SOS1 promotes epithelial-mesenchymal transition of Epithelial Ovarian Cancer(EOC) cells through AKT independent NF-κB signaling pathway

We aimed to explore the role and mechanism of SOS1 (Son of sevenless homolog 1) in malignant behaviors of epithelial ovarian cancer (EOC) cells Hey with high metastatic potential. Firstly, compared with Hey-WT (wild type) and Hey-NT (none targeted) cells, Hey-SOS1i cells showed decreased polarities,...

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Main Authors: Min Cheng, Xiaolin Ye, Jiemin Dai, Feiji Sun
Format: Article
Language:English
Published: Elsevier 2021-09-01
Series:Translational Oncology
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S1936523321001522
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author Min Cheng
Xiaolin Ye
Jiemin Dai
Feiji Sun
author_facet Min Cheng
Xiaolin Ye
Jiemin Dai
Feiji Sun
author_sort Min Cheng
collection DOAJ
description We aimed to explore the role and mechanism of SOS1 (Son of sevenless homolog 1) in malignant behaviors of epithelial ovarian cancer (EOC) cells Hey with high metastatic potential. Firstly, compared with Hey-WT (wild type) and Hey-NT (none targeted) cells, Hey-SOS1i cells showed decreased polarities, disorders in cytoskeleton arrangement. Numbers of transwell migrated, invaded, intravasation cells and extravasated cells were decreased significantly. Hey-NT cells and Hey-SOS1i cells were employed to establish a peritoneal dissemination model in nude mice. Hey-SOS1i cells formed less implantation metastatic foci in the abdominal cavity than Hey-NT cells, especially on the intestine and diaphragm in the 5th week after the tumor cells were injected intraperitoneally. SOS1 knockdown in Hey cells resulted in increased E-cadherin and decreased Vimentin, N-cadherin, MMP2, and MMP9, together with reduced Snail and activation of NF-κB pathway. Together, these results suggest SOS1 might induce EMT through activating AKT independent NF-κB pathway and the transcriptive activity of Snail, and subsequently regulate the cytoskeleton reprogramming and cell motility of Hey, one of EOC cells with high metastatic potential. This may provide some new targets for the treatment of ovarian cancer with high metastatic potential.
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spelling doaj.art-b976af9e299b47d8b90878ef2810d60b2022-12-21T21:34:51ZengElsevierTranslational Oncology1936-52332021-09-01149101160SOS1 promotes epithelial-mesenchymal transition of Epithelial Ovarian Cancer(EOC) cells through AKT independent NF-κB signaling pathwayMin Cheng0Xiaolin Ye1Jiemin Dai2Feiji Sun3Department of Reproductive Medicine Centre, Affiliated Hospital of Zunyi Medical University, Zunyi City, 563000, Guizhou Province, P.R. ChinaDepartment of Obstetrics and Gynecology, First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. ChinaDepartment of Obstetrics and Gynecology, First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. ChinaDepartment of Neurosurgery, Affiliated Hospital of Zunyi Medical University, Zunyi City, 563000, Guizhou Province, P.R. China; Corresponding author.We aimed to explore the role and mechanism of SOS1 (Son of sevenless homolog 1) in malignant behaviors of epithelial ovarian cancer (EOC) cells Hey with high metastatic potential. Firstly, compared with Hey-WT (wild type) and Hey-NT (none targeted) cells, Hey-SOS1i cells showed decreased polarities, disorders in cytoskeleton arrangement. Numbers of transwell migrated, invaded, intravasation cells and extravasated cells were decreased significantly. Hey-NT cells and Hey-SOS1i cells were employed to establish a peritoneal dissemination model in nude mice. Hey-SOS1i cells formed less implantation metastatic foci in the abdominal cavity than Hey-NT cells, especially on the intestine and diaphragm in the 5th week after the tumor cells were injected intraperitoneally. SOS1 knockdown in Hey cells resulted in increased E-cadherin and decreased Vimentin, N-cadherin, MMP2, and MMP9, together with reduced Snail and activation of NF-κB pathway. Together, these results suggest SOS1 might induce EMT through activating AKT independent NF-κB pathway and the transcriptive activity of Snail, and subsequently regulate the cytoskeleton reprogramming and cell motility of Hey, one of EOC cells with high metastatic potential. This may provide some new targets for the treatment of ovarian cancer with high metastatic potential.http://www.sciencedirect.com/science/article/pii/S1936523321001522SOS1Ovarian cancerEpithelial-mesenchymal transitionNF-κB signaling pathway
spellingShingle Min Cheng
Xiaolin Ye
Jiemin Dai
Feiji Sun
SOS1 promotes epithelial-mesenchymal transition of Epithelial Ovarian Cancer(EOC) cells through AKT independent NF-κB signaling pathway
Translational Oncology
SOS1
Ovarian cancer
Epithelial-mesenchymal transition
NF-κB signaling pathway
title SOS1 promotes epithelial-mesenchymal transition of Epithelial Ovarian Cancer(EOC) cells through AKT independent NF-κB signaling pathway
title_full SOS1 promotes epithelial-mesenchymal transition of Epithelial Ovarian Cancer(EOC) cells through AKT independent NF-κB signaling pathway
title_fullStr SOS1 promotes epithelial-mesenchymal transition of Epithelial Ovarian Cancer(EOC) cells through AKT independent NF-κB signaling pathway
title_full_unstemmed SOS1 promotes epithelial-mesenchymal transition of Epithelial Ovarian Cancer(EOC) cells through AKT independent NF-κB signaling pathway
title_short SOS1 promotes epithelial-mesenchymal transition of Epithelial Ovarian Cancer(EOC) cells through AKT independent NF-κB signaling pathway
title_sort sos1 promotes epithelial mesenchymal transition of epithelial ovarian cancer eoc cells through akt independent nf κb signaling pathway
topic SOS1
Ovarian cancer
Epithelial-mesenchymal transition
NF-κB signaling pathway
url http://www.sciencedirect.com/science/article/pii/S1936523321001522
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