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Last update 08 May 2025

KIFC1

Last update 08 May 2025

Basic Info

Synonyms

HSET, KIFC1, kinesin family member C1

+ [4]

Introduction

Minus end-directed microtubule-dependent motor required for bipolar spindle formation (PubMed:15843429). May contribute to movement of early endocytic vesicles (By similarity). Regulates cilium formation and structure (By similarity).

Drugs associated with KIFC1

KIFC1 inhibitors (Merck)

Target

KIFC1

Mechanism

KIFC1 inhibitors

Active Org.

Merck KGaA

Originator Org.

Merck KGaA

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

AZ-82

Target

KIFC1

Mechanism

KIFC1 inhibitors

Active Org.-

Originator Org.

AstraZeneca R&D Boston, Inc.

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with KIFC1

100 Translational Medicine associated with KIFC1

0 Patents (Medical) associated with KIFC1

245

Literatures (Medical) associated with KIFC1

01 Apr 2025·Experimental Cell Research

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

Review

Author: Sabarivani, A ; Sanghvi, Gaurav ; Ray, Subhashree ; Roopashree, R ; Bhakuni, Pushpa Negi ; Kashyap, Aditya

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.

01 Mar 2025·Naunyn-Schmiedeberg's Archives of Pharmacology

Identification of RTP4 facilitating ovarian cancer by bioinformatics analysis and experimental validation

Article

Author: Han, Wenling ; Fang, Chunyun ; Tang, Chen ; Ni, Bin ; Shen, Junjing

Ovarian cancer (OV) is the most malignant gynecological tumor in women, with poor prognosis and high mortality rate. This study aims to identify hub genes in OV and explore the role of Receptor transporter 4 (RTP4) in OV progression. Common differentially expressed genes (DEGs) were screened from two microarray datasets. GO and KEGG enrichment analysis were performed. Protein-protein interaction (PPI) network was constructed by STING. Kaplan-Meier plotter was used to analyze prognosis. The effect of target gene on immune infiltration was analyzed by TIMER. The proliferation, migration, and invasion of OV cells were measured by CCK-8, wound healing assay, and trans-well assay, respectively. A total of 293 common DEGs were selected from GSE12470 and GSE16709 datasets. Hub genes, EPCAM, KIFC1, RTP4, TAGLN, and ZFP36 were selected by PPI network. Kaplan-Meier plotter demonstrated that high expression of RTP4 was related to low overall survival in OV patients. The TIMER result showed that high expression of RTP4 promoted immune infiltration of CD8⁺ T cells, B cells, neutrophils, and dendritic cells in OV. Moreover, silencing RTP4 significantly inhibited the proliferation, migration, and invasion of OV cells. RTP4 was associated with the poor prognosis in OV. In summary, silencing RTP4 inhibited the proliferation, migration, and invasion of OV cells, having the potential to be a novel therapeutic target for OV.

01 Mar 2025·Theriogenology

Loss of KIFC1 activity induces spindle instability and actin defects during porcine oocyte maturation

Article

Author: Wei, Jing-Xi ; Hu, Lin-Lin ; Tao, Le-Yan ; Wang, Peng-Jie ; Liu, Qiang-Qiang ; Wang, Yue ; Sun, Shao-Chen ; Wang, Yu-Ran

KIFC1 is a motor protein of the Kinesin family and it is involved in spindle apparatus assembly, chromosome arrangement, and microfilament-mediated biological processes in mitosis. However, the specific function of KIFC1 in pig oocytes remains unclear. Here, in order to explore the function of KIFC1 in porcine oocytes, the AZ82 inhibitor was used to inhibit the activity of KIFC1. Our results showed when KIFC1 was inhibited, the polar body extrusion rate was obviously decreased, indicating that KIFC1 plays a crucial role in porcine oocytes. We next measured the spindle structure and chromosome arrangement via immunofluorescent staining and found both the rates of abnormal spindle and chromosome disorder increased significantly. By further analyzing the causes of the abnormal spindle, we found the acetylation of tubulin was disrupted. In addition, we also found the spindle position was impaired after KIFC1 inhibition, declaring the spindle migration was affected. Further analysis found cortex actin decreased and cytoplasmic actin increased after KIFC1 inhibition. In summary, we found that KIFC1 played a critical role in porcine oocytes maturation by controlling spindle apparatus via mediating the acetylation of microtubule and regulating the spindle migration via affecting actin dynamics.

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KIFC1

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