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RBAK is upregulated in non-small cell lung cancer and promotes cell migration and invasion.

ABSTRACT: Non-small cell lung cancer (NSCLC) is a leading cause of cancer-associated mortality worldwide, NCSCLC includes lung adenocarcinoma and lung squamous cell carcinoma. Tumor metastasis is the major cause of mortality of patients with NSCLC. However, the mechanisms underlying NSCLC metastasis remain largely elusive. In present study, the authors focused on exploring the roles of RBAK in NSCLC. The present study demonstrated that RB-associated KRAB zinc finger (RBAK) was upregulated in NSCLC compared with non-tumorous tissues by analyzing Gene Expression Omnibus (GEO) datasets and The Cancer Genome Atlas (TCGA) dataset. High expression of RBAK was associated with poor disease-free survival of patients with NSCLC by analyzing TCGA dataset. Furthermore, an RBAK-mediated protein-protein interaction network was constructed to reveal the potential underlying mechanisms by which RBAK drives NSCLC progression. The authors found that RBAK was involved in regulating a number of transcription factors, including androgen receptor, forkhead box A1, tumor protein 53, and E2F transcription factor 1, 2 and 4, suggesting that RBAK may have a role in regulating gene transcription. GO and KEGG enrichment analyses of the genes co-expressed with RBAK revealed that RBAK is involved in regulating a number of biological functions, including the Wnt signaling pathway, mRNA splicing, protein polyubiquitination, cell-cell adhesion and focal adhesion. Transwell and wound healing assays demonstrated that knockdown of RBAK suppressed NSCLC cell migration and invasion. The present study enhances the current understanding of the important roles of RBAK in NSCLC metastasis and may provide useful information for the development of novel treatment approaches.

SUBMITTER: He B

PROVIDER: S-EPMC6755425 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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RBAK is upregulated in non-small cell lung cancer and promotes cell migration and invasion.

He Bingjun B Wang Bin B Wang Haiyong H Zhang Chu C Wu Yuanlin Y Fu Linhai L Yu Guangmao G

Experimental and therapeutic medicine 20190816 4

Non-small cell lung cancer (NSCLC) is a leading cause of cancer-associated mortality worldwide, NCSCLC includes lung adenocarcinoma and lung squamous cell carcinoma. Tumor metastasis is the major cause of mortality of patients with NSCLC. However, the mechanisms underlying NSCLC metastasis remain largely elusive. In present study, the authors focused on exploring the roles of RBAK in NSCLC. The present study demonstrated that RB-associated KRAB zinc finger (RBAK) was upregulated in NSCLC compare ...[more]

PMID: 31555381

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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.

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RBAK is upregulated in non-small cell lung cancer and promotes cell migration and invasion.

Publications

RBAK is upregulated in non-small cell lung cancer and promotes cell migration and invasion.

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