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Upregulated in Hepatitis B virus-associated hepatocellular carcinoma cells, miR-331-3p promotes proliferation of hepatocellular carcinoma cells by targeting ING5.
Oncotarget. 2015 Nov 10; 6(35):38093-106.O

Abstract

Hepatitis B virus (HBV) is a major risk factor for development and progression of hepatocellular carcinoma (HCC). It has been reported that viral infection can interfere with cellular microRNA (miRNA) expression and participate in the pathogenesis of oncogenicity. Our miRNAs array data indicated that miR-331-3p expression in HCC cell lines increased, but the relationship between miR-331-3p expression and HBV activity is unclear. Here, we observed elevated expression of miR-331-3p in different HCC cell lines expressing HBV. HBV, especially HBx, promotes miR-331-3p expression by enhancing its promoter activity. Using a miRNA target prediction database miRBase, we identified ING5 to be a novel target gene of miR-331-3p. miR-331-3p could inhibit ING5 expression by directly targeting its 3'-untranslated region (3'-UTR). As predicted, HBV was confirmed to repress ING5 at both mRNA and protein levels by promoting miR-331-3p expression. Our result indicated that miR-331-3p expression promotes proliferation of SMMC7721 cells by inhibiting ING5. ING5 overexpression promoted cell apoptosis in HCC cell lines. We also found ING5 expression was decreased in tumor tissue of HCC patient with HBV infection compared to its expression in para-carcinoma tissues.

CONCLUSION

These results showed that miR-331-3p is upregulated by HBV and promotes proliferation of HCC cells though repression of ING5 expression. These data provide new insights for understanding the mechanisms of HBV-related HCC pathogenesis.

Authors+Show Affiliations

Key Laboratory of Molecular Biology on Infectious Diseases, Ministry of Education, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.Key Laboratory of Molecular Biology on Infectious Diseases, Ministry of Education, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.Key Laboratory of Molecular Biology on Infectious Diseases, Ministry of Education, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.Key Laboratory of Molecular Biology on Infectious Diseases, Ministry of Education, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.Key Laboratory of Molecular Biology on Infectious Diseases, Ministry of Education, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.Key Laboratory of Molecular Biology on Infectious Diseases, Ministry of Education, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.Key Laboratory of Molecular Biology on Infectious Diseases, Ministry of Education, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China. Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Zhejiang University, Hangzhou, China.Key Laboratory of Molecular Biology on Infectious Diseases, Ministry of Education, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26497554

Citation

Cao, Yiyi, et al. "Upregulated in Hepatitis B Virus-associated Hepatocellular Carcinoma Cells, miR-331-3p Promotes Proliferation of Hepatocellular Carcinoma Cells By Targeting ING5." Oncotarget, vol. 6, no. 35, 2015, pp. 38093-106.
Cao Y, Chen J, Wang D, et al. Upregulated in Hepatitis B virus-associated hepatocellular carcinoma cells, miR-331-3p promotes proliferation of hepatocellular carcinoma cells by targeting ING5. Oncotarget. 2015;6(35):38093-106.
Cao, Y., Chen, J., Wang, D., Peng, H., Tan, X., Xiong, D., Huang, A., & Tang, H. (2015). Upregulated in Hepatitis B virus-associated hepatocellular carcinoma cells, miR-331-3p promotes proliferation of hepatocellular carcinoma cells by targeting ING5. Oncotarget, 6(35), 38093-106. https://doi.org/10.18632/oncotarget.5642
Cao Y, et al. Upregulated in Hepatitis B Virus-associated Hepatocellular Carcinoma Cells, miR-331-3p Promotes Proliferation of Hepatocellular Carcinoma Cells By Targeting ING5. Oncotarget. 2015 Nov 10;6(35):38093-106. PubMed PMID: 26497554.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Upregulated in Hepatitis B virus-associated hepatocellular carcinoma cells, miR-331-3p promotes proliferation of hepatocellular carcinoma cells by targeting ING5. AU - Cao,Yiyi, AU - Chen,Juan, AU - Wang,Dan, AU - Peng,Hong, AU - Tan,Xixi, AU - Xiong,Dongmei, AU - Huang,Ailong, AU - Tang,Hua, PY - 2015/05/14/received PY - 2015/10/02/accepted PY - 2015/10/27/entrez PY - 2015/10/27/pubmed PY - 2016/9/7/medline KW - HBV KW - HCC KW - ING5 KW - miR-331-3p KW - miRNA SP - 38093 EP - 106 JF - Oncotarget JO - Oncotarget VL - 6 IS - 35 N2 - UNLABELLED: Hepatitis B virus (HBV) is a major risk factor for development and progression of hepatocellular carcinoma (HCC). It has been reported that viral infection can interfere with cellular microRNA (miRNA) expression and participate in the pathogenesis of oncogenicity. Our miRNAs array data indicated that miR-331-3p expression in HCC cell lines increased, but the relationship between miR-331-3p expression and HBV activity is unclear. Here, we observed elevated expression of miR-331-3p in different HCC cell lines expressing HBV. HBV, especially HBx, promotes miR-331-3p expression by enhancing its promoter activity. Using a miRNA target prediction database miRBase, we identified ING5 to be a novel target gene of miR-331-3p. miR-331-3p could inhibit ING5 expression by directly targeting its 3'-untranslated region (3'-UTR). As predicted, HBV was confirmed to repress ING5 at both mRNA and protein levels by promoting miR-331-3p expression. Our result indicated that miR-331-3p expression promotes proliferation of SMMC7721 cells by inhibiting ING5. ING5 overexpression promoted cell apoptosis in HCC cell lines. We also found ING5 expression was decreased in tumor tissue of HCC patient with HBV infection compared to its expression in para-carcinoma tissues. CONCLUSION: These results showed that miR-331-3p is upregulated by HBV and promotes proliferation of HCC cells though repression of ING5 expression. These data provide new insights for understanding the mechanisms of HBV-related HCC pathogenesis. SN - 1949-2553 UR - https://www.unboundmedicine.com/medline/citation/26497554/Upregulated_in_Hepatitis_B_virus_associated_hepatocellular_carcinoma_cells_miR_331_3p_promotes_proliferation_of_hepatocellular_carcinoma_cells_by_targeting_ING5_ L2 - http://www.impactjournals.com/oncotarget/misc/linkedout.php?pii=5642 DB - PRIME DP - Unbound Medicine ER -