MIR1299 (MicroRNA 1299)

Finally, dual-luciferase reporter assays confirmed that circAGFG1 acts as a sponge for miR-1299, thereby potentially modulating the miR-1299 signaling pathway. Collectively, our findings delineate the critical role of the circAGFG1 in promoting TNBC progression, highlighting its potential as a novel therapeutic target.

In summary, inhibiting the oncogenic miRNAs and ectopic expression of tumor-suppressive miRNAs can decrease prolactin secretion, reduce tumor invasion and migration, enhance dopamine agonist efficacy, and inhibit prolactinoma development. These findings can serve as a blueprint for future translational studies investigating miR-based therapeutics for prolactinoma.

Importantly, the data indicated that the suppression of Hsa_circ_0007718 led to a marked decrease in the proliferation rates, migratory potential, and invasive capabilities of CRC cells. Furthermore, the study confirmed that Hsa_circ_0007718 acts as a downstream target of miR-1299, exerting its regulatory effects by inhibiting miR-1299 and thereby promoting the expression of PSMC2.

The miRNA targets were enriched in pancreatic carcinogenesis/progression-related pathways. Our study suggests that circulating miRNAs may identify individuals at high risk for pancreatic cancer ≤5 years prior to diagnosis, indicating its potential utility in cancer screening and surveillance.

Finally, KCNQ1OT1 was bound to miR-1299 to upregulate PDPK1 expression in CESC cells. Collectively, miR-1299 was regulated by KCNQ1OT1 and inhibited CESC progression in vivo and in vitro, suggesting the tumor-suppressor role of miR-1299 for CESC.

We present four models involving eleven miRNAs to differentiate healthy controls from different types of BC cases. Our models scarcely overlap with those previously reported.

In addition, circ_0088046 silencing constrained tumour formation in vivo. Circ_0088046 contributed to HCC cell malignancy via modulating the miR-1299/RTKN2 axis.

Silencing LINC01133 or IGF2BP3 and/or overexpressing miR-1299 limited pancreatic cancer cell proliferation, invasion, epithelial-mesenchymal transition, and suppressed tumorigenic abilities in mice lacking T cells (nude mice). Overall, our findings identified that silencing LINC01133 downregulates IGF2BP3 by upregulating miR-1299 expression, ultimately leading to the prevention of pancreatic cancer.

Silencing circEGFR inhibited the malignant progression of the tumor. These results revealed circEGFR is a promising biomarker for TNBC diagnosis, therapeutic and prognosis.

Our findings showed that hsa_circ_0001925 mediated TNBC progression via regulating miR-1299/YY1 axis, providing a potential target for BC treatment.

Radiosensitivity in vivo was also elevated by silence of circPPFIA1 via regulating miR-1299 and TXNRD1 levels. All experimental data showed that knockdown of circPPFIA1 contributed to radiosensitivity in ESCC by inducing miR-1299-related downregulation of TXNRD1.

HMGB3 elevation offset the suppressive impact of miR-1299 mimic on the malignancy of NSCLC cells under TSIIA treatment. TSIIA curbed NSCLC progression by the circ_0020123/miR-1299/HMGB3 axis, manifesting that the TSIIA/circ_0020123/miR-1299/HMG regulatory network might be a potential treatment strategy for NSCLC.