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OLFM4 抑制宫颈癌上皮-间质转化和转移潜能。

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

机构信息

Department of Pathology, Qianfoshan Hospital Affiliated with Shandong University, Jinan, Shandong, P.R. China.

Department of Combined Traditional Chinese and Western Medicine, Medical College of Qingdao University, Qingdao, Shandong, P.R. China.

出版信息

Oncol Res. 2019 Jul 12;27(7):763-771. doi: 10.3727/096504018X15399955297355. Epub 2019 Feb 14.

DOI:10.3727/096504018X15399955297355
PMID:30764901
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7848444/
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.

摘要

OLFM4 在肿瘤的发生和发展中起着重要作用。本研究旨在探讨 OLFM4 在转移性宫颈癌中的作用及其潜在机制。在这里,我们发现 OLFM4 的表达在转移性宫颈癌中显著降低。因此,OLFM4 的过表达抑制了人宫颈癌细胞的上皮-间充质转化(EMT)、迁移和侵袭。为了进一步探讨其分子机制,我们揭示了 OLFM4 的增强干扰了 mTOR 信号通路,并且 PA 诱导的 mTOR 信号激活大大减弱了 OLFM4 对细胞迁移和侵袭的抑制作用,这表明 mTOR 通路在 OLFM4 相关的宫颈癌转移中具有潜在作用。总之,我们的结果证实 OLFM4 是一种肿瘤抑制因子,通过调节 mTOR 信号通路抑制宫颈癌的转移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/543b/7848444/0e276dab07b3/OR-27-763-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/543b/7848444/a06d5542ca97/OR-27-763-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/543b/7848444/ca8484cdcf0d/OR-27-763-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/543b/7848444/eea24faf9920/OR-27-763-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/543b/7848444/7e563320b77b/OR-27-763-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/543b/7848444/0e276dab07b3/OR-27-763-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/543b/7848444/a06d5542ca97/OR-27-763-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/543b/7848444/ca8484cdcf0d/OR-27-763-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/543b/7848444/eea24faf9920/OR-27-763-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/543b/7848444/7e563320b77b/OR-27-763-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/543b/7848444/0e276dab07b3/OR-27-763-g005.jpg

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