miR-200-b overexpression

Silencing of MATN1-AS1 in cervical cancer cell lines can reduce the expression of Mir-200b. Matn1-as1 can regulate the expression of Mir-200b and participate in the occurrence and development of cervical cancer.

L-Fucose inhibited the progression of CCA via the miR-200b/MAPK7 and signal transducer and activator of transcription 3 signaling pathways.

Some of them showed a fair accuracy and strong relationship between specific miRNA over or under-expression and survival outcomes. However, results from these studies are preliminary and miRNAs use in routine clinical practice is still far to come.

CCAT2 promoted the migration and invasion of ESCC cells in vitro, and tumorigenesis in vivo by upregulating TK1 expression, while overexpression of miR-200b reversed these effects of CCAT2. Overall, this study suggests that CCAT2 competitively binds to miR-200b to alleviate its inhibitory effects on IGF2BP2 expression, resulting in elevated TK1 expression, and an ensuing promotion of the development of ESCC.

Using rescue experiments, the increased migratory ability of the miR‑200b‑overexpressing cells was reversed by ETS1 overexpression. In summary, this study showed that miR‑200b overexpression serves a carcinogenic role and promotes the migration of BEAS‑2B cells following long‑term exposure to CS by targeting ETS1.

Overall, our results demonstrated that miR-200b was highly expressed in the plasma-derived exosome of ovarian cancer patients, and promoted the proliferation and invasion of ovarian cancer cells through inducing macrophage M2 polarization by suppressing KLF6 expression. Our results suggested that miR-200b might be a novel target for ovarian cancer treatment.