Lidao Bao1, Jianfen Zhao2, Xiaoxia Dai3, Yi Wang4, Ruilian Ma4, Yila Su5, Hongwei Cui5, Jianxiang Niu6, Shiming Bai7, Zhiying Xiao8, Hongwei Yuan9, Zhou Yang10, Changqing Li11, Rui Cheng4, Xianhua Ren12. 1. Department of Pharmacy, Affiliated Hospital of Inner Mongolia Medical University, 010059 Hohhot, PR China. Electronic address: lidao_bao@dfci.harvard.edu. 2. Department of Health Care for Cadres, Binzhou People's Hospital, 256610 Binzhou, PR China. 3. Department of Respiratory Medicine, Binzhou People's Hospital, 256610 Binzhou, PR China. 4. Department of Pharmacy, Affiliated Hospital of Inner Mongolia Medical University, 010059 Hohhot, PR China. 5. Molecular Biotechnology Center of Inner Mongolia Medical University, 010059 Hohhot, PR China. 6. Department of Hepatobiliary Surgery, Inner Mongolia Medical University, 010059 Hohhot, PR China. 7. Kitami Institute of Technology, 090-8507 Kitami, Japan. 8. College of Chemistry and Chemical Engineering, Inner Mongolia University for Nationalities, 028043 Tongliao, PR China. 9. Department of Pathology, Inner Mongolia Medical University, 010059 Hohhot, PR China. 10. Department of Imaging, Affiliated Hospital of Inner Mongolia Medical University, 010059 Hohhot, PR China. 11. Department of Geriatrics, Affiliated Hospital of Inner Mongolia Medical University, 010059 Hohhot, PR China. 12. Department of Pharmacy, Affiliated Hospital of Inner Mongolia Medical University, 010059 Hohhot, PR China. Electronic address: renxianhua237@163.com.
Abstract
BACKGROUND AND AIMS: To clarify the role of miR-23a in the onset and development of hepatocarcinoma on the cellular, genetic and molecular levels. PATIENTS AND METHODS: Seventy-eight patients were included after hepatectomy. Relationships between the clinical pathological factors of tumor and paracancerous tissues were analyzed. Risk factors of overall and recurrence-free survival rates were subject to multi-variable analysis. Tissues were sequenced by digital miRNA expression profiling, and new miRNA was subject to target gene prediction. RESULTS: miR-23a expression was correlated with the stage of the TNM Classification of Malignant Tumours most significantly, followed by tumor size (P=0.041 and 0.047). High miR-23a, vascular invasion, tumor size≥7cm, tumor capsule and late pathological stage were the risk factors of overall survival rate, and those of recurrence-free survival rate also included alpha-fetoprotein level≥200μg/L and multiple tumors. Compared with normal hepatic cell line L-02, the miR-23a expression levels in tumor cell lines SMMC-7721 and HepG2 were up-regulated and down-regulated respectively. Transfecting miR-23a inhibitor suppressed cell growth. Apoptotic rates of the control and those transfected with inhibitor-NC and miR-23a inhibitor for 48h were similar. CONCLUSION: High miR-23a expression is the independent prognostic factor of overall and recurrence-free survival rates, and miR-23a may be involved in the onset of hepatocarcinoma as an oncogene.
BACKGROUND AND AIMS: To clarify the role of miR-23a in the onset and development of hepatocarcinoma on the cellular, genetic and molecular levels. PATIENTS AND METHODS: Seventy-eight patients were included after hepatectomy. Relationships between the clinical pathological factors of tumor and paracancerous tissues were analyzed. Risk factors of overall and recurrence-free survival rates were subject to multi-variable analysis. Tissues were sequenced by digital miRNA expression profiling, and new miRNA was subject to target gene prediction. RESULTS:miR-23a expression was correlated with the stage of the TNM Classification of Malignant Tumours most significantly, followed by tumor size (P=0.041 and 0.047). High miR-23a, vascular invasion, tumor size≥7cm, tumor capsule and late pathological stage were the risk factors of overall survival rate, and those of recurrence-free survival rate also included alpha-fetoprotein level≥200μg/L and multiple tumors. Compared with normal hepatic cell line L-02, the miR-23a expression levels in tumor cell lines SMMC-7721 and HepG2 were up-regulated and down-regulated respectively. Transfecting miR-23a inhibitor suppressed cell growth. Apoptotic rates of the control and those transfected with inhibitor-NC and miR-23a inhibitor for 48h were similar. CONCLUSION: High miR-23a expression is the independent prognostic factor of overall and recurrence-free survival rates, and miR-23a may be involved in the onset of hepatocarcinoma as an oncogene.
Authors: Stefan Hatzl; Olivia Geiger; Maja Kim Kuepper; Veronica Caraffini; Till Seime; Tobias Furlan; Erika Nussbaumer; Rotraud Wieser; Martin Pichler; Marcel Scheideler; Katarzyna Nowek; Mojca Jongen-Lavrencic; Franz Quehenberger; Albert Wölfler; Jakob Troppmair; Heinz Sill; Armin Zebisch Journal: Cancer Res Date: 2016-04-15 Impact factor: 12.701