteristics, expression regulation mechanisms and biological functions of the miR‑200 family in BC. Special emphasis is given to their roles in epithelial‑mesenchymal transition, cell proliferation, apoptosis, maintenance of stemness, and remodeling of the tumor microenvironment. Furthermore, members of the miR‑200 family have potential as diagnostic and prognostic biomarkers and are closely linked to chemotherapy resistance. The present review aims to provide novel insights and a theoretical foundation for the diagnosis, treatment, and deeper investigation of BC by comprehensively examining the functional mechanisms of the miR‑200.