FAM225A promotes sorafenib resistance in hepatocarcinoma cells through modulating miR-130a-5p-CCNG1 interaction

Yan Tong Liu1, Guo Qing Liu2, Jing Min Huang2

  • 1Xi'an Medical University, Xi'an, China.

Bioscience Reports
|November 27, 2020
PubMed

Insights

Long non-coding RNA FAM225A promotes hepatocellular carcinoma resistance to sorafenib. Targeting the FAM225A/miR-130a-5p/CCNG1 network may restore sensitivity to this liver cancer therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Hepatocellular carcinoma (HCC) treatment faces challenges due to chemotherapy resistance.
  • Understanding molecular mechanisms of acquired resistance is crucial for effective liver cancer therapy.

Purpose of the Study:

  • To investigate the role of lncRNA FAM225A in sorafenib resistance in HCC.
  • To elucidate the molecular pathway involving FAM225A, miR-130a-5p, and CCNG1 in HCC drug resistance.

Main Methods:

  • Quantitative analysis of FAM225A expression in HCC tissues and cell lines.
  • FAM225A knockdown experiments in HepG2/SOR cells and in vivo tumor xenograft models.
  • Assessment of cell viability using MTT assay.
  • Investigation of interactions between FAM225A, miR-130a-5p, and CCNG1 using molecular biology techniques.

Main Results:

  • FAM225A was significantly upregulated in HCC tissues, cell lines, and sorafenib-resistant cells.
  • FAM225A knockdown reduced sorafenib resistance in HCC cells and tumor xenografts.
  • FAM225A directly interacts with miR-130a-5p, which targets CCNG1, modulating sorafenib sensitivity.

Conclusions:

  • The FAM225A/miR-130a-5p/CCNG1 network plays a key role in regulating sorafenib resistance in HCC.
  • Targeting this network offers a potential strategy to re-sensitize HCC to sorafenib treatment.