Curcumin suppress the growth of hepatocellular carcinoma via down-regulating SREBF1

Zhen You1, Bei Li1, Jingchang Xu1

  • 1Department of Biliary Surgery, West China Hospital of Sichuan University, Chengdu 610041, Sichuan, China.

Oncology Research
|April 5, 2018
PubMed

Insights

Curcumin effectively inhibits hepatocellular carcinoma (HCC) cell growth and promotes apoptosis. This anticancer effect is achieved by down-regulating the sterol regulatory element binding transcription factor 1 (SREBF1) gene, suppressing tumor progression.

Area of Science:

  • Pharmacology
  • Molecular Biology
  • Oncology

Background:

  • Hepatocellular carcinoma (HCC) is a prevalent cancer with limited treatment options.
  • Curcumin, a natural compound, exhibits potential anticancer properties.
  • Understanding the molecular mechanisms of curcumin's action is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the pharmacological effects of curcumin on HCC cell lines (Huh7 and PLC).
  • To explore the underlying molecular mechanisms, including the identification of target genes.
  • To evaluate curcumin's impact on cell viability, morphology, and apoptosis.

Main Methods:

  • Cell viability was assessed using MTT assays.
  • Apoptosis was analyzed via flow cytometry.
  • Gene expression databases and network analysis were employed to identify potential target genes, including SREBF1 (sterol regulatory element binding transcription factor 1).
  • In vitro experiments and Western Blotting confirmed the role of SREBF1.

Main Results:

  • Curcumin demonstrated a time- and dose-dependent inhibition of HCC cell growth.
  • Morphological changes, including cytoplasmic shrinkage, were observed.
  • Curcumin significantly accelerated apoptosis in HCC cells.
  • Curcumin down-regulated SREBF1 expression in vitro.
  • Down-regulation of SREBF1 suppressed tumor growth.

Conclusions:

  • Curcumin possesses significant pharmacological effects against HCC.
  • The anticancer activity of curcumin is mediated, in part, by the down-regulation of SREBF1.
  • Targeting SREBF1 represents a potential therapeutic strategy for HCC treatment using curcumin.

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