MicroRNA-21 regulates biological behavior by inducing EMT in human cholangiocarcinoma
MicroRNAs (miRNAs) have recently been demonstrated to play a crucial role in malignant progression including differentiation, proliferation, metastasis and invasion, MicroRNA-21 (mir-21) also has been reported to have association with tumor invasion and metastasis in some tumors including cholangioc...
Saved in:
Published in | International journal of clinical and experimental pathology Vol. 8; no. 5; pp. 4684 - 4694 |
---|---|
Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
e-Century Publishing Corporation
01.01.2015
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | MicroRNAs (miRNAs) have recently been demonstrated to play a crucial role in malignant progression including differentiation, proliferation, metastasis and invasion, MicroRNA-21 (mir-21) also has been reported to have association with tumor invasion and metastasis in some tumors including cholangiocarcinoma (CCA). In this study, we further investigated the association of mir-21 with CCA biological behavior by transfecting miR-21 mimics or mir-21 inhibitor into QBC939 and RBE cells accompanied with the tumor xenografts experiment. Results indicated that over-expression of miR-21 significantly promoted cell migration, invasion and xenografts growth, whereas contrary phenomenon was observed in mir-21 inhibitor group. Furthermore, we explored the expression of EMT related proteins in CCA cells and tumor xenografts. Results showed that E-cadherin was decreased and N-cadherin, Vimentin were up-regulated significantly when miR-21 was over-expressed. In conclusion, microRNA-21 is crucial for CCA carcinogenesis and metastasis, which could induce EMT process, thereby promote the invasion and migration of CCA cells. These findings may provide new strategy for prevention and treatment of CCA in the future. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Co-first authors. |
ISSN: | 1936-2625 |