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Intermedin promotes hepatic carcinoma cell proliferation through upregulation of miR-155

Hai Shang1, Zhi Qiang Hao1, Xi Bo Fu1

  • 1Department of Hepatobiliary Surgery, Liaoning Cancer Hospital & Institute Shenyang 110042, Liaoning Province, China.

International Journal of Clinical and Experimental Pathology
|January 18, 2020
PubMed
Abstract

Insights

Intermedin (IMD) promotes hepatic carcinoma cell growth by increasing microRNA-155 (miR-155) levels. Inhibiting miR-155 partially blocks this IMD-induced proliferation, suggesting miR-155 is key in liver cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • MicroRNAs (miRNAs) are crucial in malignant carcinoma development.
  • Intermedin (IMD), a small peptide, is known to enhance hepatic carcinoma cell proliferation.

Purpose of the Study:

  • To investigate the role of miR-155 in IMD-mediated hepatic carcinoma cell proliferation.
  • To elucidate the molecular mechanism linking IMD and liver cancer growth.

Main Methods:

  • Hepatic carcinoma SMMC7721 cell proliferation was assessed using CCK-8 assays.
  • Expression levels of proliferating cell nuclear antigen (PCNA) and miR-155 were quantified via real-time PCR.

Main Results:

  • IMD demonstrated a time- and dose-dependent promotion of SMMC7721 cell proliferation.
  • IMD was found to upregulate miR-155 expression.
  • Blocking miR-155 partially inhibited IMD-induced SMMC7721 cell proliferation.

Conclusions:

  • IMD promotes human hepatic carcinoma cell line SMMC7721 proliferation by upregulating miR-155.
  • This finding offers potential therapeutic targets for hepatic cancer prevention and treatment.
Keywords:
Intermedinhepatic carcinomamiR-155proliferation

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