MIR449A (MicroRNA 449a)

Finally, NOTCH1 could reduce the radiosensitivity of cervical cancer cells to radiotherapy both in vitro and in vivo; whereas has-miR-449a, as an upstream regulatory miRNA of NOTCH1, could inhibit cervical cancer cell proliferation and enhance radiosensitivity by inhibiting NOTCH1 expression. This study clarifies NOTCH1's role in promoting cervical cancer progression and reducing radiosensitivity, with has-miR-449a as a negative regulator, providing targets for optimizing cervical cancer radiotherapy.

In summary, we discovered that ablation of miR-34/449 led to hyperactivation of the Wnt/β-catenin signaling pathway, which resulted in the differentiation impairment of ciliated cells, thus resulting in infertility in the mice. This study revealed a novel mechanism describing how miR-34/449 affects oviductal ciliated cell differentiation and oviductal epithelial homeostasis through the Wnt/β-catenin signaling pathway and finally affects fertility.

This is the first study to provide insights into the FGT miRNA profiles following Nb and HSV-2 single and co-infection, as well as the predicted genes and pathways they regulate, which may influence host immunity and pathology. This study highlights the role of miRNAs in regulating FGT immunity and pathology in the context of STH/HSV-2 co-infection.

Extracellular vesicle miRNAs add a layer of complexity, acting as mediators in CD's systemic effects. Finally, we outline future perspectives, envisioning how the evolving landscape of miRNA research can propel advancements in understanding, diagnosis, and treatment, marking this review as a cornerstone for researchers and clinicians in the dynamic field of miRNAs and CD.

Overall, our findings suggest that hsa-miR-27a-5p and hsa-miR-449a, identified through bioinformatics and microarray-based expression analyses, could serve as promising biomarkers for BC detection. Their significant association with the MAPK signaling pathway was determined through bioinformatics analysis.

These findings suggest that this miRNA signature has potential to be used as a diagnostic and prognostic biomarker and could serve as a foundation for future therapeutic strategies for endometrial cancer. However, further experimental validation is needed to confirm its clinical applicability.

Our findings demonstrate, for the first time, that cisplatin-treated medulloblastoma cells from distinct molecular subgroups secrete EVs with altered miRNA expression profiles that either inhibit or promote the growth of recipient cancer cells. This underscores the potential of targeting EV-mediated communication as a novel therapeutic strategy in medulloblastoma.

Finally, a nomogram was constructed to forecast the 1-year, 3-year, and 5-year survival probabilities of PCa patients. In summary, our study demonstrates the significant role of the ceRNA-based LINC01122/TPD52 axis in the progression of PCa and its correlation with prognosis.

Moreover, microRNAs-449 overexpression and FASN inhibition decreased cell proliferation and sensitized cells to trastuzumab treatment by inhibiting the PI3K/AKT signaling pathway. Together, these results suggest the microRNAs-449/FASN axis as a potential therapeutic target in combination with anti-HER2 agents to overcome trastuzumab resistance and to improve treatment response in HER2-positive breast cancer patients.

The study demonstrated that these miRNAs could influence critical processes such as angiogenesis, proliferation, inflammation, tumorigenesis, and apoptosis in cancer cells, highlighting their potential as therapeutic targets. However, the varied effects observed with the co-transfection of mimics and inhibitors suggest a complex interplay that requires further investigation.

Pharmacological MPC inhibition induces a similar metabolic shift, reducing metastatic potential and leading to cell cycle exit. Overall, miR-449 and miR-340 orchestrate FN-RMS cell identity, positioning MPC inhibition as a strategy to shift FN-RMS cells toward a non-tumorigenic, quiescent state.

The present study demonstrated that lncRNA EGFR-AS1 was essential for the development of NSCLC through its function as a competitive endogenous RNA binding to miR-449a and upregulating histone deacetylase 1. In brief, it identified a novel signaling pathway that mediated the invasion and metastasis of NSCLC and may therefore provide a new treatment target for NSCLC.