Background
Aberrant expression of long non-coding RNA cancer susceptibility 15 (lncRNA CASC15) has been documented in various human tumors, and upregulation of CASC15 is closely correlated with cancer progression. However, the expression profile and potential biological functions of lncRNA CASC15 in non-small cell lung cancer (NSCLC) have not been fully characterized.
Conclusion
In summary, our findings suggest CASC15 exhibits an oncogenic role in promoting NSCLC tumorigenesis via regulating EMT.
Methods
The expression levels of CASC15 were assessed by qRT-PCR in human NSCLC tissues and by in situ hybridization in NSCLC tissue microarray. The relationship between CASC15 expression and clinical parameters, as well as prognosis were analyzed and validated in TCGA NSCLC datasets. The biological functions of CASC15 were analyzed by CCK-8 assay, cell migration and invasion assay in NSCLC cell lines in vitro. In addition, a mouse xenograft model was established to evaluate the effect of CASC15 knockdown on NSCLC tumor growth in vivo. Epithelial-mesenchymal transition (EMT) related molecules were examined by western blot and immunohistochemistry staining.
Results
We found that CASC15 was upregulated in NSCLC tissues and cell lines. High expression levels of CASC15 were correlated with malignancies and poor survival rate in NSCLC patients. Multivariate analysis revealed that CASC15 was an independent risk factor of prognosis. In addition, we demonstrated that CASC15 knockdown inhibited NSCLC cell proliferation, migration and invasion in vitro. Xenograft model showed CASC15 knockdown significantly suppressed NSCLC tumor growth. Mechanistically, we revealed that CASC15 regulated EMT-related molecules and promoted the NSCLC progression and metastasis.