TY - JOUR
T1 - LncRNA FTX sponges miR-215 and inhibits phosphorylation of vimentin for promoting colorectal cancer progression
AU - Yang, Yi
AU - Zhang, Jinpei
AU - Chen, Xi
AU - Xu, Xin
AU - Cao, Gang
AU - Li, Hua
AU - Wu, Tao
N1 - Publisher Copyright:
© 2018, Macmillan Publishers Limited, part of Springer Nature.
PY - 2018/8/1
Y1 - 2018/8/1
N2 - Recent researches have reported that long noncoding RNA (lncRNA) five prime to Xist (FTX) plays a crucial role in the initiation and progression of cancers. In the current study, the clinical significance and functional roles of lncRNA FTX in colorectal cancer (CRC) progression were investigated. A significant increase of lncRNA FTX expression in CRC tissue and cell lines was observed. Overexpression of lncRNA FTX was significantly associated with the bigger tumor diameter, the advanced TNM stage, the lymph node, and distant metastasis, and also predicted poor prognosis of patients with CRC. Functional analyses demonstrated that knockdown of lncRNA FTX markedly inhibited CRC cell proliferation, migration, and invasion in vitro. Mechanistically, FTX directly interacted with miR-215 and suppressed miR-215 expression. FTX also bind to vimentin and reduced its phosphorylation level on Ser83 in CRC cells. Finally, using siRNAs against lncRNA FTX could dramatically inhibit CRC growth and distant metastasis in vivo. Taken together, our data demonstrated an oncogenic role of lncRNA FTX in CRC tumorigenesis and progression via interaction with miR-215 and vimentin. Then, a promising therapeutic target for CRC was provided.
AB - Recent researches have reported that long noncoding RNA (lncRNA) five prime to Xist (FTX) plays a crucial role in the initiation and progression of cancers. In the current study, the clinical significance and functional roles of lncRNA FTX in colorectal cancer (CRC) progression were investigated. A significant increase of lncRNA FTX expression in CRC tissue and cell lines was observed. Overexpression of lncRNA FTX was significantly associated with the bigger tumor diameter, the advanced TNM stage, the lymph node, and distant metastasis, and also predicted poor prognosis of patients with CRC. Functional analyses demonstrated that knockdown of lncRNA FTX markedly inhibited CRC cell proliferation, migration, and invasion in vitro. Mechanistically, FTX directly interacted with miR-215 and suppressed miR-215 expression. FTX also bind to vimentin and reduced its phosphorylation level on Ser83 in CRC cells. Finally, using siRNAs against lncRNA FTX could dramatically inhibit CRC growth and distant metastasis in vivo. Taken together, our data demonstrated an oncogenic role of lncRNA FTX in CRC tumorigenesis and progression via interaction with miR-215 and vimentin. Then, a promising therapeutic target for CRC was provided.
UR - https://www.scopus.com/pages/publications/85048730078
U2 - 10.1038/s41434-018-0026-7
DO - 10.1038/s41434-018-0026-7
M3 - 文章
C2 - 29925853
AN - SCOPUS:85048730078
SN - 0969-7128
VL - 25
SP - 321
EP - 330
JO - Gene Therapy
JF - Gene Therapy
IS - 5
ER -
