KIF14 affects cell cycle arrest and cell viability in cervical cancer by regulating the p27Kip1 pathway

Zhang, Jie; Buranjiang, Gulimire; Mutalifu, Zuohelaguli; Jiang, Hua; Li-yan, Yao

doi:10.1186/s12957-022-02585-3

Cited by 5 publications

(5 citation statements)

References 35 publications

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“…Knockdown experiments have shown that KIF14 suppression inhibits cell proliferation and induces apoptosis through inactivation of AKT signaling [ 24 ]. KIF14 has been associated with cervical cancer, and a knockdown model of KIF14 impacted the cell cycle by affecting cell viability, proliferation, and migration, thus placing it as a potential therapeutic target [ 70 ]. KIF14 has not yet been associated with SARS-CoV-2 infection, but it does interact with nsp9 and nsp4 ( Figure 3 B).…”

Section: Discussionmentioning

confidence: 99%

Buffy Coat Transcriptomic Analysis Reveals Alterations in Host Cell Protein Synthesis and Cell Cycle in Severe COVID-19 Patients

Cavalcante

Fonseca²,

Leon³

et al. 2022

IJMS

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Transcriptome studies have reported the dysregulation of cell cycle-related genes and the global inhibition of host mRNA translation in COVID-19 cases. However, the key genes and cellular mechanisms that are most affected by the severe outcome of this disease remain unclear. For this work, the RNA-seq approach was used to study the differential expression in buffy coat cells of two groups of people infected with SARS-CoV-2: (a) Mild, with mild symptoms; and (b) SARS (Severe Acute Respiratory Syndrome), who were admitted to the intensive care unit with the severe COVID-19 outcome. Transcriptomic analysis revealed 1009 up-regulated and 501 down-regulated genes in the SARS group, with 10% of both being composed of long non-coding RNA. Ribosome and cell cycle pathways were enriched among down-regulated genes. The most connected proteins among the differentially expressed genes involved transport dysregulation, proteasome degradation, interferon response, cytokinesis failure, and host translation inhibition. Furthermore, interactome analysis showed Fibrillarin to be one of the key genes affected by SARS-CoV-2. This protein interacts directly with the N protein and long non-coding RNAs affecting transcription, translation, and ribosomal processes. This work reveals a group of dysregulated processes, including translation and cell cycle, as key pathways altered in severe COVID-19 outcomes.

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Section: Discussionmentioning

confidence: 99%

Buffy Coat Transcriptomic Analysis Reveals Alterations in Host Cell Protein Synthesis and Cell Cycle in Severe COVID-19 Patients

Cavalcante

Fonseca²,

Leon³

et al. 2022

IJMS

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“…KIF14 can act as a chromokinesin via binding to microtubules and chromatin during the bipolar spindle formation. Many studies have reported that KIF14 could promote tumorigenesis and progression by acting on many signaling pathways ( Yang et al, 2019 ; Zhang J. et al, 2022 ). Zhang J. et al (2022) found that KIF14 is an oncogene in cervical cancer, and knocking down KIF14 causes cell cycle arrest by inhibiting p27 degradation, thus affecting cell viability, proliferation, and migration.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have reported that KIF14 could promote tumorigenesis and progression by acting on many signaling pathways ( Yang et al, 2019 ; Zhang J. et al, 2022 ). Zhang J. et al (2022) found that KIF14 is an oncogene in cervical cancer, and knocking down KIF14 causes cell cycle arrest by inhibiting p27 degradation, thus affecting cell viability, proliferation, and migration. Similarly, silencing of KIF14 repressed tumor cell growth by interfering with cytokinesis and the p27Kip1 ubiquitination pathway in hepatocellular carcinoma ( Xu et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Novel circular RNA circ-0002727 regulates miR-144-3p/KIF14 pathway to promote lung adenocarcinoma progression

Li,

Hong,

Zhai

et al. 2023

Front. Cell Dev. Biol.

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Objective: Circular RNAs (circRNAs) have been shown to participate in various cancers via sponging miRNAs (microRNAs). However, their role in lung adenocarcinoma (LUAD) remains elusive.Methods: The transcriptome data and corresponding clinical information of lung adenocarcinoma samples were extracted from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database. Differentially expressed circRNAs (DEcircRNAs), differentially expressed miRNAs (DEmiRNAs), and differentially expressed genes (DEgenes) were identified and further used to constructed a circRNA-associated competing endogenous RNA (ceRNA) network. Real-Time qPCR analysis was conducted to examine gene expression at transcriptional level. The regulatory mechanisms of circRNA-miRNA-gene were validated by dual-luciferase reporter array and RNA pull-down assay. Cell growth, migration and invasion were evaluated by CCK-8 assay, colony formation assay and transwell assay, respectively.Results: Based on public microarray data, we systematically constructed a circRNA-associated ceRNA network including 11 DEcircRNAs, 8 DEmiRNAs and 49 DEgenes. Among the ceRNA network, we found that circ-0002727 was a key regulatory and was further confirmed to be upregulated in LUAD cancer cells. Subsequently, we found that silencing of circ-0002727 significantly suppressed the LUAD cell proliferation, migration and invasion in vitro. Mechanistically, we showed that circ-0002727 could competitively bind miR-144-3p to enhance the KIF14 expression in LUAD cells. Rescue assays indicated that circ-0002727 could regulate LUAD cell proliferation through modulating miR-144-3p/KIF14 pathway. Besides, KIF14 expression level was positively correlated with TNM stage and metastasis, and patients with high KIF14 expression suffered poor prognosis.Conclusion: Taken together, our study revealed that circ-0002727 could act as a ceRNA to regulate LUAD progression via modulating miR-144-3p/KIF14 pathway, providing a potential therapeutic target for LUAD.

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“…Belonging to the kinesin-3 family, the functions of kinesin family member 14 (KIF14) are also dependent on microtubules. Notably, KIF14 has been proposed as a tumor promoter in multiple human malignancies, including cervical cancer ( 18 ), gastric cancer ( 19 ) and retinoblastoma ( 20 ). Notably, Wang et al has suggested that KIF14, targeted by microRNA (miR)-200c, activates Akt to elicit pro-proliferation activities in CRC ( 21 ).…”

Section: Introductionmentioning

confidence: 99%

RFC3 drives the proliferation, migration, invasion and angiogenesis of colorectal cancer cells by binding KIF14

Yu,

Wu,

Qian

et al. 2024

Exp Ther Med

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Colorectal cancer (CRC) is a deadly and aggressive type of cancer that has a high fatality rate. The expression levels of replication factor C subunit 3 (RFC3) and kinesin family member 14 (KIF14) have been reported to be increased in CRC. The current study aimed to explore the effects of RFC3 on the malignant behaviors of CRC cells and its possible underlying mechanism involving KIF14. RFC3 and KIF14 expression levels in CRC tissues were analyzed using TNMplot database and Gene Expression Profiling Interactive Analysis database bioinformatics tools. RFC3 and KIF14 levels in CRC cells were examined using reverse transcription-quantitative PCR and western blotting. Cell Counting Kit-8 and 5-ethynyl-2'-deoxyuridine assays were performed to assess cell proliferation. Cell apoptosis was determined using flow cytometric analysis. Wound healing and Transwell assays were adopted for the evaluation of cell migration and invasion. Tube formation assay in human umbilical vein endothelial cells was used to measure angiogenesis. Western blotting analysis was performed to determine the expression of apoptosis-, migration- and angiogenesis-associated proteins. Additionally, bioinformatics tools predicted the co-expression and interaction of RFC3 and KIF14, which was verified by a co-immunoprecipitation assay. RFC3 displayed elevated expression in CRC tissues and cells, and depletion of RFC3 halted the proliferation, migration, invasion and angiogenesis, while increasing the apoptosis of CRC cells; this was accompanied by changes in the expression levels of related proteins. In addition, RFC3 bound to KIF14 and interference with RFC3 reduced KIF14 expression. Moreover, KIF14 upregulation reversed the effects of RFC3 depletion on the aggressive cellular behaviors in CRC. In conclusion, RFC3 might interact with KIF14 to function as a contributor to the malignant development of CRC.

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KIF14 affects cell cycle arrest and cell viability in cervical cancer by regulating the p27Kip1 pathway

Cited by 5 publications

References 35 publications

Buffy Coat Transcriptomic Analysis Reveals Alterations in Host Cell Protein Synthesis and Cell Cycle in Severe COVID-19 Patients

Buffy Coat Transcriptomic Analysis Reveals Alterations in Host Cell Protein Synthesis and Cell Cycle in Severe COVID-19 Patients

Novel circular RNA circ-0002727 regulates miR-144-3p/KIF14 pathway to promote lung adenocarcinoma progression

RFC3 drives the proliferation, migration, invasion and angiogenesis of colorectal cancer cells by binding KIF14

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