MiR-92b regulates the cell growth, cisplatin chemosensitivity of A549 non small cell lung cancer cell line and target PTEN
•We found that miR-92b is significantly up-regulated in NSCLC tissues.•We demonstrated that miR-92b regulate A549 cell growth.•We claimed miR-92b regulates the resistance of NSCLC A549 cells to CDDP.•We suggested miR-92b directly target PTEN in NSCLC. MicroRNAs (miRNAs) have emerged to play importan...
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Published in | Biochemical and biophysical research communications Vol. 440; no. 4; pp. 604 - 610 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.11.2013
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Subjects | |
Online Access | Get full text |
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Summary: | •We found that miR-92b is significantly up-regulated in NSCLC tissues.•We demonstrated that miR-92b regulate A549 cell growth.•We claimed miR-92b regulates the resistance of NSCLC A549 cells to CDDP.•We suggested miR-92b directly target PTEN in NSCLC.
MicroRNAs (miRNAs) have emerged to play important roles in tumorigenesis and drug resistance of human cancer. Fewer studies were explored the roles of miR-92b on human lung cancer cell growth and resistance to cisplatin (CDDP). In this paper, we utilized real-time PCR to verify miR-92b was significantly up-regulated in non-small cell lung cancer (NSCLC) tissues compared to matched adjacent normal tissues. In vitro assay demonstrated that knock-down of miR-92b inhabits cell growth and sensitized the A549/CDDP cells to CDDP. Furthermore, we found miR-92b could directly target PTEN, a unique tumor suppressor gene, which was downregulated in lung cancer tissues compared to the matched adjacent normal tissues. These data indicate that the miR-92b play an oncogene roles by regulates cell growth, cisplatin chemosensitivity phenotype, and could serve as a novel potential maker for NSCLC therapy. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0006-291X 1090-2104 1090-2104 |
DOI: | 10.1016/j.bbrc.2013.09.111 |