Apigenin inhibits migration and induces apoptosis of human endometrial carcinoma Ishikawa cells via PI3K-AKT-GSK-3β pathway and endoplasmic reticulum stress
Liang, Yan-Cui | Zhong, Qian | Ma, Run-Hui | Ni, Zhi-Jing | Thakur, Kiran | Khan, Mohammad Rizwan | Busquets, Rosa | Zhang, Jian-Guo | Wei, Zhao-Jun
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.
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Эту запись предоставил National Agricultural Library