Serinc2 Drives the Progression of Cervical Cancer Through Regulating Myc Pathway

ABSTRACT Background As one of the most common malignancies, cervical cancer (CC) seriously affects women's health. This study aimed to investigate the biological function of Serinc2 in CC. Methods Serinc2 expression was surveyed utilizing immunohistochemistry, western blot, and qRT‐PCR. CC cell...

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Main Authors: Xiaoping Wang, Chen Jiang, Qing Li
Format: Article
Language:English
Published: Wiley 2024-10-01
Series:Cancer Medicine
Subjects:
Online Access:https://doi.org/10.1002/cam4.70296
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author Xiaoping Wang
Chen Jiang
Qing Li
author_facet Xiaoping Wang
Chen Jiang
Qing Li
author_sort Xiaoping Wang
collection DOAJ
description ABSTRACT Background As one of the most common malignancies, cervical cancer (CC) seriously affects women's health. This study aimed to investigate the biological function of Serinc2 in CC. Methods Serinc2 expression was surveyed utilizing immunohistochemistry, western blot, and qRT‐PCR. CC cell viability, invasion, proliferation, migration, and apoptosis, were detected via CCK‐8, Transwell assay, colony formation, wound healing assay, and flow cytometry. Glucose consumption, lactate production, and ATP levels were determined by the corresponding kit. The protein expression of c‐Myc, PDK1, HK2, PFKP, LDHA, Snail, Vimentin, N‐cadherin, and E‐cadherin was detected via western blot. The interaction between the promoter of PFKP and Myc was confirmed through luciferase reporter assay and Chip assay. In vivo, to evaluate the function of Serinc2 on tumor growth, a xenograft mouse model was used. Results In CC tissues and cells, Serinc2 was upregulated. In CC cells, knockdown of Serinc2 suppressed cell invasion, proliferation, migration, decreased the expression of Snail, Vimentin, N‐cadherin, HK2, PFKP, LDHA, and PDK1, increased E‐cadherin expression, reduced glucose consumption and the production of lactate and ATP, and induced cell apoptosis; Serinc2 overexpression led to the opposite results. Mechanically, Serinc2 promoted Myc expression, and Myc induced PFKP expression. Furthermore, overexpressed Myc abolished the inhibitive influences of Serinc2 knockdown on the malignant behaviors of CC cells. Additionally, knockdown of Serinc2 inhibited tumor growth and reduced the protein expression of c‐Myc, PFKP, LDHA, and PDK1 in vivo. Conclusions Knockdown of Serinc2 inhibited the malignant progression of CC, which was achieved via Myc pathway. Our study provides novel insight into CC pathogenesis.
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spelling doaj-art-b227a7269ba54e0580cef74ff5eec79e2025-08-20T02:32:11ZengWileyCancer Medicine2045-76342024-10-011319n/an/a10.1002/cam4.70296Serinc2 Drives the Progression of Cervical Cancer Through Regulating Myc PathwayXiaoping Wang0Chen Jiang1Qing Li2Department of Obstetrics and Gynecology Jinan Maternity and Child Care Hospital Jinan Shandong People's Republic of ChinaDepartment of Obstetrics and Gynecology Jinan Maternity and Child Care Hospital Jinan Shandong People's Republic of ChinaDepartment of Obstetrics and Gynecology Jinan Maternity and Child Care Hospital Jinan Shandong People's Republic of ChinaABSTRACT Background As one of the most common malignancies, cervical cancer (CC) seriously affects women's health. This study aimed to investigate the biological function of Serinc2 in CC. Methods Serinc2 expression was surveyed utilizing immunohistochemistry, western blot, and qRT‐PCR. CC cell viability, invasion, proliferation, migration, and apoptosis, were detected via CCK‐8, Transwell assay, colony formation, wound healing assay, and flow cytometry. Glucose consumption, lactate production, and ATP levels were determined by the corresponding kit. The protein expression of c‐Myc, PDK1, HK2, PFKP, LDHA, Snail, Vimentin, N‐cadherin, and E‐cadherin was detected via western blot. The interaction between the promoter of PFKP and Myc was confirmed through luciferase reporter assay and Chip assay. In vivo, to evaluate the function of Serinc2 on tumor growth, a xenograft mouse model was used. Results In CC tissues and cells, Serinc2 was upregulated. In CC cells, knockdown of Serinc2 suppressed cell invasion, proliferation, migration, decreased the expression of Snail, Vimentin, N‐cadherin, HK2, PFKP, LDHA, and PDK1, increased E‐cadherin expression, reduced glucose consumption and the production of lactate and ATP, and induced cell apoptosis; Serinc2 overexpression led to the opposite results. Mechanically, Serinc2 promoted Myc expression, and Myc induced PFKP expression. Furthermore, overexpressed Myc abolished the inhibitive influences of Serinc2 knockdown on the malignant behaviors of CC cells. Additionally, knockdown of Serinc2 inhibited tumor growth and reduced the protein expression of c‐Myc, PFKP, LDHA, and PDK1 in vivo. Conclusions Knockdown of Serinc2 inhibited the malignant progression of CC, which was achieved via Myc pathway. Our study provides novel insight into CC pathogenesis.https://doi.org/10.1002/cam4.70296cell proliferationcervical cancerglycolysisMycSerinc2
spellingShingle Xiaoping Wang
Chen Jiang
Qing Li
Serinc2 Drives the Progression of Cervical Cancer Through Regulating Myc Pathway
Cancer Medicine
cell proliferation
cervical cancer
glycolysis
Myc
Serinc2
title Serinc2 Drives the Progression of Cervical Cancer Through Regulating Myc Pathway
title_full Serinc2 Drives the Progression of Cervical Cancer Through Regulating Myc Pathway
title_fullStr Serinc2 Drives the Progression of Cervical Cancer Through Regulating Myc Pathway
title_full_unstemmed Serinc2 Drives the Progression of Cervical Cancer Through Regulating Myc Pathway
title_short Serinc2 Drives the Progression of Cervical Cancer Through Regulating Myc Pathway
title_sort serinc2 drives the progression of cervical cancer through regulating myc pathway
topic cell proliferation
cervical cancer
glycolysis
Myc
Serinc2
url https://doi.org/10.1002/cam4.70296
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AT qingli serinc2drivestheprogressionofcervicalcancerthroughregulatingmycpathway