Knockdown of S100A2 inhibits the aggressiveness of endometrial cancer by activating STING pathway

Background Endometrial cancer is a kind of gynaecological cancer. S100A2 is a newfound biomarker to diagnose endometrial cancer. This study was to investigate the role of S100A2 on regulating migration and invasion of endometrial cancer.Methods The mRNA and protein levels of S100A2 were obtained by...

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Main Authors: Chengcheng Li, Dandan Zhu, Xun Cao, Ying Li, Xiaoyuan Hao
Format: Article
Language:English
Published: Taylor & Francis Group 2024-12-01
Series:Journal of Obstetrics and Gynaecology
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Online Access:https://www.tandfonline.com/doi/10.1080/01443615.2024.2361849
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author Chengcheng Li
Dandan Zhu
Xun Cao
Ying Li
Xiaoyuan Hao
author_facet Chengcheng Li
Dandan Zhu
Xun Cao
Ying Li
Xiaoyuan Hao
author_sort Chengcheng Li
collection DOAJ
description Background Endometrial cancer is a kind of gynaecological cancer. S100A2 is a newfound biomarker to diagnose endometrial cancer. This study was to investigate the role of S100A2 on regulating migration and invasion of endometrial cancer.Methods The mRNA and protein levels of S100A2 were obtained by quantitative real-time polymerase chain reaction, immunohistochemistry and western blot methods. Cell viability was measured by the Cell Counting Kit-8 assay. Cell migration and invasion were quantified using transwell assays. Western blot assay was conducted to quantify protein expressions of epithelial to mesenchymal transition-related proteins (N-cadherin and E-cadherin). Furthermore, in vivo tumour formation experiments were performed to evaluate the role of S100A2 on tumour xenografts.Results S100A2 was significantly up-regulated in endometrial cancer tissues. Knockdown of S100A2 inhibited cell viability, migration and invasion of endometrial cancer cells. Meanwhile, STING pathway was activated by the inhibited S100A2. STING inhibitor C-176 significantly reversed the effects of S100A2 knockdown on aggressive behaviours of endometrial cancer cells. Inhibition of S100A2 dramatically suppresses the tumour growth in vivo.Conclusions S100A2 functions as an oncogene in endometrial cancer. Targeting S100A2 may be a promising therapeutic method to treat endometrial carcinoma.
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publishDate 2024-12-01
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series Journal of Obstetrics and Gynaecology
spelling doaj-art-d057abf5834c492882fadb9095db714c2025-01-09T12:13:17ZengTaylor & Francis GroupJournal of Obstetrics and Gynaecology0144-36151364-68932024-12-0144110.1080/01443615.2024.2361849Knockdown of S100A2 inhibits the aggressiveness of endometrial cancer by activating STING pathwayChengcheng Li0Dandan Zhu1Xun Cao2Ying Li3Xiaoyuan Hao4Gynaecology and Obstetrics, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, ChinaGynaecology and Obstetrics, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, ChinaRehabilitation Medicine Department, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, ChinaGynaecology and Obstetrics, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, ChinaGynaecology and Obstetrics, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, ChinaBackground Endometrial cancer is a kind of gynaecological cancer. S100A2 is a newfound biomarker to diagnose endometrial cancer. This study was to investigate the role of S100A2 on regulating migration and invasion of endometrial cancer.Methods The mRNA and protein levels of S100A2 were obtained by quantitative real-time polymerase chain reaction, immunohistochemistry and western blot methods. Cell viability was measured by the Cell Counting Kit-8 assay. Cell migration and invasion were quantified using transwell assays. Western blot assay was conducted to quantify protein expressions of epithelial to mesenchymal transition-related proteins (N-cadherin and E-cadherin). Furthermore, in vivo tumour formation experiments were performed to evaluate the role of S100A2 on tumour xenografts.Results S100A2 was significantly up-regulated in endometrial cancer tissues. Knockdown of S100A2 inhibited cell viability, migration and invasion of endometrial cancer cells. Meanwhile, STING pathway was activated by the inhibited S100A2. STING inhibitor C-176 significantly reversed the effects of S100A2 knockdown on aggressive behaviours of endometrial cancer cells. Inhibition of S100A2 dramatically suppresses the tumour growth in vivo.Conclusions S100A2 functions as an oncogene in endometrial cancer. Targeting S100A2 may be a promising therapeutic method to treat endometrial carcinoma.https://www.tandfonline.com/doi/10.1080/01443615.2024.2361849Endometrial carcinomaS100A2STINGcGAS
spellingShingle Chengcheng Li
Dandan Zhu
Xun Cao
Ying Li
Xiaoyuan Hao
Knockdown of S100A2 inhibits the aggressiveness of endometrial cancer by activating STING pathway
Journal of Obstetrics and Gynaecology
Endometrial carcinoma
S100A2
STING
cGAS
title Knockdown of S100A2 inhibits the aggressiveness of endometrial cancer by activating STING pathway
title_full Knockdown of S100A2 inhibits the aggressiveness of endometrial cancer by activating STING pathway
title_fullStr Knockdown of S100A2 inhibits the aggressiveness of endometrial cancer by activating STING pathway
title_full_unstemmed Knockdown of S100A2 inhibits the aggressiveness of endometrial cancer by activating STING pathway
title_short Knockdown of S100A2 inhibits the aggressiveness of endometrial cancer by activating STING pathway
title_sort knockdown of s100a2 inhibits the aggressiveness of endometrial cancer by activating sting pathway
topic Endometrial carcinoma
S100A2
STING
cGAS
url https://www.tandfonline.com/doi/10.1080/01443615.2024.2361849
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