Overexpressed NEK2 contributes to progression and cisplatin resistance through activating the Wnt/β-catenin signaling pathway in cervical cancer.

IF 5.3 2区 医学 Q1 ONCOLOGY Cancer Cell International Pub Date : 2025-02-14 DOI:10.1186/s12935-025-03644-x
Jiang Haiye, Wang Xiangzhu, Zhang Yunfei, Gui Shumin, Ni Chang, Jiang Yaohui, Yin Heng, Nie Xinmin
{"title":"Overexpressed NEK2 contributes to progression and cisplatin resistance through activating the Wnt/β-catenin signaling pathway in cervical cancer.","authors":"Jiang Haiye, Wang Xiangzhu, Zhang Yunfei, Gui Shumin, Ni Chang, Jiang Yaohui, Yin Heng, Nie Xinmin","doi":"10.1186/s12935-025-03644-x","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Cervical cancer ranks as the fourth most common cancer among women, with cisplatin resistance posing a significant challenge to the long-term survival of patients.</p><p><strong>Methods: </strong>The roles of NEK2 in cervical cancer were examined through bioinformatics analysis. Transfection efficiency and molecular mechanisms were assessed using real-time quantitative polymerase chain reaction (qRT-PCR) and western blotting (WB). To evaluate cell functions, a series of assays, including cell counting kit-8 (CCK-8), wound healing, transwell, colony formation, and flow cytometry (FCM), were performed on HeLa, SiHa, and HeLa/DDP (cisplatin-resistant) cell lines.</p><p><strong>Results: </strong>We found that NEK2 is upregulated in cervical cancer tissues compared to normal tissues and is further elevated in cisplatin-resistant cervical cancer compared to cisplatin-sensitive cases. The overexpression of NEK2 is associated with enhanced cancer progression, poorer prognosis, and increased cisplatin resistance in cervical cancer patients. Notably, in the presence of cisplatin, the knockdown of NEK2 inhibited cell viability, proliferation, migration, invasion, and G2/M phase arrest in cervical cancer cells, while also enhancing the sensitivity of cisplatin-resistant cervical cancer cells through the inactivation of the Wnt/β-catenin signaling pathway.</p><p><strong>Conclusions: </strong>NEK2 is upregulated in cervical squamous cell carcinoma (CESC) compared to normal tissues and exhibits higher levels in cisplatin-resistant CESC than in sensitive counterparts, correlating with disease progression and poor prognosis. Thus, NEK2 is implicated in the cisplatin resistance of CESC via the activation of the Wnt/β-catenin signaling pathway, suggesting its potential as a prognostic marker and a novel target for the diagnosis and treatment of cisplatin-resistant CESC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"45"},"PeriodicalIF":5.3000,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Cell International","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s12935-025-03644-x","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Cervical cancer ranks as the fourth most common cancer among women, with cisplatin resistance posing a significant challenge to the long-term survival of patients.

Methods: The roles of NEK2 in cervical cancer were examined through bioinformatics analysis. Transfection efficiency and molecular mechanisms were assessed using real-time quantitative polymerase chain reaction (qRT-PCR) and western blotting (WB). To evaluate cell functions, a series of assays, including cell counting kit-8 (CCK-8), wound healing, transwell, colony formation, and flow cytometry (FCM), were performed on HeLa, SiHa, and HeLa/DDP (cisplatin-resistant) cell lines.

Results: We found that NEK2 is upregulated in cervical cancer tissues compared to normal tissues and is further elevated in cisplatin-resistant cervical cancer compared to cisplatin-sensitive cases. The overexpression of NEK2 is associated with enhanced cancer progression, poorer prognosis, and increased cisplatin resistance in cervical cancer patients. Notably, in the presence of cisplatin, the knockdown of NEK2 inhibited cell viability, proliferation, migration, invasion, and G2/M phase arrest in cervical cancer cells, while also enhancing the sensitivity of cisplatin-resistant cervical cancer cells through the inactivation of the Wnt/β-catenin signaling pathway.

Conclusions: NEK2 is upregulated in cervical squamous cell carcinoma (CESC) compared to normal tissues and exhibits higher levels in cisplatin-resistant CESC than in sensitive counterparts, correlating with disease progression and poor prognosis. Thus, NEK2 is implicated in the cisplatin resistance of CESC via the activation of the Wnt/β-catenin signaling pathway, suggesting its potential as a prognostic marker and a novel target for the diagnosis and treatment of cisplatin-resistant CESC.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
求助全文
约1分钟内获得全文 去求助
来源期刊
CiteScore
10.90
自引率
1.70%
发文量
360
审稿时长
1 months
期刊介绍: Cancer Cell International publishes articles on all aspects of cancer cell biology, originating largely from, but not limited to, work using cell culture techniques. The journal focuses on novel cancer studies reporting data from biological experiments performed on cells grown in vitro, in two- or three-dimensional systems, and/or in vivo (animal experiments). These types of experiments have provided crucial data in many fields, from cell proliferation and transformation, to epithelial-mesenchymal interaction, to apoptosis, and host immune response to tumors. Cancer Cell International also considers articles that focus on novel technologies or novel pathways in molecular analysis and on epidemiological studies that may affect patient care, as well as articles reporting translational cancer research studies where in vitro discoveries are bridged to the clinic. As such, the journal is interested in laboratory and animal studies reporting on novel biomarkers of tumor progression and response to therapy and on their applicability to human cancers.
期刊最新文献
Mcl-1 downregulation enhances BCG treatment efficacy in bladder cancer by promoting macrophage polarization. Mechanistic insights of lenvatinib: enhancing cisplatin sensitivity, inducing apoptosis, and suppressing metastasis in bladder cancer cells through EGFR/ERK/P38/NF-κB signaling inactivation. The role of mitochondrial biogenesis, mitochondrial dynamics and mitophagy in gastrointestinal tumors. Overexpressed NEK2 contributes to progression and cisplatin resistance through activating the Wnt/β-catenin signaling pathway in cervical cancer. Arcyriaflavin A, a cyclin D1/CDK4 inhibitor, suppresses tumor growth, migration, and invasion of metastatic melanoma cells.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1