Background: Previous studies have reported the role of circular RNAs (circR-NAs) in the progression of non-small-cell lung cancer (NSCLC). SWT1-derived circRNAs were confirmed to affect the apoptosis of cardiomyocytes; however, the biological functions of SWT1-derived circRNAs in cancers are still unknown.Here, we investigated the potential role of SWT1-derived circRNAs in NSCLC.Methods: We used quantitative real-time polymerase chain reaction (qRT-PCR) to measure the expression of circSWT1 in NSCLC tissues and paired normal tissues. The potential functions of circSWT1 in tumor progression were assessed by CCK-8, colony formation, wound healing, and matrigel transwell assays in vitro and by xenograft tumor models in vivo. Next, epithelial-mesenchymal transition (EMT) was evaluated by western blotting, immunofluorescence, and immunohistochemistry (IHC). Moreover, circRIP, RNA pulldown assays, luciferase reporter gene assays, and FISH were conducted to illuminate the molecular mechanisms of circSWT1 via the miR-370-3p/SNAIL signal pathway. Then, we knocked out SNAIL in A549 and H1299 cells to identify the roles of circSWT1 in the progression and EMT of NSCLC through SNAIL. Finally, circSWT1 functions were confirmed in vivo using xenograft tumor models. Results: CircSWT1 expression was significantly upregulated in NSCLC tissues, and high expression of circSWT1 predicted poor prognosis in NSCLC via survival analysis. In addition, overexpression of circSWT1 promoted the invasion and migration of NSCLC cells. Subsequently, we found that overexpression of circ-SWT1 induced EMT and that knockdown of circSWT1 inhibited EMT in NSCLC cells. Mechanistically, circSWT1 relieved the inhibition of downstream SNAIL by sponging miR-370-3p. Moreover, we found that these effects could be reversed by knocking out SNAIL. Finally, we verified that circSWT1 promoted NSCLC progression and EMT in xenograft tumor models.
The role of TELO2-interacting protein 1 (TTI1) in the progression of several types of cancer has been reported recently. The aim of this study was to estimate the expression and potential value of TTI1 in non-small-cell lung cancer (NSCLC) patients.The expression of TTI1 and its prognostic value in NSCLC from The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) database were analyzed.To verify the bioinformatics findings, a tissue microarray containing 160 NSCLC and paired peritumoral tissues from NSCLC patients was analyzed by immunohistochemistry for TTI1. Subsequently, the roles of TTI1 in NSCLC cells were investigated in vivo by establishing xenograft models in nude mice and in vitro by transwell, CCK-8, wound healing, and colony formation assays. In addition, quantitative real-time polymerase
Background: The role of TTI1 in the progression of several types of cancer has been reported recently. The aim of this study was to estimate the expression and the potential value of TTI1 in non-small cell lung cancer (NSCLC) patients.Methods: The expression of TTI1 and its prognostic value in NSCLC from The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) database were analyzed. To verify the bioinformatics findings, a tissue microarrays (TMAs) containing 160 NSCLC and paired peritumoral tissues from NSCLC patients was analysed by immunohistochemistry for TTI1. Subsequently, the roles of TTI1 in NSCLC cells were investigated in vivo by establishing xenograft models in nude mice, and in vitro by transwell, CCK-8 assay, wound healing and colony formation assays. In addition, qRT-PCR and western blot were applied to explore the underlying mechanism by which TTI1 promotes tumor progression. Finally, the relation between TTI1 and KI67 expression level of NSCLC was probed, and Kaplan-Meier and Cox's analyses were performed to assess the prognostic merit of TTI1 and KI67 in NSCLC patients. Results: The expression of TTI1 was significantly upregulated in NSCLC tissues compared to paired peritumoral tissues, which was coincide with the bioinformatics findings from TCGA and GEO database. TTI1 was highly expressed in NSCLC patients with large tumor, advanced tumor stage, and lymphatic metastasis. In addition, the prognostic analysis identified the TTI1 as an independent indication for poor prognosis of NSCLC patients. In vitro, Up-regulation of TTI1 in NSCLC cells could facilitate cell invasion, metastasis, viability and proliferation. Mechanistically, our study verified that TTI1 could regulate mTOR activity which has a pivotal role in human cancer. Consistently, the TTI1 and KI67 expression had a positive relationship in NSCLC cells and tissues. Notably, compared with patients with low expression of TTI1 or KI67, patients with overexpression of TTI1 or KI67 had a shorter overall survival rate (OS) and a higher disease-free survival rate (DFS), and the combination of TTI1 and KI67 was an independent parameter predicting the prognosis and recurrence of NSCLC patients. Conclusions: TTI1 promotes NSCLC cell proliferation, metastasis and invasion by regulating mTOR activity and the combination of TTI1 and KI67 is a valuable molecular biomarker for the survival and recurrence of NSCLC patients.
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