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Atractylenolide II Suppresses Glycolysis and Induces Apopto-sis by Blocking the PADI3-ERK Signaling Pathway in Endo-metrial Cancer Cells

ABSTRACT: Atractylenolide II (AT-II), the major bioactive compound of Atractylodes macrocephala exhibits anticancer activity against many types of tumors, but the roles and the potential mechanisms in endometrial cancer remain unclear. To explore a novel therapeutic target of AT-II for the clinical therapy of endometrial cancer, the high-throughput sequence was performed.

ORGANISM(S): Homo sapiens

PROVIDER: GSE252780 | GEO | 2024/03/20

REPOSITORIES: GEO

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Atractylenolide II Suppresses Glycolysis and Induces Apopto-sis by Blocking the PADI3-ERK Signaling Pathway in Endo-metrial Cancer Cells

Project description:Atractylenolide II Suppresses Glycolysis and Induces Apopto-sis by Blocking the PADI3-ERK Signaling Pathway in Endo-metrial Cancer Cells

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Atractylenolide II Suppresses Glycolysis and Induces Apoptosis by Blocking the PADI3-ERK Signaling Pathway in Endometrial Cancer Cells.

Project description:Atractylenolide II (AT-II), the major bioactive compound of Atractylodes macrocephala, exhibits anti-cancer activity against many types of tumors, but the roles and the potential mechanisms in endometrial cancer remain unclear. In the present study, AT-II treatment was found to significantly suppress RL95-2 and AN3CA cell proliferation and glycolysis, and induced their apoptosis by inactivating the ERK signaling pathway, accompanied by the changing expression of the glycolytic key enzymes and apoptotic-related proteins. Peptidyl arginine deiminase 3 (PADI3), as the candidate target gene of AT-II, was highly expressed in the endometrial cancer tissues and associated with a poor prognosis according to bioinformatics analysis. PADI3 knockdown inhibited proliferation and glycolysis in endometrial cancer cells and induced cell apoptosis. Furthermore, AT-II negatively regulated the expression of PADI3, and PADI3 overexpression reversed the effects of AT-II on endometrial cancer cells. Our findings suggested that the anti-cancer function of AT-II is associated with the suppression of glycolysis and induction of apoptosis by blocking the PADI3-ERK signaling pathway. Thus, AT-II represents a novel therapeutic target for endometrial cancer and targeting AT-II may serve as a potential strategy for the clinical therapy of endometrial cancer.

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