1p36.33

MIRN200A,mir-200a

Tumor cell proliferation

MiR-200a showed its roles in regulation of tumor cell proliferation. In human endometrial adenocarcinoma cell line HEC-1B, repression of miR-200a could increase the tumor suppressor gene PTEN and thus inhibit cell proliferation and promote cell apoptosis, which showed the oncogenic role of miR-200a (Li, He et al. 2014). However, studies in breast cancer also demonstrated that miR-200a could attenuate cell proliferation by targeting Mitochondrial Transcription Factor A (Yao, Zhou et al. 2014). As well, miR-200a was also proved to impair glioma cell growth by targeting SIM2-s (Su, He et al. 2014).

Tumor cells invasion and cancer metastasis

As a member of miR-200 family, miR-200a showed its regulation roles in cancer cells invasion and migration. By targeting SIM-2, miR-200a could inhibit glioma cell migration and invasion (Su, He et al. 2014). In CD133/1+ ovarian cancer stem cells, miR-200a could inhibit cell migration and invasion by repressing expression of Zeb2 (which is a repressor of E-cadherin) (Wu, Guo et al. 2011). However, in human breast cancer cells, it was found that miR-200a could target YAP1 thus induce anoikis resistance and metastasis (Yu, Hu et al. 2013).

Repression of epithelial-mesenchymal transition (EMT)

Roles of miR-200 family in EMT regulation were intensively studied. As miR-200a, it was reported that miR-200a could regulate EMT by targeting SIRT1 and mammary epithelial cells (Eades, Yao et al. 2011). In hepatic oval cells, downregulation of miR-200a induces EMT phenotypes and CSC-like signatures by directly targeting beta-catenin (Liu, Ruan et al. 2013).