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ESM-1 Regulates PI3K-AKT-mTOR Signaling to Promote the Progression of Cervical Cancer
Authors:  Zhengxia Zhu, B.S., Jianyang Zhang, M.M., and Peng Wu, B.S.
  Objective: To study the effect of endothelial cell- specific molecule-1 (ESM-1) on the biological behavior of cervical cancer cells and the molecular mechanism involved.
Study Design:
qRT-PCR was used to detect ESM-1 expression in cervical cancer tissues and normal tissues adjacent to cancer, human normal cervical epithelial cell lines (H8), and human cervical cancer cell lines (HeLa, CaSki, C-33A, and SiHa). After silencing ESM-1 expression in C-33A and SiHa cells, MTT, flow cytometry, and Transwell assay were administered to measure cell proliferation, apoptosis, invasion, and migration, respectively. ESM-1 protein expression in tissues and PI3K-AKT-mTOR pathway related protein in cervical cancer cells were detected by western blot.
ESM-1 expression was upregulated significantly in cervical cancer tissues and cells. Knockdown of ESM-1 inhibited the proliferation, invasion, and migration of cervical cancer cells, promoted cancer cell apoptosis, and significantly inhibited the activation of PI3K-AKT-mTOR signaling pathway. Additionally, knockdown of ESM-1 restrained the cancer-promoting effect of the PI3K activator (740Y-P) on cells.
Knockdown of ESM-1 can inhibit the activation of PI3K/Akt/mTOR signaling pathway to hinder cell proliferation, invasion, and migration. Meanwhile, knockdown of ESM-1 can promote cervical cancer cell apoptosis and slow down the development of cervical cancer. Additionally, it can be used as a molecular target for the treatment and prognosis of cervical cancer.
Keywords:  cervical cancer, ESM-1, invasion, migration, PI3K-AKT-mTOR signaling pathway, proliferation
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