Journal
CANCER BIOLOGY & THERAPY
Volume 9, Issue 7, Pages 554-561Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/cbt.9.7.11267
Keywords
biological therapy of cancer; microRNA; adenoviral vector; liver cancer; miR-122; apoptosis; cell cycle
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Funding
- National Natural Sciences Foundation of China [30872984]
- 973 Project [2010CB529406, 2004CB518804]
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Background: microRNA-122 (miR-122) plays an important role in both of hepatic physiology and pathology Down regulation of miR-122 was reported in human primary hepatocellular carcinoma (HCC) and restoration of miR-122 could suppress the growth of cancer cells. In this study, we presented a novel strategy for cancer therapy based on gene transfer of miR-122 by adenoma! vector. Results: Our data showed that Ad-miR122 could express functional miR-122 in tumor cells at a high level. Infection of tumor cells with Ad-miR122 resulted in inhibition of growth of cancer cells originating from liver (HepG2, Hep3B, Huh7 and PLC/PRF/5), lung (NCI-H460) and uterine cervix (HeLa). This antitumor activity was related to the induction of apoptosis and/or cell cycle arrest in cancer cells. Infection with Ad-miR122 resulted in decreased expression of Bcl-W and CCNG1 in cancer cells. Methods: We generated a recombinant adenoviral vector expressing miR-122 (Ad-rniR122). The miR-122 expression was measured by quantitative real-time PCR (qRT-PCR) Cell survival rate was determined by MTT assay. Conclusion: The antitumor activity of Ad-miR122 was probably due to the induction of apoptosis and/or cell cycle arrest in cancer cells through inhibiting Bcl-W and/or CCNG1 expression. We concluded that expression of therapeutic microRNA, such as miR-122, via adenoviral vector is a promising strategy for cancer treatment.
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