Abstract
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•API inhibited Ishikawa cells growth with IC50 value of 45.55 μM and blocked Ishikawa cells in G2/M phase.•API induced apoptosis through the mitochondrial pathway by increasing the ROS level and lowering the MMP.•API triggered apoptosis via activating the ERS pathway by increasing the Ca2+ level.•API could impede cell migration and invasion through PI3K-AKT-GSK-3β signaling pathway.
Several experimental and biological studies have emphasized the tumor suppression efficacy and low toxicity of Apigenin (API); however, its exact underlying mechanism on human endometrial carcinoma Ishikawa cell line (EC) is still unknown. We found that API could inhibit the proliferation of Ishikawa cells at IC50 of 45.55 μM, arrest the cell cycle at G2/M phase, induce apoptosis by inhibiting Bcl-xl and increasing Bax, Bak and Caspases. Further, API could induce apoptosis by activating the endoplasmic reticulum (ER) stress pathway by increasing the Ca2+, ATF4, and CHOP. It could impede cell migration and invasion through PI3K-AKT-GSK-3β signaling pathway, preventing wound healing, restraining cells migration from the upper chamber to the lower chamber. This study demonstrated that API can be used as a promising dietary supplement and an adjuvant chemotherapeutic agent for cancer treatment.