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Published on: June 13, 2020
Sodium butyrate restores ASC expression and induces apoptosis in LS174T cells
Shuai Zhang1, Jingqiao Bai, Shuangyi Ren
1Department of Clinical Biochemistry, Dalian Medical University, Dalian 116044, P.R. China.
Abstract:
Sodium butyrate (NaBu) is a short-chain fatty acid (SCFA), which has been proposed as a potential anticancer agent. Apoptosis-associated speck-like protein (ASC) is a pro-apoptotic signaling factor that is subjected to epigenetic silencing in human cancers. Modulation by the aberrant methylation of CpG islands of ASC is a well-characterized epigenetic mechanism, and the methylation-induced silencing of ASC has been observed in several types of tumors. NaBu induces cell cycle arrest, markers of cell differentiation and apoptosis in colon cancer. NaBu promotes transcriptional activation by relaxing the DNA conformation and displays anti-proliferative and differentiating activity in a wide variety of cancers. Thus, we used NaBu to investigate the relationship between the status of cell proliferation and the re-expression of ASC in colon carcinoma LS174T cells. Our experiments determined ASC re-expression at the protein level using western blotting. In addition, we used reverse transcription-polymerase chain reaction to detect the expression levels of ASC mRNA and an MTT assay to detect the inhibitory rate of cell growth. The apoptosis rate was also detected for further validation of the re-expression of ASC. The results showed that ASC re-expression was significantly increased in the LS174 cells following NaBu treatment in a time- and dose-dependent manner. The expression of ASC also induced the apoptosis of LS174T cells. These results suggest that NaBu plays a role in the reactivation of ASC expression and that the latter promotes the apoptosis of LS174T cells.
Insights
Sodium butyrate (NaBu) reactivates the apoptosis-associated speck-like protein (ASC) in colon cancer cells. This reactivation of ASC by NaBu promotes cancer cell apoptosis, suggesting a potential anticancer therapeutic strategy.
Area of Science:
- Epigenetics
- Cancer Biology
- Molecular Oncology
Background:
- Sodium butyrate (NaBu), a short-chain fatty acid, is investigated for its anticancer properties.
- Apoptosis-associated speck-like protein (ASC) is crucial for apoptosis but often epigenetically silenced in cancers via DNA methylation.
- Aberrant methylation of ASC's CpG islands leads to its silencing in various tumor types.
Purpose of the Study:
- To investigate the effect of NaBu on ASC re-expression in colon carcinoma LS174T cells.
- To explore the relationship between NaBu-induced cell proliferation inhibition and ASC reactivation.
- To validate the role of ASC re-expression in promoting colon cancer cell apoptosis.
Main Methods:
- Western blotting to detect ASC protein levels.
- Reverse transcription-polymerase chain reaction (RT-PCR) for ASC mRNA expression.
- MTT assay to quantify cell growth inhibition.
- Apoptosis assays to confirm ASC's functional role.
Main Results:
- NaBu treatment significantly increased ASC re-expression in LS174T cells.
- ASC re-expression occurred in a time- and dose-dependent manner following NaBu administration.
- NaBu treatment inhibited cell proliferation and induced apoptosis in LS174T cells, correlating with ASC re-expression.
Conclusions:
- Sodium butyrate effectively reactivates silenced ASC expression in colon cancer cells.
- Re-expression of ASC induced by NaBu plays a critical role in promoting colon cancer cell apoptosis.
- NaBu demonstrates potential as an epigenetic therapy for colon cancer by restoring ASC function.
