Dataset Information

CRTC2 promotes non-small cell lung cancer A549 migration and invasion in vitro.

ABSTRACT:

Background

CRTC2 is highly expressed in lung cancer and contributes to lung cancer pathogenesis; however, whether CRTC2 promotes lung cancer metastasis remains unknown. In the present study, we investigated the role of CRTC2 in lung cancer metastasis in vitro.

Methods

CRTC2 stable knockdown of lung cancer cell A549 was generated with small hairpin RNA and confirmed by quantitative reverse transcription-PCR and Western blot. Wound healing and invasion transwell assays were performed to explore migration and invasion activity, and Western blot was conducted to detect the expression of related proteins.

Results

Suppression of CRTC2 significantly inhibited A549 cell migration and invasion in vitro. Mechanistic studies showed that knockdown of CRTC2 greatly downregulated MMP2 and MMP9 expression. CRTC2 silencing remarkably suppressed epithelial-mesenchymal transition by modulating the expression of E-cadherin and vimentin. Furthermore, suppression of CRTC2 expression significantly reduced MAPK/c-Jun N-terminal kinase activity.

Conclusion

CRTC2 may promote A549 migration and invasion by modulation of c-Jun N-terminal kinase-mediated epithelial-mesenchymal transition and matrix metalloproteinase expression.

SUBMITTER: Shi S

PROVIDER: S-EPMC5754302 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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Publications

CRTC2 promotes non-small cell lung cancer A549 migration and invasion in vitro.

Shi Shaoqing S Luo Wei W Zhang Rui R Wang Chu C Zheng Yuanyuan Y Song Yunhua Y Wang Rongchun R Zhang Liyan L Zhang Lihua L Li Weimin W Luo Zhuang Z

Thoracic cancer 20171103 1

<h4>Background</h4>CRTC2 is highly expressed in lung cancer and contributes to lung cancer pathogenesis; however, whether CRTC2 promotes lung cancer metastasis remains unknown. In the present study, we investigated the role of CRTC2 in lung cancer metastasis in vitro.<h4>Methods</h4>CRTC2 stable knockdown of lung cancer cell A549 was generated with small hairpin RNA and confirmed by quantitative reverse transcription-PCR and Western blot. Wound healing and invasion transwell assays were performe ...[more]

PMID: 29105369

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Project description:BackgroundIt has been shown that circular RNAs (circRNAs) are involved in the pathogenesis of non-small cell lung cancer (NSCLC). However, the molecular mechanisms of circRNAs in tumor malignant progression and tyrosine kinase inhibitors (TKI) resistance remain undefined. Hereby, we explored the mechanisms by which circRBM33 promotes NSCLC progression and epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) resistance.MethodsTranscriptome sequencing (RNA-seq) was carried out to obtain the circRBM33 we investigated. Quantitative reverse transcriptase-polymerase chain reaction was performed to detect the expression of circRBM33. Cell counting kit-8 assay was performed to detect cell proliferation as well as flow cytometry to detect cell cycle and apoptosis. Transwell assay was performed to detect cell migration and invasion. In vivo tumourigenesis assays were performed to further validate the function of circRBM33. The transcriptome was sequenced after RNA-pulldown and knockdown of cirRBM33 to identify the proteins bound by cirRBM33 and the downstream mechanisms involved in the regulation of cirRBM33.ResultsThe sequencing results revealed that cirRBM33 was highly expressed in the cell line of osimertinib resistant H1975. In vitro functional validation demonstrated that knockdown of circRBM33 inhibited H1975 proliferation, migration and invasion, changed cell cycle and promoted apoptosis. In vivo, knockdown of circRBM33 inhibited tumour growth. Mass spectrometry results and sequencing analysis of knockdown circRBM33 suggest that circRBM33 may mediate resistance to osimertinib in H1975-OR cells through regulate the DNMT1/interleukin-6 (IL-6) axis.ConclusionsCircRBM33 is upregulated in NSCLC and that knockdown of circRBM33 inhibits the progression of NSCLC. CircRBM33 may combine with DNMT1, and regulate the resistance of H1975 osimertinib-resistant cells to osimertinib that mediated by IL6. CircRBM33 is a promising diagnostic and prognostic marker to provide effective treatment strategies for NSCLC patients.

Dataset Information

CRTC2 promotes non-small cell lung cancer A549 migration and invasion in vitro.

Background

Methods

Results

Conclusion

Publications

CRTC2 promotes non-small cell lung cancer A549 migration and invasion in vitro.

Similar Datasets

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