C Wang1, S Li1, J Xu2, W Niu3, S Li1. 1. a Respiratory Medicine Department , The First Affiliated Hospital of JIAMUSI University , Jia Mu Si , PR China. 2. b Intensive Care Unit , The First Affiliated Hospital of JIAMUSI University , Jia Mu Si , PR China. 3. c Urinary Surgery , The First Affiliated Hospital of JIAMUSI University , Jia Mu Si , PR China.
Abstract
BACKGROUND: A potential role for microRNA-935 (miR-935) has been identified in several cancers but not in non-small cell lung cancer (NSCLC). We hypothesised changes in miR-935 in NSCLC, and proposed mechanisms that may further explain its role in carcinogenesis. METHODS: NSCLC tissue and nearby normal tissue was obtained from 101 patients and was probed by qRT-PCR for miR-935 expression. The role of miR-935 and a potential target (signal transduction factor E2F7) was determined in cell lines by a dual luciferase assay. The function of miR-935 was investigated through metabolic activity (MTT) and transwell migration assays. Western blot and immunocytochemical assays examined protein expression level. Growth of miR-935 transfected or untransfected cells was measured via xenograft tumour formation. RESULTS: miR-935 was reduced in cancer tissue and was related to lymph node metastases, tumour node metastasis status and poor prognosis (all p < 0.02). In vitro, miR-935 suppressed cell proliferation, migration and invasion in NSCLC cells through targeting E2F7. Furthermore, E2F7 was upregulated in NSCLC tissue associated with poor prognosis (p = 0.0203) of NSCLC patients. miR-935 suppressed the epithelial-mesenchymal transition and AKT pathways in NSCLC and inhibited the tumour growth in vivo. CONCLUSION: Altered miR-935 in lung cancer biopsy tissue may be a diagnostic tool and could direct treatment. Involvement in carcinogenesis is implied by its suppression of the development of NSCLC via targeting E2F7 and inhibiting AKT pathway.
BACKGROUND: A potential role for microRNA-935 (miR-935) has been identified in several cancers but not in non-small cell lung cancer (NSCLC). We hypothesised changes in miR-935 in NSCLC, and proposed mechanisms that may further explain its role in carcinogenesis. METHODS:NSCLC tissue and nearby normal tissue was obtained from 101 patients and was probed by qRT-PCR for miR-935 expression. The role of miR-935 and a potential target (signal transduction factor E2F7) was determined in cell lines by a dual luciferase assay. The function of miR-935 was investigated through metabolic activity (MTT) and transwell migration assays. Western blot and immunocytochemical assays examined protein expression level. Growth of miR-935 transfected or untransfected cells was measured via xenograft tumour formation. RESULTS:miR-935 was reduced in cancer tissue and was related to lymph node metastases, tumour node metastasis status and poor prognosis (all p < 0.02). In vitro, miR-935 suppressed cell proliferation, migration and invasion in NSCLC cells through targeting E2F7. Furthermore, E2F7 was upregulated in NSCLC tissue associated with poor prognosis (p = 0.0203) of NSCLCpatients. miR-935 suppressed the epithelial-mesenchymal transition and AKT pathways in NSCLC and inhibited the tumour growth in vivo. CONCLUSION: Altered miR-935 in lung cancer biopsy tissue may be a diagnostic tool and could direct treatment. Involvement in carcinogenesis is implied by its suppression of the development of NSCLC via targeting E2F7 and inhibiting AKT pathway.
Entities:
Keywords:
AKT pathway; E2F7; miR-935; non-small cell lung cancer
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