KIFC1 in cancer: Understanding its expression, regulation, and therapeutic potential

IF 3.5 3区 生物学 Q3 CELL BIOLOGY Experimental cell research Pub Date : 2025-04-01 Epub Date: 2025-03-08 DOI:10.1016/j.yexcr.2025.114510
Gaurav Sanghvi , R. Roopashree , Aditya Kashyap , A. Sabarivani , Subhashree Ray , Pushpa Negi Bhakuni
{"title":"KIFC1 in cancer: Understanding its expression, regulation, and therapeutic potential","authors":"Gaurav Sanghvi ,&nbsp;R. Roopashree ,&nbsp;Aditya Kashyap ,&nbsp;A. Sabarivani ,&nbsp;Subhashree Ray ,&nbsp;Pushpa Negi Bhakuni","doi":"10.1016/j.yexcr.2025.114510","DOIUrl":null,"url":null,"abstract":"<div><div>Kinesins are a family of motor proteins essential for intracellular transport and cellular dynamics, with kinesin family member C1 (KIFC1) emerging as a key regulator of cancer progression. Recent studies highlight KIFC1's crucial role in mitotic spindle assembly, chromosome segregation, and cell migration—processes frequently dysregulated in cancer. Its involvement in promoting malignant cell proliferation and metastasis underscores its significance in tumor biology. In various cancer types, aberrant KIFC1 expression correlates with poor prognosis and aggressive phenotypes, suggesting its potential as a biomarker for disease severity. Mechanistically, KIFC1 influences signaling pathways linked to cell cycle regulation and programmed cell death, reinforcing its role in oncogenesis. Given its pivotal function in cancer cell dynamics, KIFC1 represents a promising therapeutic target. Strategies aimed at modulating its activity, including small molecules or RNA interference, could disrupt cancer cell viability and proliferation. The current review article highlights KIFC1's importance in cancer biology, advocating for further investigation into its mechanisms and the development of KIFC1-targeted therapies to enhance treatment efficacy and improve patient outcomes across various malignancies.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114510"},"PeriodicalIF":3.5000,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental cell research","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0014482725001065","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/3/8 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Kinesins are a family of motor proteins essential for intracellular transport and cellular dynamics, with kinesin family member C1 (KIFC1) emerging as a key regulator of cancer progression. Recent studies highlight KIFC1's crucial role in mitotic spindle assembly, chromosome segregation, and cell migration—processes frequently dysregulated in cancer. Its involvement in promoting malignant cell proliferation and metastasis underscores its significance in tumor biology. In various cancer types, aberrant KIFC1 expression correlates with poor prognosis and aggressive phenotypes, suggesting its potential as a biomarker for disease severity. Mechanistically, KIFC1 influences signaling pathways linked to cell cycle regulation and programmed cell death, reinforcing its role in oncogenesis. Given its pivotal function in cancer cell dynamics, KIFC1 represents a promising therapeutic target. Strategies aimed at modulating its activity, including small molecules or RNA interference, could disrupt cancer cell viability and proliferation. The current review article highlights KIFC1's importance in cancer biology, advocating for further investigation into its mechanisms and the development of KIFC1-targeted therapies to enhance treatment efficacy and improve patient outcomes across various malignancies.
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
癌症中的KIFC1:了解其表达、调节和治疗潜力
运动蛋白是一个对细胞内运输和细胞动力学至关重要的运动蛋白家族,其中运动蛋白家族成员C1 (KIFC1)成为癌症进展的关键调节因子。最近的研究强调了KIFC1在有丝分裂纺锤体组装、染色体分离和细胞迁移过程中的关键作用,这些过程在癌症中经常失调。它参与促进恶性细胞的增殖和转移,强调了它在肿瘤生物学中的重要性。在各种癌症类型中,异常的KIFC1表达与不良预后和侵袭性表型相关,这表明它有可能作为疾病严重程度的生物标志物。在机制上,KIFC1影响与细胞周期调节和程序性细胞死亡相关的信号通路,加强其在肿瘤发生中的作用。鉴于其在癌细胞动力学中的关键功能,KIFC1代表了一个有希望的治疗靶点。旨在调节其活性的策略,包括小分子或RNA干扰,可能会破坏癌细胞的生存能力和增殖。当前的综述文章强调了KIFC1在癌症生物学中的重要性,提倡进一步研究其机制和开发KIFC1靶向治疗,以提高各种恶性肿瘤的治疗效果和改善患者预后。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Experimental cell research
Experimental cell research 医学-细胞生物学
CiteScore
7.20
自引率
0.00%
发文量
295
审稿时长
30 days
期刊介绍: Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.
期刊最新文献
The antineoplastic agent streptozotocin induces short-term telomere instability in Epstein-Barr virus-transformed human lymphoblastoid cells Serum-free medium modulates the immunomodulatory and anabolic function of equine bone marrow-derived mesenchymal stromal cells EP300/NCOA1 complex drives glioma angiogenesis via H3K27 acetylation–dependent activation of VEGFA Zn2+-dependent modulation of the mitochondrial Ca2+ uniporter underlies resveratrol-mediated protection against myocardial ischemia-reperfusion injury The role of MBD3 in cell biology and disease: Recent advances and future directions
×
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:604180095
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