MIR134 (MicroRNA 134)

The overexpression of miR-139-3p in BC cells enhanced cisplatin, olaparib, and irradiation (IR) sensitivity. The diagnostic model based on the four circulating miRNAs could serve as a tool for the liquid biopsy of BC. Targeting the miR-139-3p/RPA2 axis may have potential in modulating the DNA damage pathway in BC.

In particular, strategies that restore or inhibit miRNA activity using mimics or antagomiRs show promise in improving drug sensitivity and complementing current treatment options. Overall, emerging evidence supports the integration of miRNA profiling into precision oncology for SCLC, with the aim of refining diagnosis, risk assessment and therapeutic decision-making.

Tumor suppressor miR-1343-3p inhibited gastric cancer cell proliferation by regulating OGDHL/PDHB-pyruvate glucose metabolism axis, which lay a better basis for targeted therapeutic strategy in cancers.

In addition, comparative analyses revealed conserved gene signatures in human basal cell carcinoma of the eyelids, emphasizing the importance of canine models in translational oncology. This comprehensive molecular characterization provides new insights into the pathogenesis of canine eyelid melanoma and identifies key biomarkers and pathways that may be relevant for future therapeutic interventions in veterinary and comparative oncology.

Propofol exerted an antitumor role in EC advancement at least partly through the circ-PTK2/miR-134-5p/PARP9 axis, providing new insight into the involvement of circRNAs in propofol-mediated effect on EC progression. This study also provides evidence that circ-PTK2 could be developed as a potential therapeutic target for EC patients.

Increased TYMSOS was linked to adverse prognosis, malignant progression, and immune escape in cervical cancer by modulating miR-134-5p/KRAS axis.

Mechanistically, ELDR functions as a competitive endogenous RNA (ceRNA) by sequestering tumor-suppressive miR-1343-3p in the cytoplasm, which consequently leads to the upregulation of the oncogene TRIM44. Our findings unveil the ELDR/miR-1343-3p/TRIM44 axis as a crucial pathway in BCa progression, establishing ELDR as a promising prognostic biomarker and an attractive candidate for the development of targeted therapies.

Validation across the total dataset and five GSE datasets (GSE106817, GSE112264, GSE113486, GSE113740, and GSE164174) yielded AUCs of 0.997, 0.999, 1.000, 1.000, 0.996, and 0.994, respectively. The novel miRNA set comprising miR-1290, miR-5100, miR-1343-3p, miR-8073, miR-4706, and miR-4787-3p holds promise as a diagnostic classifier for GC screening.

This preliminary study demonstrated that miR-107, miR-134-5p, miR-149-5p, and miR-370-3p were significantly overexpressed in PCa patients compared to the BPH group. ROC analysis highlighted their diagnostic potential in distinguishing BPH from PCa. Despite the limited sample size, these findings provide early evidence to guide future research on the diagnostic value of miRNAs in prostate cancer.

In this study, we demonstrated that LINC01063 can be used as an independent prognostic marker for colon cancer and explored its promotion of colon cancer cancer progression through the miR-134-5p/KRAS axis. Future studies will focus on in vivo validation and elucidation of downstream signaling cascades, while clinically, LINC01063 holds potential as a prognostic indicator and a therapeutic target for KRAS-mutant colon cancer, aiding in personalized treatment strategies.

In contrast, GC cells in the miR-1343-3p inhibitor group showed decreased expression of miR-1343-3p and increased expression of SOX18 mRNA and protein (all P < 0.05). Salidroside may inhibit the proliferation of GC cells by regulating the miR-1343-3p/SOX18 signaling axis and these regulators may present new potential therapeutic targets or biomarkers for gastric cancer.

Additionally, the external validation datasets showed an AUC exceeding 95%, confirming the robustness and reliability of our findings. Furthermore, functional annotation analysis revealed the involvement of several miRNA-mediated pathways in the pathogenesis of CRC.