KIFC3

Last update 08 May 2025

Basic Info

Synonyms

KIFC3, kinesin family member C3, Kinesin-like protein KIFC3

Introduction

Minus-end microtubule-dependent motor protein. Involved in apically targeted transport (By similarity). Required for zonula adherens maintenance.

100 Clinical Results associated with KIFC3

100 Translational Medicine associated with KIFC3

0 Patents (Medical) associated with KIFC3

Literatures (Medical) associated with KIFC3

01 Dec 2024·Molecules and Cells

Transport of Golgi-localized β-catenin p-S47 by KIF11 or KIFC3 induces primary ciliogenesis

Article

Author: Lee, Na Yeong ; Kim, Sun-Ok ; Lim, Key-Hwan ; Lee, Kyung Ho ; Kyun, Mi-Lang ; Yu, Ji Eun

Primary cilium is an important hub for cell signaling and dysregulation of primary cilia assembly and disassembly is associated with the development of cancer and chemotherapeutic drug resistance, as well as the genetic disorders collectively known as ciliopathy. β-catenin plays a major role in canonical Wnt signaling; however, its association with primary cilia has only recently been highlighted in reports of β-catenin-mediated primary ciliogenesis. In this study, we found that β-catenin p-S47 was localized to the Golgi apparatus and the nucleus, and the amount of β-catenin p-S47 at these locations was significantly higher during primary ciliogenesis compared with asynchronous cell growth conditions. In addition, the novel β-catenin-binding motor proteins KIF11 and KIFC3 were shown to have a lower binding affinity in β-catenin S47A than in β-catenin wild-type. Knockdown of KIF11 or KIFC3 resulted in primary cilia deficiency and increased β-catenin p-S47 levels in the Golgi apparatus and were accompanied by a decrease in β-catenin p-S47 at the centrosome. The accumulation of β-catenin p-S47 in the nucleus was increased during primary ciliogenesis along with β-catenin-dependent transcriptional activity. The collective findings indicate the existence of a novel mechanism of primary ciliogenesis involving KIF11-/KIFC3-associated β-catenin p-S47 in the Golgi apparatus and β-catenin p-S47 transcriptional activity in the nucleus. This study revealed a new mechanism for the study of ciliopathies, cancer, and chemotherapeutic drug resistance caused by primary ciliogenesis dysregulation and provides new targets for drug development to treat these diseases.

01 Nov 2024·Thoracic Cancer

KIFC3 promotes the progression of non–small cell lung cancer cells through the PI3K/Akt pathway

Article

Author: Mu, Yu ; Zhang, Qingxiang ; Luo, Anni ; Liu, Haoxiang

AbstractBackgroundKinesin family member C3 (KIFC3), as reported, plays important roles in several tumor types. Nevertheless, it is unknown whether KIFC3 has effects on non–small cell lung cancer (NSCLC) development.Materials and methodsKIFC3 expression was detected by RT‐PCR, and its correlation with prognosis was analyzed by GEPIA website. Small interfering RNA against KIFC3 were adopted for modulating KIFC3 expression in NSCLC cells. KIFC3 effects on NSCLC cell proliferation were determined using the MTT and clone formation assay. Matrigel invasion and wound healing assays were adopted for measuring the invasion and migration capability of NSCLC cells. Western blot was applied for measuring the levels of proteins associated with the phosphatidylinositol‐3‐kinase/protein kinase B (PI3K/Akt) pathway in NSCLC cells.ResultsKIFC3 was markedly increased in NSCLC samples and cells. KIFC3 knockdown suppressed the proliferation, invasion, and migration in NSCLC. Mechanically, KIFC3 silencing suppressed NSCLC progression through inhibiting the PI3K/Akt pathway.ConclusionsKIFC3 lack suppressed the proliferation, invasion, and migration which works, at least partially, by the PI3K/Akt pathway. These findings suggest that targeting KIFC3 via the PI3K/Akt pathway may offer a novel therapeutic strategy for NSCLC.

08 Oct 2024·Current Medicinal Chemistry

Unveiling the Power of Mitochondrial Fission and Fusion: A Five-Gene Signature for Personalized Prognosis in Gastric Cancer

Article

Author: Tie, Ping ; Li, Dongbing ; Zhou, Bin ; Lu, You ; Liu, Yuanhua

Background:Mitochondrial fission and fusion play important roles in tumorigenesis, progression and therapy. Dysregulation of these processes may lead to tumor progression, and regulation of these processes may provide novel strategies for cancer therapy. The involvement of genes related to mitochondrial fission and fusion (MD) in gastric cancer (GC) remains poorly understood.Objective:The aim of this study was to establish an MD gene signature for GC patients and to investigate its association with prognosis, tumor microenvironment and treatment response in GC.Methods:We use the TCGA-GC database as the cohort, focusing specifically on genes associated with MD. We conducted identification and consistency clustering analysis of differentially expressed genes in MD, conducted MD gene mutation and copy number variation analysis, as well as correlation and functional enrichment analysis between MD gene cluster classification and immune infiltration. TCGA-GC and GSE15459 were used to construct training and validation cohorts for the model. We used various statistical methods, including Cox and Lasso regression, to develop the model. We validated the model using bulk transcriptome and single- cell transcriptome datasets (GSE13861, GSE26901, GSE66229, and GSE13450). We used GSEA enrichment, CIBERSORT algorithm, ESTIMATE, and TIDE to gain insight into the annotation of MD signature and the characterization of the tumor microenvironment. OncoPredict was used to analyze the relationship between the PRG signature and the drug sensitivity. We validated the expression of several key genes in MD signature on GC cell lines using quantitative real-time PCR (qRT-PCR).Conclusion:The MD signature has the capacity to significantly contribute to the prediction of personalized outcomes and the advancement of novel therapeutic strategies tailored for GC patients.Results:These MDs-related subtypes exhibited different prognosis and immune filtration patterns. A five-gene signature, comprising AGT, HCFC1, KIFC3, NOX4, and RIN1, was developed. There was a clear distinction in overall survival between low- and high-risk patients. The analyses showed further confirmation of the independent prognostic value of the gene signature. There was a notable correlation between the MD signature, immune infiltration and drug susceptibility. The expression levels of AGT, HCFC1, KIFC3, NOX4 and RIN1 mRNA were all increased in these GC cells.

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KIFC3

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