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Article

Clinical effects of miR-101 on prognosis of hepatocellular carcinoma and carcinogenic mechanism of anti-miR-101

  • Authors:
    • Xuecheng Lv
    • Jinghua Li
    • Bingnan Yang
  • View Affiliations / Copyright

    Affiliations: Department of Pharmacy, The First People's Hospital of Shangqiu, Shangqiu, Henan 476100, P.R. China, Department of Cardiovascular Surgery, Henan Provincial People's Hospital, Zhengzhou, Henan 450000, P.R. China, Department of Neurosurgery, Henan Provincial People's Hospital, Zhengzhou, Henan 450000, P.R. China
  • Pages: 2184-2192
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    Published online on: July 28, 2016
       https://doi.org/10.3892/or.2016.4980
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Abstract

The aim of this study was to verify whether anti-miR-101 participates in the treatment of hepatocellular carcinoma (HCC) as a small-molecule antitumor agent, and to explore the effect on phosphatase and tensin homolog deleted on chromosome 10 (PTEN). Patients who received consecutive hepatectomies were followed-up, and miR-101 expressions in their tumor and paracancerous tissues were detected. Correlation between miR-101 expression and clinical pathological factors and prognosis was studied. High‑throughput sequencing was used to detect the genetic and microRNA (miRNA) levels of tumor tissues. Expression of anti-miR-101 in different HCC cell lines was determined, and those of desired genes and proteins were detected by qRT-PCR and western blotting to obtain the target gene. miR-101 was significantly upregulated in HCC patients compared with that in paracancerous tissues. High miR-101 expression, vascular invasion, tumor size ≥7 cm and late pathological stage were the risk factors of recurrence-free survival rate. High miR-101 expression was the independent prognostic factor of total and recurrence-free survival rates. CXCL12, IL6R, FOXO3 and PTEN were screened as desired genes, and only PTEN was expressed significantly differently in three cell lines. miR-101 could bind 3'-UTR of WT-PTEN with reduced fluorescent intensity, suggesting that PTEN was the target gene. SMMC-7721, HepG2 and Huh7 were eligible cell lines for miR-101 studies. miR-101 was an applicable molecular marker of HCC. Anti-miR-101 regulated the transcription of PTEN and may promote cell proliferation, differentiation and apoptosis by regulating downstream genes with PTEN. The regulatory effects of anti-miR-101 on PTEN provide valuable evidence for finding novel miRNA drugs.
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Copy and paste a formatted citation
Spandidos Publications style
Lv X, Li J and Yang B: Clinical effects of miR-101 on prognosis of hepatocellular carcinoma and carcinogenic mechanism of anti-miR-101. Oncol Rep 36: 2184-2192, 2016.
APA
Lv, X., Li, J., & Yang, B. (2016). Clinical effects of miR-101 on prognosis of hepatocellular carcinoma and carcinogenic mechanism of anti-miR-101. Oncology Reports, 36, 2184-2192. https://doi.org/10.3892/or.2016.4980
MLA
Lv, X., Li, J., Yang, B."Clinical effects of miR-101 on prognosis of hepatocellular carcinoma and carcinogenic mechanism of anti-miR-101". Oncology Reports 36.4 (2016): 2184-2192.
Chicago
Lv, X., Li, J., Yang, B."Clinical effects of miR-101 on prognosis of hepatocellular carcinoma and carcinogenic mechanism of anti-miR-101". Oncology Reports 36, no. 4 (2016): 2184-2192. https://doi.org/10.3892/or.2016.4980
Copy and paste a formatted citation
x
Spandidos Publications style
Lv X, Li J and Yang B: Clinical effects of miR-101 on prognosis of hepatocellular carcinoma and carcinogenic mechanism of anti-miR-101. Oncol Rep 36: 2184-2192, 2016.
APA
Lv, X., Li, J., & Yang, B. (2016). Clinical effects of miR-101 on prognosis of hepatocellular carcinoma and carcinogenic mechanism of anti-miR-101. Oncology Reports, 36, 2184-2192. https://doi.org/10.3892/or.2016.4980
MLA
Lv, X., Li, J., Yang, B."Clinical effects of miR-101 on prognosis of hepatocellular carcinoma and carcinogenic mechanism of anti-miR-101". Oncology Reports 36.4 (2016): 2184-2192.
Chicago
Lv, X., Li, J., Yang, B."Clinical effects of miR-101 on prognosis of hepatocellular carcinoma and carcinogenic mechanism of anti-miR-101". Oncology Reports 36, no. 4 (2016): 2184-2192. https://doi.org/10.3892/or.2016.4980
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