OLFM4 Inhibits Epithelial-Mesenchymal Transition and Metastatic Potential of Cervical Cancer Cells.

Abstract

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.

• Authors: Juan Li, Chunyan Liu, Dawei Li, Meng Wan, Hong Zhang, Xiaoxia Zheng, Xuemei Jie, Pengju Zhang, Jingjing Li, Hongchun Hou, Qing Sun
• Journal: Oncology research (Oncol Res) Vol. 27 Issue 7 Pg. 763-771 (Jul 12 2019) ISSN: 1555-3906 [Electronic] United States
• PMID: 30764901 (Publication Type: Journal Article)

Chemical References

• OLFM4 protein, human
• Granulocyte Colony-Stimulating Factor
• MTOR protein, human
• TOR Serine-Threonine Kinases

Topics

• Cell Movement (physiology)
• Down-Regulation
• Epithelial-Mesenchymal Transition
• Female
• Granulocyte Colony-Stimulating Factor (biosynthesis, genetics, metabolism)
• HeLa Cells
• Humans
• Neoplasm Invasiveness
• Neoplasm Metastasis
• Signal Transduction
• TOR Serine-Threonine Kinases (antagonists & inhibitors, metabolism)
• Uterine Cervical Neoplasms (genetics, metabolism, pathology)