Andrographolide enhanced radiosensitivity by downregulating glycolysis via the inhibition of the PI3K-Akt-mTOR signaling pathway in HCT116 colorectal cancer cells

Objective Radiotherapy plays an important role in the treatment of colorectal cancer (CRC). However, some patients benefit minimally from radiotherapy because of radioresistance. This study investigated the effects of andrographolide on radiosensitivity in HCT116 CRC cells and examined its mechanism...

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Bibliographic Details
Published in:Journal of international medical research 2020-08, Vol.48 (8), p.300060520946169-300060520946169
Main Authors: Li, Xiaofei, Tian, Ruifang, Liu, Lan, Wang, Lihui, He, Dong, Cao, Ke, Ma, John K., Huang, Chenghui
Format: Article
Language:English
Subjects:
Apoptosis
Cell Line, Tumor
Cell Proliferation
Colorectal cancer
Colorectal Neoplasms - drug therapy
Colorectal Neoplasms - radiotherapy
Diterpenes
Glycolysis
HCT116 Cells
Humans
Kinases
Phosphatidylinositol 3-Kinase - metabolism
Phosphatidylinositol 3-Kinases - metabolism
Pre-Clinical Research Report
Proto-Oncogene Proteins c-akt - metabolism
Radiation therapy
Radiation Tolerance
Signal Transduction
Sirolimus
TOR Serine-Threonine Kinases - metabolism
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Summary:Objective Radiotherapy plays an important role in the treatment of colorectal cancer (CRC). However, some patients benefit minimally from radiotherapy because of radioresistance. This study investigated the effects of andrographolide on radiosensitivity in HCT116 CRC cells and examined its mechanism of action. Methods Cell survival, proliferation, apoptosis, and migration were evaluated using MTT, colony formation, flow cytometry, and Transwell cell invasion assays, respectively. Glycolysis-related indicators were measured to examine cell glycolytic activity. The expression of related proteins was detected by western blotting. Results After andrographolide treatment, the expression of phosphoinositide 3-kinase (PI3K)-Akt-mammalian target of rapamycin (mTOR) signaling pathway-related proteins, glycolytic activity, and cell survival and invasion rates were decreased in HCT116 cells. Andrographolide plus irradiation increased apoptosis and decreased survival, invasion, and colony formation compared with the effects of irradiation alone. Conclusion Andrographolide enhanced radiosensitivity by downregulating glycolysis via inhibition of the PI3K-Akt-mTOR signaling pathway in HCT116 cells.
ISSN:0300-0605
1473-2300
DOI:10.1177/0300060520946169