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SODD promotes glucose uptake of colorectal cancer cells via AKT pathway
Rui Zhang1, Jibin Li1, Xiaofei Yan1
1Department of Colorectal Surgery.
Abstract:
Altered glucose metabolism has been found in a variety of malignant diseases and recognized as one of the hallmarks of cancer. However, the molecular mechanism behind it is far from well understood. In current study, we found silencer of death domains (SODD) regulates glucose uptake of colorectal cancer cells. When cultured under low level of glucose, SODD overexpressing RKO and SW1417 cells generated more colonies, compared with control cells, in clonogenic assay. SODD upregulation enhanced RKO and SW1417 cells viability. Furthermore, SODD induced more GLUT1 (Glucose transporter 1) expression and enhanced glucose uptake. AKT phosphorylation was upregulated in SODD overexpression cells. Moreover, inhibition of GLUT1 or AKT could reverse SODD induced glucose uptake enhancement. In conclusion, our findings indicate that SODD positively regulates glucose uptake and may be a potential therapeutic target of colorectal cancer.
Insights
Silencer of death domains (SODD) promotes colorectal cancer growth by increasing glucose uptake. Inhibiting SODD may offer a new therapeutic strategy for colorectal cancer.
Area of Science:
- Oncology
- Cancer Metabolism
- Molecular Biology
Background:
- Altered glucose metabolism is a hallmark of cancer, but its underlying mechanisms remain unclear.
- Understanding cancer-specific metabolic regulation is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the role of silencer of death domains (SODD) in regulating glucose metabolism in colorectal cancer.
- To explore SODD as a potential therapeutic target for colorectal cancer.
Main Methods:
- Clonogenic assays were performed on colorectal cancer cell lines (RKO and SW1417) with varying SODD expression levels under low glucose conditions.
- Cell viability, glucose transporter 1 (GLUT1) expression, glucose uptake, and AKT phosphorylation were assessed.
- The effects of GLUT1 and AKT inhibition on SODD-induced glucose uptake were evaluated.
Main Results:
- SODD overexpression enhanced colorectal cancer cell viability and colony formation, particularly under low glucose conditions.
- SODD upregulation led to increased GLUT1 expression and elevated glucose uptake.
- AKT phosphorylation was upregulated in SODD-overexpressing cells, and inhibiting GLUT1 or AKT reversed the enhanced glucose uptake.
Conclusions:
- SODD positively regulates glucose uptake in colorectal cancer cells.
- SODD plays a significant role in promoting colorectal cancer cell growth and survival.
- SODD represents a potential therapeutic target for colorectal cancer treatment.
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