MIR141 (MicroRNA 141)

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.

Furthermore, we identified miR-141 as a negative regulator of NPY1R, highlighting its potential as a therapeutic agent. Collectively, our results identified the UHRF1/NPY1R regulatory axis as a critical epigenetic mechanism in intestinal inflammation and underscored its dual promise for IBD diagnostics and therapy.

Although promising, clinical implementation of miRNA-based assays requires further validation, standardization of protocols, and large-scale prospective studies. Harnessing circulating miRNAs could usher in a new era of precision oncology for PCa, improving early diagnosis, prognostication, and real-time therapeutic guidance.

This review synthesizes the current evidence on the ncRNA-mediated regulatory networks that influence CRC radiosensitivity, emphasizing their potential as therapeutic targets to overcome RT resistance and improve outcomes in advanced CRC. By bridging mechanistic insights with clinical applications, this work aims to guide future research and the implementation of precision RT strategies.

We established the new radiotranscriptomic signatures specifically optimized for differentiating T3b stage from T2c stage by decoding stage-specific imaging-genomic crosstalk. This new approach may overcome TNM staging limitations.

Among the miRNA alterations associated with stage I adenocarcinoma in nonsmokers, we found alterations in all 5 miR-200 family members (miR-200b, miR-200a, miR-141, miR-429, and miR-200c). Our identification of miRNA alterations associated with early-stage lung adenocarcinoma in nonsmokers, especially alterations in the miR-200 family, suggests that these miRNAs may play a unique role in the early stages of lung carcinogenesis and progression in nonsmokers and that they may be useful as markers for the early detection of lung cancer.

These findings suggest that hsa-miR-150-5p is a key regulator in HCV-associated liver disease, with upregulation observed in both HCV and HIV-HCV coinfection groups, potentially influencing transcriptional and network-level regulation. This systems-level framework highlights miR-150-5p as a potential biomarker for HCV and HIV-HCV associated liver pathology, providing a basis for future studies toward precision interventions in viral coinfection-mediated oncogenesis.

Key markers such as miR-141, miR-375, and PCA3 showed strong diagnostic and risk stratification value in PCa. This non-invasive approach holds promise for improving early detection and clinical risk assessment.

Both the authors and the Editor of International Journal of Molecular Medicine apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 37: 1601‑1610, 2016; DOI: 10.3892/ijmm.2016.2553].

Evaluation of miRNAs commonly deregulated between the three groups showed 14 shared upregulated miRNAs (miR-429, miR-425-5p, miR-200c-3p, miR-200c-5p, miR-200b-3p, miR-200a-3p, miR-183-5p, miR-182-5p, miR-141-5p, miR-141-3p, miR-96-5p, miR-93-5p, miR-10a-5p, miR-10a-3p) with a progressive increase in expression levels, from ovarian EMS to TL and ultimately to ECOC. The identified miRNA expression profiles associated with the progression from ovarian EMS, TL and ECOC provide valuable insights into the molecular progression from benign to malignant lesions and could represent potential biomarkers for the early detection of ECOC.

By integrating RCA with HCR-mediated MNAzyme assembly in a programmable DNA logic framework, this design provides multi-level cascade amplification at room temperature, significantly improving both sensitivity and specificity. The platform thus represents a versatile tool with strong potential for precision oncology, clinical diagnostics, and point-of-care testing.

Moreover, circANKRD52 could bind to miR-141-3p, leading to upregulation of PRKACB, and downregulation of miR-141-3p restored melanoma cell growth and invasion. Our findings demonstrate that circANKRD52 promotes the growth and angiogenesis of melanoma cells by sponging miR-141-3p and upregulating PRKACB.