Evidence map›Paper›PMID 40857057›Full record

ArticleJournal of cellular and molecular medicine2025

KIFC1 Overexpression Promotes Pancreatic Carcinoma Progression via Stabilising BUB1B.

Ao Cui, Ying-Xue Yu, Mei-Xue Xiong, Ji-Yang Wang, Ye-Qing Zou, Ya-Qiong Zhu, Long-Jian Ran, Yu Zhang, Rui-Xiang Liu, Ming-Yi Dong and 3 more

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In one paragraph

Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Ao CuiDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, China.ORCID 0009-0002-5125-7159
Ying-Xue YuDepartment of Neurology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Mei-Xue XiongDepartment of General Surgery, The People's Hospital of Gongqingcheng, Gongqingcheng, China.
Ji-Yang WangDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Ye-Qing ZouJiangxi Province Key Laboratory of Molecular Medicine, Nanchang, China.
Ya-Qiong ZhuJiangxi Province Key Laboratory of Molecular Medicine, Nanchang, China.
Long-Jian RanDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Yu ZhangDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Rui-Xiang LiuDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Ming-Yi DongJiangxi Province Key Laboratory of Molecular Medicine, Nanchang, China.
Hui WangJiangxi Province Key Laboratory of Molecular Medicine, Nanchang, China.
Lu FangDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Xiao-Wei FuDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, China.

Funding

Foundation of Jiangxi Educational Commission GJJ2200227Foundation of Jiangxi Educational Commission GJJ2200237Scientific Research Incubation Project, The Second Affiliated Hospital of Nanchang University 2022YNF12020Scientific Research Incubation Project, The Second Affiliated Hospital of Nanchang University 2022YNFY12002The National Natural Science Foundation of China 82360220The National Natural Science Foundation of China 82360513The National Natural Science Foundation of China 82460600The Natural Science Foundation of Jiangxi Province 20224BAB216050The Natural Science Foundation of Jiangxi Province 20232BAB206078The Natural Science Foundation of Jiangxi Province 20232BAB216076
6 · The paper itself

Abstract

Pancreatic cancer (PC) is a highly lethal tumour of the gastrointestinal tract. New molecular targets are urgently needed for its treatment. Kinesin family member C1 (KIFC1) is implicated in the development and progression of several types of cancer. Previous studies from our group demonstrated that KIFC1 overexpression in hepatocellular carcinoma promotes malignant behaviours via the PI3K/AKT pathway. However, the molecular and functional mechanisms of KIFC1 in PC are not yet fully elaborated. In this study, KIFC1 and BUB1B were significantly upregulated in PC patient samples, and high KIFC1 expression was closely associated with the malignant phenotype and poorer overall survival (OS) in PC patients. Functional experiments showed that KIFC1 knockdown inhibited PC cell growth in vivo and in vitro, blocked cell cycle progression and hindered cell migration and invasion. In addition, rescue experiments showed that KIFC1 induced PC cell malignant behaviours dependent on BUB1B. Mechanistically, KIFC1 regulates BUB1B expression by competitively binding to BUB1B and reducing its ubiquitination and degradation. We have shown for the first time the molecular regulatory mechanism between KIFC1 and BUB1B on PC. Therefore, KIFC1 shows promise as an attractive therapeutic target for PC in the future.

Indexed as

Cell Cycle ProteinsGene Expression Regulation, NeoplasticKinesinsPancreatic NeoplasmsProtein Serine-Threonine KinasesAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleHumansMaleMiceMice, NudeMiddle AgedBUB1B protein, humanCell Cycle ProteinsKIFC1 protein, humanKinesinsProtein Serine-Threonine KinasesBUB1BKIFC1pancreatic cancerprotein interactionstumorigenesisubiquitination

Identifiers

PMID40857057
PMCPMC12379544

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.