OLFM4 Inhibits Epithelial-Mesenchymal Transition and Metastatic Potential of Cervical Cancer Cells
Autor: | Meng Wan, Hong Zhang, Juan Li, Qing Sun, Hongchun Hou, Xuemei Jie, Xiaoxia Zheng, Chunyan Liu, Dawei Li, Jingjing Li, Pengju Zhang |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Cancer Research Epithelial-Mesenchymal Transition Down-Regulation Uterine Cervical Neoplasms Tumor initiation OLFM4 Article law.invention Metastasis 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Downregulation and upregulation law Cell Movement Granulocyte Colony-Stimulating Factor Medicine Humans Neoplasm Invasiveness Epithelial–mesenchymal transition Neoplasm Metastasis PI3K/AKT/mTOR pathway Epithelial–mesenchymal transition (EMT) business.industry TOR Serine-Threonine Kinases Cell migration General Medicine Phosphatidic acid 030104 developmental biology Oncology chemistry 030220 oncology & carcinogenesis Cancer research Cervical cancer mTOR Suppressor Female Signal transduction business HeLa Cells Signal Transduction |
Zdroj: | Oncology Research |
ISSN: | 1555-3906 |
Popis: | OLFM4 has been shown to play an important role in tumor initiation and progression. This study aims to investigate the role of OLFM4 in metastatic cervical cancer and its underlying mechanism. Here we discover that OLFM4 expression is significantly reduced in metastatic cervical cancer. Accordingly, overexpression of OLFM4 inhibits epithelial‐mesenchymal transition (EMT), migration, and invasion in human cervical cancer cells. To further explore its molecular mechanisms, we reveal that OLFM4 augmentation interferes with mTOR signaling pathway, and the suppressive effects of OLFM4 on cell migration and invasion are largely weakened by phosphatidic acid (PA)-induced mTOR signal activation, which implicates the potential role of the mTOR pathway in OLFM4-related cervical metastasis. In conclusion, our results confirm OLFM4 as a tumor suppressor that inhibits cervical cancer metastasis by regulating mTOR signal pathway. |
Databáze: | OpenAIRE |
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