Yong-Gang Liu1, Jia Li2, Fang Nie1, Gao-Wa Jin3. 1. Department of Thoracic Oncology, Baotou Cancer Hospital Baotou 014000, Inner Mongolia, China. 2. Department of Immunization Planning, Baotou Disease Control and Defense Center Baotou 014000, Inner Mongolia, China. 3. Department of Oncology, Ordos Central Hospital Ordos 017000, Inner Mongolia, China.
Abstract
BACKGROUND: This study set out to explore the regulatory relationship between LINC00961/miR-3127 axis and non-small-cell lung carcinoma (NSCLC), so as to provide a new and effective molecular target for targeted therapy of NSCLC. METHODS: RNA-seq and miRNA-seq data of NSCLC and normal samples were obtained from The Cancer Genome Atlas (TCGA) database for analyzing LINC00961 and miR-3127 expression. Eighty-six pairs of clinical NSCLC tissues and adjacent normal tissues as well as NSCLC cell lines were obtained. Measurements of LINK00961 and miR-3127 levels were done using real-time-quantitative polymerase chain reaction (RT-qPCR). Furthermore, LINK00961 and miR-3127 in NSCLC cell were regulated respectively. The NSCLC cell proliferation, invasion and migration were determined with MTT assay, Transwell and wound healing assays, respectively. The levels of invasion- and apoptosis-related proteins were detected using western blots, and the connection of LINC00961 and miR-3127 was identified using dual luciferase reporter (DLR) assay. RESULTS: Differential analysis results of TCGA databases identified that LINC00961 was ubiquitously expressed at low levels in NSCLC, while miR-3127 was highly expressed. Similar expression trends of LINC00961 and miR-3127 were observed in clinical NSCLC samples and cell lines. Overexpression of LINC00961 and knockdown of miR-3127 significantly reduced NCI-H1299 cell migration, invasiveness, and multiplication, decreased MMP-2, MMP-9 and Bcl-2 protein levels, and increased E-cadherin, Bax and Caspase-3 protein levels. The DLR assay confirmed that miR-3127 can be targeted by LINC00961. CONCLUSION: LINC00961 functions as an anti-oncogene in NSCLC by modulating miR-3127. AJTR
BACKGROUND: This study set out to explore the regulatory relationship between LINC00961/miR-3127 axis and non-small-cell lung carcinoma (NSCLC), so as to provide a new and effective molecular target for targeted therapy of NSCLC. METHODS: RNA-seq and miRNA-seq data of NSCLC and normal samples were obtained from The Cancer Genome Atlas (TCGA) database for analyzing LINC00961 and miR-3127 expression. Eighty-six pairs of clinical NSCLC tissues and adjacent normal tissues as well as NSCLC cell lines were obtained. Measurements of LINK00961 and miR-3127 levels were done using real-time-quantitative polymerase chain reaction (RT-qPCR). Furthermore, LINK00961 and miR-3127 in NSCLC cell were regulated respectively. The NSCLC cell proliferation, invasion and migration were determined with MTT assay, Transwell and wound healing assays, respectively. The levels of invasion- and apoptosis-related proteins were detected using western blots, and the connection of LINC00961 and miR-3127 was identified using dual luciferase reporter (DLR) assay. RESULTS: Differential analysis results of TCGA databases identified that LINC00961 was ubiquitously expressed at low levels in NSCLC, while miR-3127 was highly expressed. Similar expression trends of LINC00961 and miR-3127 were observed in clinical NSCLC samples and cell lines. Overexpression of LINC00961 and knockdown of miR-3127 significantly reduced NCI-H1299 cell migration, invasiveness, and multiplication, decreased MMP-2, MMP-9 and Bcl-2 protein levels, and increased E-cadherin, Bax and Caspase-3 protein levels. The DLR assay confirmed that miR-3127 can be targeted by LINC00961. CONCLUSION: LINC00961 functions as an anti-oncogene in NSCLC by modulating miR-3127. AJTR