1p36.33

MIRN200B,mir-200b

Tumor cell proliferation

Multiple roles of miR-200b in cell cycles regulation and tumor cell proliferation were reported in human cancers. MiR-200b could directly target RND3 which could induce expression of cyclin D1 thereby promoting S-phase entry (Xia, Li et al. 2010). MiR-200b could also regulate cell cycle by targeting GATA4 and its downstream protein cyclin D1 which could affect cell proliferation (Yao, Wei et al. 2013). In human TGFBR2-null colorectal cancers, miR-200b could stimulate tumor growth by targeting CDKN1B (p27/kip1). It was also found that miR-200b could promoter cell proliferation by targeting p27/kip1 (Fu, Liu et al. 2014).

Tumor cells invasion and cancer metastasis

Abnormal expressions of miR-200b were found in various cancers, including breast cancer, colon cancer, nasopharyngeal carcinoma, urothelial carcinoma and prostate cancer. MiR-200b could directly targeting SUZ12 and ROCK2 thus inhibit cholangiocarcinoma tumourigenesis and metastasis (Peng, Jiang et al. 2013). In gastric carcinoma, miR-200b was found to target ZEB2 and thereby repress tumor cell invasion and migration (Kurashige, Kamohara et al. 2012).

Repression of epithelial-mesenchymal transition (EMT)

EMT is an important pathological progression and studies revealed vital roles of miR-200b in EMT regulation. MiR-200b could inhibit TGFB1-induced epithelial-mesenchymal transition by targeting SMAD2 intestinal epithelial cells and SMAD2 could repress expression of vimentin, which indicated regulation role of miR-200b on vimentin (Chen, Xiao et al. 2013). Also, the role of miR-200b in EMT regulation was observed in EMT induced by transforming growth factor-beta1 in kidney proximal tubular cells by directly target the 3-UTR of fibronectin (Tang, Chen et al. 2013).

Chemoresistance

Chemoresistance is the main cause of tumor relapse. Ectopic expression of miR-200b could reduce the chemoresistance of cells by targeting BIM1 in human tongue cancer cells. In human lung adenocarcinoma cells, miR-200b could target E2F3 to sensitize tumor cells to chemotherapy agents.