miR-1306 Mediates the Feedback Regulation of the TGF-ß/SMAD Signaling Pathway in Granulosa Cells

Yang, Liu; Du, Xing; Liu, Lu; Cao, Qiuyu; Pan, Zengxiang; Li, Qifa

The expression of TGFBR2, in vivo or in vitro, is controlled by multiple factors, including genetic and epigenetic factors [10] [11] [12] [13] . At the genetic level, for instance, the TGFBR2 protein was truncated and inactivated because of TGFBR2 mutations, thus inhibiting its growth regulatory functions in microsatellite instability-high (MSI-H) cancers [14] . Besides, TGFBR2 is also known to be regulated by several transcription factors such as zinc finger protein 32 (ZNF32) [15] and/or co-activators such as yes-associated protein 1 (YAP-1) [16] . At the epigenetic level, TGFBR2 expression is widely regulated by various factors, such as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) [17, 18] . For example, miR-93 down-regulates its target gene, TGFBR2, in prostate cancer and leads to acceleration of cell growth and invasion [19] . miRNA-520f and miR-7 are known to suppress TGFBR2 and inhibit epithelial-mesenchymal transition of epithelial cells [20, 21] . Furthermore, lncRNAs usually regulate TGFBR2 expression by interacting with miRNAs. A recent study reported that lnc-small nucleolar RNA host gene 1 (lnc-SNHG1), an overexpressed lncRNA found in the tumor tissues and cells lines originating from invasive pituitary cancer, directly binds to miR-302/372/373/520 and promotes expression of their common target, TGFBR [22] .