Effects of Cx43 gene modification on the proliferation and migration of the human lung squamous carcinoma cell line NCI-H226

Jp, Zang; Wei, Ran

doi:10.4238/2015.october.26.7

Cited by 4 publications

(3 citation statements)

References 11 publications

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“…Some in vitro studies have suggested a tumour suppressor role for connexins in the lung. Notably, Cx43 gene transfection can inhibit the migration of the human lung squamous carcinoma cell line NCI-H226 [17]. Other work showed that Cx43 may recruit E-cadherin to inhibit the malignant behaviour of lung cancer cells [18].…”

Section: Introductionmentioning

confidence: 99%

Insight into the Role and Regulation of Gap Junction Genes in Lung Cancer and Identification of Nuclear Cx43 as a Putative Biomarker of Poor Prognosis

Aasen

Sansano

Montero

et al. 2019

Cancers

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Direct intercellular communication, mediated by gap junctions formed by the connexin transmembrane protein family, is frequently dysregulated in cancer. Connexins have been described as tumour suppressors, but emerging evidence suggests that they can also act as tumour promoters. This feature is connexin- and tissue-specific and may be mediated by complex signalling pathways through gap junctions or hemichannels or by completely junction-independent events. Lung cancer is the number one cancer in terms of mortality worldwide, and novel biomarkers and therapeutic targets are urgently needed. Our objective was to gain a better understanding of connexins in this setting. We used several in silico tools to analyse TCGA data in order to compare connexin mRNA expression between healthy lung tissue and lung tumours and correlated these results with gene methylation patterns. Using Kaplan-Meier plotter tools, we analysed a microarray dataset and an RNA-seq dataset of non-small cell lung tumours in order to correlate connexin expression with patient prognosis. We found that connexin mRNA expression is frequently either upregulated or downregulated in lung tumours. This correlated with both good and poor prognosis (overall survival) in a clear connexin isoform-dependent manner. These associations were strongly influenced by the histological subtype (adenocarcinoma versus squamous cell carcinoma). We present an overview of all connexins but particularly focus on four isoforms implicated in lung cancer: Cx26, Cx30.3, Cx32 and Cx43. We further analysed the protein expression and localization of Cx43 in a series of 73 human lung tumours. We identified a subset of tumours that exhibited a unique strong nuclear Cx43 expression pattern that predicted worse overall survival (p = 0.014). Upon sub-stratification, the prognostic value remained highly significant in the adenocarcinoma subtype (p = 0.002) but not in the squamous carcinoma subtype (p = 0.578). This finding highlights the importance of analysis of connexin expression at the protein level, particularly the subcellular localization. Elucidation of the underlying pathways regulating Cx43 localization may provide for novel therapeutic opportunities.

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Section: Introductionmentioning

confidence: 99%

Insight into the Role and Regulation of Gap Junction Genes in Lung Cancer and Identification of Nuclear Cx43 as a Putative Biomarker of Poor Prognosis

Aasen

Sansano

Montero

et al. 2019

Cancers

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“…Existing reports have suggested that the pathogenesis and progression of lung carcinoma are related with various genes. For instance, the transfection of Cx43 gene could hinder the cell migration and proliferation of LUSC cell line NCI-H226 [28]. CDK7 suppression has been reported as an available therapeutic strategy in LUSC via regulating SOX2 amplification [29].…”

Section: Discussionmentioning

confidence: 99%

The effect and mechanism of miR-607/CANT1 axis in lung squamous carcinoma

Qiao¹,

Wang

Duan

et al. 2021

Anti-Cancer Drugs

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Lung squamous carcinoma (LUSC) is the second most frequent subtype of non-small cell lung cancer. Rarely gene alterations are identified in LUSC. Therefore, identifying LUSC-related genes to explain the relevant molecular mechanism is urgently needed. A potential biomarker, calcium-activated nucleotidase 1 (CANT1), was elevated in tissues of LUSC patients relative to normal cases based on the TCGA and/or GTEx database. CCK-8 and transwell tests were then implemented to measure the proliferative, invasive and migratory capacities, and showed that knockdown of CANT1 blocked LUSC cells proliferation. miR-607, predicted as an upstream factor for CANT1, was declined in LUSC using TargetScan analysis and luciferase activity test. Low miR-607 expression was related with unfavorable outcomes of LUSC patients. Moreover, miR-607 downregulation elevated cell viability, invasion and migration in LUSC cells, which was antagonized by si-CANT1. GEPIA website was accessed to estimate the relevance between CANT1 and epithelial-mesenchymal transition (EMT)-related positive factors. The protein levels of Fibronectin, Vimentin, Snail and β-catenin were altered due to the abnormal CANT1 and miR-607 expression. Together, these data unveiled that miR-607/CANT1 pair may exert a vital role in the progression of LUSC through mediating EMT process, which would furnish an available therapeutic therapy for LUSC.

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“…Therefore, the present study used EGFR-negative SqCC cell lines (13,14). NCI-H520 and NCI-H226 cells, which are human lung SqCC cell lines, which were purchased from the Food Industry Research and Development Institute (15,16). These cells were maintained in RPMI-1640 supplemented with 10% FBS and an antibiotic-antimycotic agent containing amphotericin B, penicillin and streptomycin.…”

Section: Methodsmentioning

confidence: 99%

Pterostilbene inhibits lung squamous cell carcinoma growth in�vitro and in�vivo by inducing S phase arrest and apoptosis

Tan

Chen

et al. 2019

Oncol Lett

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Natural dietary components have become the subject of an increasing amount of interest due to the side effects of anticancer treatment. Pterostilbene, an analog of resveratrol, is primarily found in grapes, and has been suggested to exert antioxidant and anticancer effects in different tumor types. The present study aimed to investigate the antitumor effects and molecular mechanisms of pterostilbene in the human lung squamous cell carcinoma (SqCC) cell line, H520. The results of the present study indicate that pterostilbene significantly reduced cell viability and induced S phase arrest, and that treatment with pterostilbene was associated with the downregulation of cyclin A and cyclin E, as with the upregulation of p21 and p27 expression in H520 cells. In the apoptosis analysis, pterostilbene induced S phase accumulation and the activation of caspase-3, −8 and −9 in H520 cells, potentially through the activation of extrinsic and intrinsic apoptotic pathways. Additionally, the in vivo study demonstrated that pterostilbene effectively inhibited lung SqCC growth in a H520 ×enograft model. Given the in vitro and in vivo antitumor effects of pterostilbene demonstrated in the present study, pterostilbene may serve a novel and effective therapeutic agent to for patients with SqCC.

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Effects of Cx43 gene modification on the proliferation and migration of the human lung squamous carcinoma cell line NCI-H226

Cited by 4 publications

References 11 publications

Insight into the Role and Regulation of Gap Junction Genes in Lung Cancer and Identification of Nuclear Cx43 as a Putative Biomarker of Poor Prognosis

Insight into the Role and Regulation of Gap Junction Genes in Lung Cancer and Identification of Nuclear Cx43 as a Putative Biomarker of Poor Prognosis

The effect and mechanism of miR-607/CANT1 axis in lung squamous carcinoma

Pterostilbene inhibits lung squamous cell carcinoma growth in�vitro and in�vivo by inducing S phase arrest and apoptosis

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