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Radiosensitivity of Cancer Stem Cells in Lung Cancer Cell Lines
Published on: August 21, 2019
Antiproliferative Effect of Aminoethyl-Chitooligosaccharide on Human Lung A549 Cancer Cells
Dai Hung Ngo1, Dai Nghiep Ngo2, Se-Kwon Kim3
1Faculty of Natural Sciences, Thu Dau Mot University, Thu Dau Mot City 820000, Binh Duong province, Vietnam. hungnd@tdmu.edu.vn.
Abstract:
The aminoethyl-chitooligosaccharide (AE-COS) was reported to inhibit human gastric cancer cell proliferation and human fibrosarcoma cell invasion. In this study, the role of AE-COS in down-regulation of proliferation of human lung A549 cancer cells was evaluated. It was found that AE-COS was able to reduce A549 cell proliferation to (32 ± 1.3)% at a concentration of 500 µg/ml. Moreover, AE-COS treatment caused suppression on COX-2 expression in a dose-dependent manner. Notably, the role of AE-COS in induction of cell apoptosis was observed via decreasing Bcl-2 expression and increasing caspase-3 and -9 activation. Accordingly, the antiproliferative effect of AE-COS was indicated due to suppression of cell proliferation and induction of cell apoptosis, suggesting AE-COS as a promising chemotherapy agent for treatment of lung cancer.
Insights
Aminoethyl-chitooligosaccharide (AE-COS) effectively inhibits lung cancer cell proliferation and promotes apoptosis. This suggests AE-COS is a potential chemotherapy agent for lung cancer treatment.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Aminoethyl-chitooligosaccharide (AE-COS) has demonstrated inhibitory effects on gastric cancer cell proliferation and fibrosarcoma cell invasion.
- Lung cancer remains a significant global health challenge, necessitating novel therapeutic strategies.
Purpose of the Study:
- To evaluate the antiproliferative and pro-apoptotic effects of AE-COS on human lung A549 cancer cells.
- To investigate the underlying molecular mechanisms of AE-COS action in lung cancer.
Main Methods:
- Human lung A549 cancer cells were treated with varying concentrations of AE-COS.
- Cell proliferation was quantified using standard assays.
- Expression levels of COX-2, Bcl-2, and activation of caspase-3 and -9 were assessed.
Main Results:
- AE-COS significantly reduced A549 cell proliferation by up to 68% at a concentration of 500 µg/ml.
- AE-COS treatment led to a dose-dependent suppression of cyclooxygenase-2 (COX-2) expression.
- AE-COS induced apoptosis by decreasing Bcl-2 expression and increasing the activation of caspase-3 and caspase-9.
Conclusions:
- AE-COS exhibits potent antiproliferative effects on human lung A549 cancer cells.
- The mechanism involves the suppression of COX-2 and induction of apoptosis via the caspase pathway.
- AE-COS shows promise as a novel chemotherapeutic agent for lung cancer.
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