LncRNA SNHG7 sponges miR-216b to promote proliferation and liver metastasis of colorectal cancer through upregulating GALNT1.
LncRNA SNHG7 sponges miR-216b to promote proliferation and liver metastasis of colorectal cancer through upregulating GALNT1.
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DOI:
10.1038/s41419-018-0759-7
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发表时间:
2018-06-18
影响因子:
9
通讯作者:
Jia L
中科院分区:
文献类型:
--
作者:
Shan Y;Ma J;Pan Y;Hu J;Liu B;Jia L
Accumulating evidence suggests long noncoding RNAs (lncRNAs) play an important role in cancer progression. However, the function of lncRNA SNHG7 in colorectal cancer (CRC) remains unclear. In this study, SNHG7 expression was significantly upregulated in CRC tissues, especially in aggressive cases. In accordance, high level of SNHG7 was observed in CRC cell lines compared to normal colon cells. Furthermore, SNHG7 overexpression promoted the proliferation, migration, and invasion of CRC cell lines, while SNHG7 depletion inhibited invasion and cell viability in vitro. Mechanistically, knockdown of SNHG7 inhibited GALNT1 and EMT markers (E-cadherin and Vimentin). Importantly, SNHG7 directly interacted with miR-216b and downregulation of miR-216b reversed efficiently the suppression of GALNT1 induced by SNHG7 siRNA. Moreover, overexpression of SNHG7 significantly enhanced the tumorigenesis and liver metastasis of SW480 cells in vivo. SNHG7 positively regulated GALNT1 level through sponging miR-216b, and played an oncogenic role in CRC progression. Together, our study elucidated the role of SNHG7 as an miRNA sponge in CRC, and shed new light on lncRNA-directed diagnostics and therapeutics in CRC.
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影响因子:
2
作者:
Cheng, SL;Liu, RH;Tsay, GJ
通讯作者:
Tsay, GJ
影响因子:
9
作者:
Liu FY;Zhou SJ;Deng YL;Zhang ZY;Zhang EL;Wu ZB;Huang ZY;Chen XP
通讯作者:
Chen XP
影响因子:
--
作者:
Huang MJ;Hu RH;Chou CH;Hsu CL;Liu YW;Huang J;Hung JS;Lai IR;Juan HF;Yu SL;Wu YM;Huang MC
通讯作者:
Huang MC
影响因子:
50.3
作者:
Anh Tuan Nguyen;Chia, Joanne;Bard, Frederic
通讯作者:
Bard, Frederic
影响因子:
8.8
作者:
Li, Z.;Yamada, S.;Inenaga, S.;Imamura, T.;Wu, Y.;Wang, K-Y;Shimajiri, S.;Nakano, R.;Izumi, H.;Kohno, K.;Sasaguri, Y.
通讯作者:
Sasaguri, Y.