&lt;p&gt;CDKN3 promotes tumor progression and confers cisplatin resistance via RAD51 in esophageal cancer&lt;/p&gt;

Wang, Jiansong; Che, Wencheng; Wang, Weimin; Su, Gongzhang; Zhen, Tianchang; Jiang, Zhongmin

doi:10.2147/cmar.s193793

Cited by 30 publications

(23 citation statements)

References 18 publications

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“…The experiments performed by Wang et al (29) focused on the functions of CDKN3 in ESCA progression and chemoresistance. ESCA includes EAC and ESCC.…”

Section: Discussionmentioning

confidence: 99%

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CDKN3 promotes cell proliferation, invasion and migration by activating the AKT signaling pathway in esophageal squamous cell carcinoma

Yao

et al. 2019

Oncol Lett

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In China, esophageal squamous cell carcinoma (ESCC), capable of direct invasion and early metastasis, exhibits high mortality. Identification of the molecular basis driving ESCC progression and development of new diagnostic biomarkers are urgently needed. Cyclin-dependent kinase inhibitor 3 (CDKN3) performs crucial roles in the modulation of tumor development. The present study aimed to explore the functions and underlying mechanism of CDKN3 in regulating ESCC cell proliferation and invasion. The expression levels of CDKN3 in ESCC cells were evaluated by reverse transcription-quantitative PCR. Cell counting kit-8 and colony forming assays were used to evaluate cell viability. Wound-healing assay was performed to explore cell migration. Transwell invasion analysis was conducted to investigate the invasive capacity of ESCC cells. Protein levels were detected by western blot assay. The results demonstrated that the expression of CDKN3 was significantly upregulated in ESCC tissues, as predicted using the UALCAN and Gene Expression Omnibus databases. PCR and western blot assays confirmed that CDKN3 was upregulated in ESCC cell lines. Functional assays revealed that CDKN3 knockdown with small interfering RNA decreased the ability of ESCC cells to proliferate, invade and migrate and suppressed G1/S transition. Further mechanistic analyses demonstrated that CDKN3 promoted cell proliferation and invasion by activating the AKT signaling pathway in ESCC cells. To the best of our knowledge, the present study is the first to identify the functions of CDKN3 in ESCC and provide evidence that CDKN3 regulates tumor progression by activating the AKT signaling pathway. Therefore, CDKN3 may serve as a potential effective therapeutic target for ESCC treatment.

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“…The experiments performed by Wang et al (29) focused on the functions of CDKN3 in ESCA progression and chemoresistance. ESCA includes EAC and ESCC.…”

Section: Discussionmentioning

confidence: 99%

“…Neither of the two studies investigated the role of CDKN3 in regulating ESCC cell proliferation, invasion and migration (19,29). A recent study by Liu et al (30) has reported that CDKN3 promoted the ESCC cell cycle, invasion and migration by modulating the p-AKT-p53-p21-axis.…”

Section: Discussionmentioning

confidence: 99%

CDKN3 promotes cell proliferation, invasion and migration by activating the AKT signaling pathway in esophageal squamous cell carcinoma

Yao

et al. 2019

Oncol Lett

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“…A recent study demonstrated that CCNA2 is a crucial regulator of NSCLC cells metastasis promoting invasion and migration of NSCLC cells through integrin αVβ3 signaling pathway 49 . CDKN3 gene encodes a dual-specificity protein phosphatase, which was previously thought to suppress tumors by controlling mitosis via CDK1 / CDK2 50 . It is well known that CDKN3 is overexpressed in multiple human tumor tissues and cell lines 51 , 52 .…”

Section: Discussionmentioning

confidence: 99%

Independent prognostic implications of RRM2 in lung adenocarcinoma

Luo

Cao

et al. 2020

J. Cancer

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Background: Ribonucleoside-diphosphate reductase subunit M2 ( RRM2 ) is the catalytic subunit of ribonucleotide reductase and modulates the enzymatic activity, which is essential for DNA replication and repair. However, the role of RRM2 in lung adenocarcinoma (LUAD) remains unclear. Methods: In this study, we explored the expression pattern and prognostic value of RRM2 in LUAD across TCGA, GEO, Oncomine, UALCAN, PrognoScan, and Kaplan-Meier Plotter, and confirmed its independent prognostic value via Cox analyses. LinkedOmics and GEPIA2 were applied to investigate co-expression and functional networks associated with RRM2 . Besides, we used TIMER to assess the correlation between RRM2 and the main six types of tumor-infiltrating immune cells. Lastly, the correlations between immune signatures of immunomodulators, chemokines, and 28 tumor-infiltrating lymphocytes (TILs) and RRM2 were examined by tumor purity-corrected partial Spearman's rank correlation coefficient through TIMER portal. Results: RRM2 was found upregulated in tumor tissues in TCGA-LUAD, and validated in multiple independent cohorts. Moreover, whether in TCGA or other cohorts, high RRM2 expression was found to be associated with poor survival. Cox analyses showed that high RRM2 expression was an independent risk factor for overall survival, disease-specific survival, and progression-free survival of LUAD. Functional network analysis suggested that RRM2 regulates RNA transport, oocyte meiosis, spliceosome, ribosome biogenesis in eukaryotes, and cellular senescence signaling through pathways involving multiple cancer-related kinases and E2F family. Also, RRM2 expression correlated with infiltrating levels of B cells, CD4+ T cells, and neutrophils. Subsequent analysis found that B cells and dendritic cells could predict the outcome of LUAD. B cells were identified as an independent risk factor among six types of immune cells through Cox analyses. At last, the correlation analysis showed RRM2 correlated with 67.68% (624/922) of the immune signatures we performed. Conclusion: Our research showed that RRM2 could independently predict the prognosis of LUAD and was associated with immune infiltration. In particular, the tight relationship between RRM2 and B cell marker genes are the potential epicenter of the immune response and one of the critical factors affecting the prognosis. Our findings laid the foundation for further research on the immunomodulatory role of RRM2 in LUAD.

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“…The knockdown of CDKN3 could inhibit the proliferation, invasion and promote the apoptosis of human ovarian cancer [40]. CDKN3 could also promote the progression of esophageal cancer [41]. Therefore, CDKN3 is quite associated with the progression of many kinds of cancer but study little in OSCC.…”

Section: Discussionmentioning

confidence: 99%

Identification of Differential Methylation Regions and Correspondence Targeted Genes in Oral Squamous Cell Carcinoma

Niu¹,

Shan²,

Guo³

2020

Preprint

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Background The differential methylation included hypermethylation and hypomethylation plays significant role in the progression of many kind of cancers but study little in oral squamous cell carcinoma (OSCC). Methods GSE123781 and GSE87053 was used to analysis the differential methylation regions (DMRs) and predict the target genes in OSCC by R software and wANNOVAR respectively. the biological process and cell pathways of common targeted genes between GSE123781 and GSE87053 were analyzed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) enrichment analysis. The hub genes (hub genes 1) in common targeted genes associated with cancer biological process was identified by protein to protein interaction network (PPI). In addition, GSE74530 and GSE30784 was used to identify common differentially expressed genes (DEGs) in OSCC by R software. The biological process and cell pathways of common DEGs was analyzed by GO and KEGG enrichment analysis. The hub genes (hub genes 2) in common DEGs associated with cancer biological process was identified by PPI network. The significant hub genes between hub genes 1 and hub genes 2 were identified by Venn picture. Finally, the expression level of significant hub genes and correspondence relationship with head and neck squamous cell carcinoma (HNSCC) patient survival were confirmed by The Cancer Genome Atlas (TCGA) dataset. Results There are 2146 common targeted genes regulated by DMRs between GSE123781 and GSE87053 and 278 hub genes in common targeted genes associated with cancer biological process. In addition, there are 895 common DEGs between GSE74530 and GSE30784 and 144 hub genes in common DEGs associated with cancer biological process. There are 9 significant hub genes between hub genes 1 and hub genes 2. Finally, these 9 significant hub genes differentially expressed in HNSCC tissues except CCR7 and quite associated with the survival of HNSCC patients. Conclusions CCR7, ETS1, RUNX3, CCR1, C3AR1, LAMB1, IRF7, LGALS3 and CDKN3 both are DEGs and regulated by DMRs in OSCC, which are quite associated with the progression of OSCC and the survival of HNSCC patients. All of these genes have much potential to be new biomarkers in targeted therapy of OSCC.

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<p>CDKN3 promotes tumor progression and confers cisplatin resistance via RAD51 in esophageal cancer</p>

Cited by 30 publications

References 18 publications

CDKN3 promotes cell proliferation, invasion and migration by activating the AKT signaling pathway in esophageal squamous cell carcinoma

CDKN3 promotes cell proliferation, invasion and migration by activating the AKT signaling pathway in esophageal squamous cell carcinoma

Independent prognostic implications of RRM2 in lung adenocarcinoma

Identification of Differential Methylation Regions and Correspondence Targeted Genes in Oral Squamous Cell Carcinoma

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