Knockdown of PFTK1 Inhibits the Migration of Glioma Cells

Fan, Shaochen; Zhao, Chengjin; Zhang, Li; Dai, Shirong; Ren, Jianbing; Zhang, Xiubing; Ban, Na; He, Xiaojuan; Yang, Lixiang; Bao, Zhen; Chen, Wenjuan; Sun, Jie; Gao, Yilu; Tao, Tao

doi:10.1007/s12031-015-0600-z

Cited by 13 publications

(16 citation statements)

References 30 publications

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“…S6), and in previous study (21). CDK14 expression was also up-regulated in other cancers, including breast cancer and glioma (26,27). Furthermore, upregulated CDK14 was highly associated with the poor prognosis of patients with breast cancer (26), or HCC (Supplementary Fig.…”

Section: Discussionsupporting

confidence: 62%

“…Moreover, analyses of transposon insertion sites from a Sleeping Beauty (SB) transposon mutagenesis screen in a HBV-related HCC mouse model revealed a significant enrichment of common insert sites (CISs) in CDK14 gene (25). Second, previous studies have shown that the CDK14 abnormalities could affect cell growth, invasion, migration and motility in various cancers cell lines, including HCC (21,24,(26)(27)(28)(29). Third, CDK14 was shown to interact with cyclin Y to activate non-canonical Wnt signaling in HCC (29).…”

Section: Discussionmentioning

confidence: 99%

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Genome-Wide Association Study Identifies a New Locus at 7q21.13 Associated with Hepatitis B Virus–Related Hepatocellular Carcinoma

Zhai

Song

et al. 2018

Clinical Cancer Research

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Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. In China, chronic hepatitis B virus (HBV) infection remains the major risk factor for HCC. In this study, we performed a genome-wide association study (GWAS) among Chinese populations to identify novel genetic loci contributing to susceptibility to HBV-related HCC. GWAS scan is performed in a collection of 205 HBV-related HCC trios (each trio includes an affected proband and his/her both parents), and 355 chronic HBV carriers with HCC (cases) and 360 chronic HBV carriers without HCC (controls), followed by two rounds of replication studies totally consisting of 3,796 cases and 2,544 controls. We identified a novel association signal within the gene at 7q21.13 (index rs10272859, OR = 1.28, = 9.46 × 10). Furthermore, we observed that the at-risk rs10272859[G] allele was significantly associated with higher mRNA expression levels of in liver tissues. Chromosome conformation capture assays in liver cells confirmed that a physical interaction exists between the promoter region of and the risk-associated SNPs in strong linkage disequilibrium with the index rs10272859 at 7q21.13. This index rs10272859 also showed significant association with the survival of HCC patients. Our findings highlight a novel locus at 7q21.13 conferring both susceptibility and prognosis to HBV-related HCC, and suggest the gene to be the functional target of the 7q21.13 locus..

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Genome-Wide Association Study Identifies a New Locus at 7q21.13 Associated with Hepatitis B Virus–Related Hepatocellular Carcinoma

Zhai

Song

et al. 2018

Clinical Cancer Research

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“…(64) The decreases in ATP probe uptake for BRAF and M4K5 in the BRAFi resistant 1205LuR cell line confirm the direct and off target inhibitory actions of vemurafenib, while CDK14 has been implicated in maintaining various hallmarks of cancer in several tumor types including ovarian, pancreatic, breast and gastric cancer as well as glioma. (65-69) Never in Mitosis Gene A (NIMA)-related protein kinase, NEK4, plays an important role in microtubule positioning and its deletion makes cancer cells either sensitive or resistant to microtubule poisons. (70) Apart from this, deletion of NEK4 was also found to delay replicative senescence and DNA damage repair in human fibroblast cells.…”

Section: Resultsmentioning

confidence: 99%

Activity-Based Protein Profiling Shows Heterogeneous Signaling Adaptations to BRAF Inhibition

et al. 2016

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Patients with BRAF V600E mutant melanoma are typically treated with targeted BRAF kinase inhibitors, such as vemurafenib and dabrafenib. Although these drugs are initially effective, they are not curative. Most of the focus to date has been upon genetic mechanisms of acquired resistance; therefore, we must better understand the global signaling adaptations that mediate escape from BRAF inhibition. In the current study, we have used activity-based protein profiling (ABPP) with ATP-analogue probes to enrich kinases and other enzyme classes that contribute to BRAF inhibitor (BRAFi) resistance in four paired isogenic BRAFi-naïve/resistant cell line models. Our analysis showed these cell line models, which differ in their PTEN status, have considerable heterogeneity in their kinase ATP probe uptake in comparing naïve cells and adaptations to chronic drug exposure. A number of kinases including FAK1, SLK and TAOK2 had increased ATP probe uptake in BRAFi resistant cells, while KHS1 (M4K5) and BRAF had decreased ATP probe uptake in the BRAFi-resistant cells. Gene ontology (GO) enrichment analysis revealed BRAFi resistance is associated with a significant enhancement in ATP probe uptake in proteins implicated in cytoskeletal organization and adhesion, and decreases in ATP probe uptake in proteins associated with cell metabolic processes. The ABPP approach was able to identify key phenotypic mediators critical for each BRAFi resistant cell line. Together, these data show that common phenotypic adaptations to BRAF inhibition can be mediated through very different signaling networks, suggesting considerable redundancy within the signaling of BRAF mutant melanoma cells.

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“…Although cell cycle proteins have long been considered to be unable to influence the migration of cells, previous studies have demonstrated that PFTK1 protein either activated or was involved in Wnt signaling and promoted migration and invasion (16). A study has previously indicated that PFTK1 can modulate oligodendrocyte differentiation via the PI3K/AKT pathway (32), whereas downregulation of PFTK1 expression inhibited glioma cell migration (17). Based on these results, PFTK1 was considered to be a potent target for cancer therapy.…”

Section: Discussionmentioning

confidence: 99%

“…PFTK1 is a novel member of the Cdc2-related serine/threonine protein kinases family, which can regulate the expression of cyclins and the cell cycle (13). Previous studies have demonstrated high expression of PFTK1 in several types of malignant tumor, including hepatocellular carcinoma (14), esophageal (11), breast (15) and gastric (16) cancers, as well as glioma (17). It is involved in cell cycle regulation, tumor proliferation, migration and invasion (18).…”

Section: Introductionmentioning

confidence: 99%

High expression of PFTK1 in cancer cells predicts poor prognosis in colorectal cancer

Mao

Jia²,

Zhu

et al. 2017

Molecular Medicine Reports

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The serine/threonine-protein kinase PFTAIRE 1 (PFTK1) is a member of the cyclin‑dependent kinase family that is highly expressed in several malignant tumors, including hepatocellular carcinoma, esophageal, breast and gastric cancers, and glioma. It contributes to tumor progression and influences tumor prognosis. However, the expression and clinicopathological significance of PFTK1 in human colorectal cancer (CRC) remain to be elucidated. The present study aimed to examine the expression of PFTK1 and to evaluate the clinical significance of its expression in human CRC. Reverse transcription‑quantitative polymerase chain reaction was performed on 10 fresh CRC and 10 surrounding normal tissue samples to detect and compare the expression of PFTK1 mRNA in CRC and normal colorectal tissues. Immunohistochemistry was performed on 179 CRC tissue specimens and 47 control samples of normal colorectal lesions to characterize the expression of PFTK1 protein. Kaplan‑Meier overall survival (OS) rate and Cox regression analyses were performed to evaluate the prognosis of patients with CRC. The expression of PFTK1 mRNA in CRC tissues (1.433±0.168) was significantly higher compared with normal tissues (0.853±0.107; t=1.97 ('t' was the value obtained from quantification of the mRNA data, following a paired t‑test), P=0.008). High PFTK1 expression in cancerous cells was detected in 92 of the CRC specimens (51.40%), and high levels of PFTK1 were associated with tumor node metastasis (TNM) stage (P=0.042), tumor classification (P=0.022) and preoperative carcinoembryonic antigen (CEA) level (P<0.001). Kaplan‑Meier OS rate and Cox regression analysis revealed that high PFTK1 expression level (hazard ratio (HR)=1.999; P=0.019) was an independent prognostic factor of CRC patients. The degree of differentiation (HR, 0.368, P=0.003), TNM classification (HR, 2.118, P=0.001) and preoperative CEA level (HR, 2.302, P=0.003) were also predictors of the prognosis of patients with CRC. The present study suggested that PFTK1 may be a potential anticancer target and prognostic marker in patients with CRC.

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Knockdown of PFTK1 Inhibits the Migration of Glioma Cells

Cited by 13 publications

References 30 publications

Genome-Wide Association Study Identifies a New Locus at 7q21.13 Associated with Hepatitis B Virus–Related Hepatocellular Carcinoma

Genome-Wide Association Study Identifies a New Locus at 7q21.13 Associated with Hepatitis B Virus–Related Hepatocellular Carcinoma

Activity-Based Protein Profiling Shows Heterogeneous Signaling Adaptations to BRAF Inhibition

High expression of PFTK1 in cancer cells predicts poor prognosis in colorectal cancer

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