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Published on: October 24, 2015
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.
Abstract:
The aim of this study is to investigate the pharmacological effect of curcumin on hepatocellular carcinoma (HCC) Huh7 and PLC cells and to explore its mechanism in the pathological process by screening possible target genes. MTT assay was used to detect the effect of curcumin on the growth of Huh7 and PLC cells. The inhibitory effect was found to be in a time- and dose- dependent manner, and the cytoplasm was shrunk with round or elliptic morphology. Flow cytometry indicated that curcumin could significantly accelerate apoptosis of Huh7 and PLC cells, showing an obvious dosage effect. Retrieval in gene expression database and related gene-drug network analysis showed that the effect of curcumin on the apoptosis of HCC cells was related to SREBF1 (sterol regulatory element binding transcription factor 1) gene. In the in-vitro experiment, adding curcumin could significantly down-regulate SREBF1, and Western Blot suggested that down-regulation of SREBF1 could suppress the tumor growth. In conclusion, Curcumin could significantly suppress the tumor growth by way of down-regulating SREBF1 expression.
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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