CDK14 expression is down-regulated by cigarette smoke in vivo and in vitro

Pollack, Daniel; Xiao, Yuxuan; Shrivasatava, Vibha; Levy, Avi; Andrusier, Miriam; DʼArmiento, Jeanine; Holz, Marina K.; Vigodner, Margarita

doi:10.1016/j.toxlet.2015.02.006

Cited by 9 publications

(5 citation statements)

References 39 publications

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“…In addition to the aforementioned studies, another study found that cigarette smoke downregulated CDK14 expression in testicular and lung cells, suggesting that CDK14 has different roles in normal lung tissue and lung cancer tissue. 21 Thus, further studies are needed to reveal the underlying molecular mechanisms of CDK14 in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: CDK14 expression is elevated in patients with non-small cell lung cancer and correlated with poor prognosis

et al. 2021

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Objective To investigate the clinical significance of cyclin-dependent kinase 14 (CDK14) expression in patients with non-small cell lung cancer (NSCLC). Methods The present prospective observational study included 193 patients diagnosed with NSCLC between January 2010 and December 2014. NSCLC tumor tissues and paired paracancerous normal tissues were obtained from all patients. CDK14, thyroid transcription factor 1 (TTF-1), cytokeratin 5/6 (CK5/6), and Ki67 expression was measured via immunohistochemistry (IHC) Results CDK14 staining was strong (>3) in 129 patients (66.49%) and weak (≤3) in 64 patients (33.16%). The mean IHC scores were markedly higher in tumor tissues than in paracancerous tissues. Pearson’s analysis demonstrated that the IHC scores of CDK14 expression were positively correlated with TTF-1, CK5/6, and Ki67 scores. Kaplan–Meier analysis illustrated that 5-year overall survival was markedly longer in patients with weak CDK14 staining. TNM stage, pleural invasion, lymph node metastasis, CDK14 expression, and Ki67 expression were risk factors for 5-year overall survival in patients with NSCLC. Conclusion CDK14 overexpression portended poor outcomes in patients with NSCLC, and CDK14 expression was correlated with TTF-1, CK5/5, and Ki67 expression.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: CDK14 expression is elevated in patients with non-small cell lung cancer and correlated with poor prognosis

et al. 2021

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“…On the other hand, we found that SNHG15 silencing induced the cycle arrest at G0/G1 phase and suppressed the apoptosis of NSCLC cells, besides, decreased the CDK14 protein. CDK14 acts as one of the important cell cycle‐regulation related genes (Li et al, ; Pollack et al, ). Meanwhile, SNHG15 regulated the apoptosis and cell‐cycle of NSCLC cells, suggesting the potential interaction within SNHG15 and cycle modulation.…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA SNHG15 promotes CDK14 expression via miR‐486 to accelerate non‐small cell lung cancer cells progression and metastasis

Ji¹,

Jin

et al. 2018

Journal Cellular Physiology

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Long non‐coding RNAs (lncRNAs) have been validated to play important role in multiple cancers, including non‐small cell lung cancer (NSCLC). In present study, our team investigate the biologic role of SNHG15 in the NSCLC tumorigenesis. LncRNA SNHG15 was significantly upregulated in NSCLC tissue samples and cells, and its overexpression was associated with poor prognosis of NSCLC patients. In vitro, loss‐of‐functional cellular experiments showed that SNHG15 silencing significantly inhibited the proliferation, promoted the apoptosis, and induced the cycle arrest at G0//G1 phase. In vivo, xenograft assay showed that SNHG15 silencing suppressed tumor growth of NSCLC cells. Besides, SNHG15 silencing decreased CDK14 protein expression both in vivo and vitro. Bioinformatics tools and luciferase reporter assay confirmed that miR‐486 both targeted the 3′‐UTR of SNHG15 and CDK14 and was negatively correlated with their expression levels. In summary, our study conclude that the ectopic overexpression of SNHG15 contribute to the NSCLC tumorigenesis by regulating CDK14 protein via sponging miR‐486, providing a novel insight for NSCLC pathogenesis and potential therapeutic strategy for NSCLC patients.

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“…Correspondingly, CDK14 played an important role in lung tumorigenesis. For example, the cigarette smoke-induced downregulation of CDK14 in lung cells correlated with β-catenin levels, suggesting impaired Wnt signaling ( Pollack et al, 2015 ). Another study also suggested that CDK14 is regulated by SNHG15 by competitively sponging miR-486, which contributed to NSCLC tumorigenesis ( Jin et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

A Novel Transcriptome Integrated Network Approach Identifies the Key Driver lncRNA Involved in Cell Cycle With Chromium (VI)-Treated BEAS-2B Cells

et al. 2021

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Hexavalent chromium [Cr(VI)] is a well-known occupational carcinogen, but the mechanisms contributing to DNA damage and cell cycle alternation have not been fully characterized. To study the dose-response effects of Cr(VI) on transcription, we exposed BEAS-2B cells to Cr(VI) at concentrations of 0.2, 0.6, and 1.8 μmol/L for 24 h. Here, we identified 1,484 differentially expressed genes (DEGs) in our transcript profiling data, with the majority of differentially expressed transcripts being downregulated. Our results also showed that these DEGs were enriched in pathways associated with the cell cycle, including DNA replication, chromatin assembly, and DNA repair. Using the differential expressed genes related to cell cycle, a weighted gene co-expression network was constructed and a key mRNA-lncRNA regulation module was identified under a scale-free network with topological properties. Additionally, key driver analysis (KDA) was applied to the mRNA-lncRNA regulation module to identify the driver genes. The KDA revealed that ARD3 (FDR = 1.46 × 10–22), SND1 (FDR = 5.24 × 10–8), and lnc-DHX32-2:1 (FDR = 1.43 × 10–17) were particularly highlighted in the category of G2/M, G1/S, and M phases. Moreover, several genes we identified exhibited great connectivity in our causal gene network with every key driver gene, including CDK14, POLA1, lnc-NCS1-2:1, and lnc-FOXK1-4:1 (all FDR < 0.05 in those phases). Together, these results obtained using mathematical approaches and bioinformatics algorithmics might provide potential new mechanisms involved in the cytotoxicity induced by Cr.

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CDK14 expression is down-regulated by cigarette smoke in vivo and in vitro

Cited by 9 publications

References 39 publications

RETRACTED: CDK14 expression is elevated in patients with non-small cell lung cancer and correlated with poor prognosis

RETRACTED: CDK14 expression is elevated in patients with non-small cell lung cancer and correlated with poor prognosis

Long non‐coding RNA SNHG15 promotes CDK14 expression via miR‐486 to accelerate non‐small cell lung cancer cells progression and metastasis

A Novel Transcriptome Integrated Network Approach Identifies the Key Driver lncRNA Involved in Cell Cycle With Chromium (VI)-Treated BEAS-2B Cells

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