Abstract
Aim: The purpose of the present study was to explore the function and mechanism of tensin 1 (TNS1) in non-small cell lung cancer (NSCLC) progression.Methods: The expression of TNS1 in NSCLC cells and tissues was assessed by RT-PCR and Western blot. Besides, Kaplan–Meier survival analysis was recruited to explore the association between TNS1 and NSCLC. Cell growth was analyzed by MTT and flow cytometry assay, while cell metastasis was determined by wound healing and transwell assays. The targeting relationship between TNS1 and miR-152 was assessed by luciferase activity assays. And Western blot was employed to determine the expression of related proteins of Akt/mTOR/RhoA pathway.Results: TNS1 level was boosted in NSCLC cells and tissues, related to the prognosis of NSCLC patients. Furthermore, it was proved that TNS1 promoted the growth and metastasis of NSCLC cells via Akt/mTOR/RhoA pathway. And miR-152 targeted TNS1 to affect the progression of NSCLC.Conclusion: miR-152/TNS1 axis inhibits the progression of NSCLC by Akt/mTOR/RhoA pathway.
Highlights
Lung cancer is one of the dominant causes of cancer-related deaths worldwide [1], among which non-small cell lung cancer (NSCLC) is the dominant histological type that accounts for ∼80% [2]
Tensin 1 (TNS1) expression in NSCLC tissues was significantly higher, compared with adjacent normal lung tissues (Figure 1A). mRNA and protein level of TNS1 were up-regulated in NSCLC cells, A549, H460, SPCA1, SK-MES-1 and H1299 compared with normal lung epithelial 16HBE cells (Figure 1B,C)
Kaplan–Meier survival analysis showed that high TNS1 expression was significantly correlated with poor prognosis in patients with NSCLC (Figure 1D)
Summary
Lung cancer is one of the dominant causes of cancer-related deaths worldwide [1], among which non-small cell lung cancer (NSCLC) is the dominant histological type that accounts for ∼80% [2]. Though the prognosis of lung cancer patients at all stages has improved in recent decades, the clinical treatment effect is not satisfactory [3]. The development of molecular-targeted drugs is the hope to improve the overall survival and quality of life of cancer patients [4], while the exact molecular mechanism of lung cancer is still unclear. Tensin 1 (TNS1), as a member of tensin family, has been reported to function as a scaffold for adhesion-related signaling through binding to actin cytoskeleton and β1-integrin [6]. Transgelin/TNS1 axis advanced proliferation and invasiveness of colorectal cancer cells [8]. Down-regulated TNS1 suppresses the proliferation of acute myeloid leukemia cells and increases the apoptosis [10]. TNS1 has been proved to be up-regulated in lung cancer cells following (-)-epigallocatechin-3-gallate treatment which was a potential anticancer agent [12]. The role of TNS1 in NSCLC tumorigenesis is still unclear
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