Exogenous Glycine Betaine Decreases Cell Proliferation and Induces Apoptosis in Human Colorectal Adenocarcinoma HT-29
Lizeth López-Castro1, Jesús Rosas-Rodríguez1, Ramona Icedo-García1
1Laboratorio de Microbiología e Inmunología, Departamento de Ciencias Químico-Biológicas y Agropecuarias, Facultad Interdiciplinaria de Ciencias Biológicas y de Salud, Universidad de Sonora, Blvd. Lázaro Cárdenas No. 100 Col. Francisco Villa, Navojoa 85880, Sonora, Mexico.
Abstract:
Studies in cervical and prostate cancer cells have reported that frequent consumption of foods rich in glycine betaine (GB) and choline have beneficial effects against some types of cancer. However, the role of GB against the human colorectal adenocarcinoma cell line HT-29 has not yet been elucidated. Therefore, this study aimed to evaluate the effect of GB on p53 and caspase-3 expression, which regulate cellular processes such as cell proliferation and apoptosis, respectively, on HT-29 cells. HT-29 cells were treated with GB at 5 mg/mL, 15.6 mg/mL, 31.2 mg/mL, and 62.5 mg/mL, after which RNA purification and cDNA synthesis were performed, followed by qPCR to detect the relative expression of p53 and caspase-3, using GAPDH as a reference gene, and protein levels were determined by ELISA. Results indicated that in HT-29 cells treated with GB at 62.5 mg/mL, the protein levels of p53 significantly (p < 0.05) increased to 45 U/mL, as compared with cells without GB (21 U/mL), whereas caspase-3 increased to 30 ng/mL, as compared with control cells (20.13 ng/mL). Therefore, we conclude that GB at high concentrations decreases cell proliferation and induces apoptosis in HT-29 cells.
Insights
Glycine betaine (GB) shows promise in combating colorectal cancer. High concentrations of GB significantly reduced HT-29 cell proliferation and induced apoptosis by upregulating p53 and caspase-3 expression.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Glycine betaine (GB) and choline are found in certain foods and have demonstrated anti-cancer effects in cervical and prostate cancer cells.
- The specific impact of GB on the human colorectal adenocarcinoma cell line HT-29 remains largely uninvestigated.
Purpose of the Study:
- To investigate the effects of glycine betaine (GB) on p53 and caspase-3 expression in HT-29 cells.
- To determine GB's role in regulating cell proliferation and apoptosis in colorectal cancer.
Main Methods:
- HT-29 cells were exposed to varying concentrations of GB (5–62.5 mg/mL).
- Quantitative PCR (qPCR) was employed to measure the relative expression of p53 and caspase-3.
- Enzyme-Linked Immunosorbent Assay (ELISA) was utilized to quantify protein levels.
Main Results:
- GB treatment at 62.5 mg/mL significantly increased p53 protein levels to 45 U/mL compared to controls (21 U/mL) in HT-29 cells (p < 0.05).
- Caspase-3 protein levels also rose to 30 ng/mL following high-dose GB treatment, compared to 20.13 ng/mL in control cells.
- These findings suggest a dose-dependent effect of GB on key apoptotic and cell cycle regulatory markers.
Conclusions:
- Glycine betaine (GB) at elevated concentrations effectively inhibits cell proliferation in HT-29 cells.
- GB treatment demonstrably induces apoptosis in colorectal adenocarcinoma cells through modulation of p53 and caspase-3 pathways.
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