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Stomatin-like protein 2 regulates survivin expression in non-small cell lung cancer cells through ?-catenin signaling pathway.

ABSTRACT: The overexpression of stomatin-like protein-2 (SLP-2) is commonly observed in non-small cell lung cancer (NSCLC) cells. In the present study, we transfected a number of NSCLC cells with an SLP-2 shRNA-expressing vector (AdSLP2i) and examined its possible effects on cell growth and apoptosis. We found that suppression of SLP-2 expression inhibited cell growth, and that the apoptosis induced by SLP-2 suppression was correlated with decreased survivin protein expression. Moreover, the reduced survivin expression was found to be associated with reduced ?-catenin nuclear localization and appeared not to be modulated through the AKT signaling pathway. By using immunoprecipitation and proteomics to analyze protein-protein interactions in A549 cells with SLP-2 overexpression, we found that annexin A2 interacted with SLP-2 and ?-catenin directly. Our data further suggested that the knockdown of SLP-2 gene affected the SLP-2/Annexin A2/?-catenin cascade formation, reduced the translocation of cytoplasmic ?-catenin into nucleus, and downregulated downstream target genes. The results presented in this study, together with our previous findings, suggest that SLP-2 promotes NSCLC cell proliferation by enhancing survivin expression mediated via ?-catenin pathway.

SUBMITTER: Yang CT

PROVIDER: S-EPMC5859036 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature

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Stomatin-like protein 2 regulates survivin expression in non-small cell lung cancer cells through β-catenin signaling pathway.

Yang Cheng-Ta CT Li Jhy-Ming JM Li Li-Fu LF Ko Yu-Shien YS Chen Jeng-Ting JT

Cell death & disease 20180401 4

The overexpression of stomatin-like protein-2 (SLP-2) is commonly observed in non-small cell lung cancer (NSCLC) cells. In the present study, we transfected a number of NSCLC cells with an SLP-2 shRNA-expressing vector (AdSLP2i) and examined its possible effects on cell growth and apoptosis. We found that suppression of SLP-2 expression inhibited cell growth, and that the apoptosis induced by SLP-2 suppression was correlated with decreased survivin protein expression. Moreover, the reduced survi ...[more]

PMID: 29556045

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Project description:Purpose:FAM110B is a member of the FAM110 family (family with sequence similarity 110), which is a component of the centrosome associated proteins. Previous studies have shown that FAM110B may be involved in the process of cell cycle and may play a role in carcinogenesis and tumor progression. Using an online database, we found that FAM110B may predict favorable prognosis in non-small cell lung cancer (NSCLC). Therefore, the role of FAM110B playing in NSCLC needs to be further investigated. Patients and Methods:Online databases and immunohistochemistry were used to predict the expression and prognostic value of FAM110B in NSCLC samples. Immunofluorescence staining was used to investigate the subcellular distribution of FAM110B. Western blot, MTT, colony formation, and matrigel invasion assay were used to detect the expression and the effect of FAM110B on mediating proliferation and invasion in NSCLC cell lines. Results:In this study, immunohistochemistry results showed that FAM110B expression significantly correlated with early TNM staging (P=0.020) and negative regional lymph node metastasis (P=0.006). Kaplan-Meier survival analysis found that the median survival time of patients with positive FAM110B expression (56.181±2.348 months) was significantly longer than those with negative FAM110B expression (47.701±2.997 months, P=0.024). Moreover, overexpression of FAM110B inhibited the proliferation and invasion of A549, H1299, and LK2 cell lines. Conversely, FAM110B RNAi exerted opposite effects in the above cell lines. Furthermore, FAM110B overexpression downregulated the active ?-catenin, phosphorylation of GSK-3? (p-GSK-3?), cyclin B1, cyclin D1, MMP2, and MMP7, and upregulated the phosphorylation of ?-catenin (p-?-catenin) in A549 and H1299 cells. Besides, the FAM110B-induced depressions of p-GSK-3? and active ?-catenin were reversed after being treated with Wnt/?-catenin inhibitor, XAV-939. Conclusion:In summary, our results demonstrated that the overexpression of FAM110B restricts the proliferation and invasion of NSCLC cells by inhibiting Wnt/?-catenin signaling. Our study reveals the antitumor function of FAM110B in NSCLC and indicates that FAM110B is a potential therapeutic target.

Dataset Information

Stomatin-like protein 2 regulates survivin expression in non-small cell lung cancer cells through ?-catenin signaling pathway.

Publications

Stomatin-like protein 2 regulates survivin expression in non-small cell lung cancer cells through β-catenin signaling pathway.

Similar Datasets

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