Finally, FBXL19-AS1/miR-203a-3p axis was found to associate with baculoviral IAP repeat-containing protein 5.1-A-like (survivin), distal-less homeobox 5, E2F transcription factor 1, and zinc finger E-box binding homeobox 2 to regulate metastasis in LUAD cells.
In conclusion, our study suggests that circAGFG1 promotes NSCLC growth and metastasis though a circAGFG1/miR-203/ZNF281 axis and may represent a novel therapeutic target.
Furthermore, the role of miR-203 in PCa cell proliferation, colony formation, cell cycle and metastasis capacities was detected through a series of in vitro experiments.
It is considered that miRNA de-regulation contributes to tumor progression and metastasis in various cancers, and MiR-203a has been identified as a tumor suppressor in cancers, such as glioma, gastric cancer and hepatocellular carcinoma.
Mechanistically, circ-ZNF652 could physically interact with miR-203 and miR-502-5p to increase the expression of their common target gene Snail (a key transcription factor that triggers EMT), thereby promoting the metastasis of HCC.
As miR‑203a‑3p was determined to target THBS2 to inhibit CRC progression and metastasis; thus, miR‑203a‑3p may be considered as a potential novel approach to treating CRC.
MicroRNA-203 is highly expressed in NSCLC, and is closely related to tumor stage, lymph node metastasis, distant metastasis and poor prognosis of NSCLC patients.
MicroRNA-203 (miR-203) is known to suppress the proliferation and metastasis of hepatocellular carcinoma, but the role in the progression of alcoholic liver disease is not clear and is warranted for further investigation.
Taken together, our research indicated a CCDC26/miR-203 pathway in regulating the growth and metastasis of gliomas, providing new viewpoints and promising targets for glioma therapy.
These findings suggest that miR-26 and miR-125b may be associated with the progression and metastasis of HNSCC and that miR-203 is associated with a more favorable prognosis.
We show that miR-203-HOTAIR interaction resulted in the inhibition of epithelial-to-mesenchymal transition (EMT) and metastatic genes as indicated by induction of key metastasis-suppressing proteins E-cadherin, claudin (epithelial markers), and PTEN along with induction of tumor suppressor genes p21 and p27.
We further showed that miR-203 expression attenuated the TGFβ pathway in both SKOV3 and OVCAR3 cells. miR-203 expression also inhibited primary tumor growth in ovaries and metastatic tumors in multiple peritoneal organs including liver and spleen.
Importantly, miR-203 overexpression markedly inhibited the proliferation, invasion and metastasis of hepatic residual HCC through suppressing expression of Ki67, CAPNS1 and lung metastasis.