ABSTRACT
Purpose: Previous studies have reported that miR-30d-5p gene expression can inhibit tumor proliferation, but its mechanism has not been fully elucidated. Methods: Based on previous findings, TGF-ß1 was used to induce epithelial mesenchymal transformation in A549 cells. The expression levels of DUSP-1, E-cadherin and Vimentin were detected by Western blot. mRNA expression levels of DUSP-1, E-cadherin and Vimentin were determined by RT-qPCR. The expression level of miR-30d-5p was determined by RT-qPCR. Results: The induction effect of TGF-ß1 could be reversed by the intervention of miR-30d-5p in A549 cells. miRNA inhibition experiment showed that miR-30d-5p inhibitor could effectively inhibit the expression of miR-30d-5p in A549 cells. After miR-30d-5p intervention, TGF-ß1 was reversed on EMT-related genes (Dusp-1, E-cadherin, Vimentin). Conclusion: TGF-ß1 can induce epithelial mesenchymal transformation of A549 cells, and miR-30d-5p may be a key regulatory mechanism in regulating gene and protein expression of TGF-ß1-mediated DUSP-1, E-cadherin and Vimentin. This provides a new perspective for understanding the anti-tumor effect of miR-30d-5p gene.
ABSTRACT
Genomic instability (GI) was associated with tumorigenesis. However, GI-related lncRNA signature (GILncSig) in lung adenocarcinoma (LUAD) is still unknown. In this study, the lncRNA expression data, somatic mutation information and clinical survival information of LUAD were downloaded from The Cancer Genome Atlas (TCGA) and performed differential analysis. Functional and prognosis analysis revealed that multiple GI-related pathways were enriched. By using univariate and multivariate Cox regression analysis, 5 GI-associated lncRNAs (AC012085.2, FAM83A-AS1, MIR223HG, MIR193BHG, LINC01116) were identified and used to construct a GILncSig model. Mutation burden analysis indicated that the high-risk GI group had much higher somatic mutation count and the risk score constructed by the 5 GI-associated lncRNAs was an independent predictor for overall survival (OS) (P < 0.05). Overall, our study provides valuable insights into the involvement of GI-associated lncRNAs in LUAD and highlights their potential as therapeutic targets.
Subject(s)
Adenocarcinoma of Lung , Biomarkers, Tumor , Gene Expression Regulation, Neoplastic , Genomic Instability , Lung Neoplasms , RNA, Long Noncoding , Humans , RNA, Long Noncoding/genetics , Adenocarcinoma of Lung/genetics , Adenocarcinoma of Lung/mortality , Adenocarcinoma of Lung/pathology , Biomarkers, Tumor/genetics , Prognosis , Lung Neoplasms/genetics , Lung Neoplasms/mortality , Lung Neoplasms/pathology , Male , Female , Gene Expression Profiling , Middle AgedABSTRACT
Aerobic exercise training is a kind of pulmonary rehabilitation for lung diseases. This was a retrospective study to assess the efficacy of aerobic exercise training in chronic obstructive pulmonary disease (COPD) at a stable stage. A total of one hundred and fifty-six stable COPD patients who had accepted self-education only or self-education combined with an aerobic exercise training between January 2017 to January 2019 were reviewed retrospectively. A total of 79 patients who had received self-education combined with an aerobic exercise training schedule comprised the aerobic exercise training group (AET group) and 77 patients who had received self-education only were regarded as the education group (EDU group). The acute incidence rate in AET group was 7.6% better than that in EDU group 20.7% (Pâ <â .05). The AET group patients expressed higher levels of 6 minutes walking distance (6MWD) (Pâ <â .05) and better evaluations of both lung function (Pâ <â .05) and T lymphocyte immune response (Pâ <â .05), as well as significantly decreased chronic obstructive pulmonary disease assessment test (CAT) scores and modified British medical research council (mMRC) grades (Pâ <â .05). Patients in EDU group did not report any changes in any of these characteristics. The aerobic exercise training intervention contributed to an increasing in 6MWD and decrease in CAT scores and mMRC grades, as well as improving the T lymphocyte immune response in stable COPD patients.
Subject(s)
Pulmonary Disease, Chronic Obstructive , Humans , Retrospective Studies , Exercise , Exercise Therapy , Exercise Tolerance , Quality of LifeABSTRACT
BACKGROUND: In the past few decades, many lines of evidence implicate the importance of liver kinase B1 (LKB1) as a tumor suppressor gene in the development and progression of solid tumours. However, the prognostic and clinicopathological value of LKB1 in patients with lung cancer are controversial. This article aimed to investigate the latest evidence on this question. METHODS: A systematic literature searched in the PubMed, Web of Science, Embase, Cochrane library, Scopus until September 20, 2020. The association between overall survival (OS), relapse-free survival (RFS), progression-free survival (PFS), clinicopathological features and LKB1 were analysed by meta-analysis. RESULTS: Eleven studies including 1507 patients were included in this meta-analysis. The pooled results revealed that low LKB1 expression was significantly associated with poor overall survival (OS) (HRâ=â1.67, 95% CI: 1.07-2.60, Pâ=â.024) in lung cancer. However, no association was found between LKB1 expression and DFS/PFS (HRâ=â1.29, 95% CI: 0.70-2.39, Pâ=â.410). Pooled results showed that low LKB1 expression was associated with histological differentiation (poor vs moderate or well, ORâ=â4.135, 95% CI:2.524-6.774, Pâ<â.001), nodal metastasis (absent vs present, ORâ=â0.503, 95% CI: 0.303-0.835, Pâ=â.008) and smoking (yes vs no, ORâ=â1.765, 95% CI: 1.120-2.782, Pâ=â.014). CONCLUSION: These results suggest that low expression of LKB1 can be considered as a unfavorable prognostic biomarker for human lung cancer, which should be further researched.