OBJECTIVE: Non-small cell lung cancer (NSCLC) is the most common type of human lung cancer, with highly aggressive, lethal malignancy and microRNAs have already been proven to be associated with NSCLC tumorigenesis. In this study, we sought to determine the expression, the clinical value and its role in NSCLC tumor progression. METHODS: Clinical NSCLC tissues and common cell lines were collected. Real-time PCR was performed to quantify the miR-498 expression. In addition, the association of miR-498 expression with clinical pathological factors and prognosis was statistically analyzed. Furthermore, cell proliferation was measured after miR-498 was overexpressed transiently in cells. RESULTS: We found that miR-498 was significantly decreased in NSCLC tumors as well as cell lines, when compared with their separated controls. Decreased miR-498 expression was associated with sex, tumor type and tumor size. Functionally, ectopic expression of miR-498 in A549 and H661 cells inhibited cell proliferation. CONCLUSION: Our data indicated that miR-498 is downregulated and correlated with tumor progression, which might be a putitive therapeutic target in NSCLC treatment.
OBJECTIVE:Non-small cell lung cancer (NSCLC) is the most common type of humanlung cancer, with highly aggressive, lethal malignancy and microRNAs have already been proven to be associated with NSCLC tumorigenesis. In this study, we sought to determine the expression, the clinical value and its role in NSCLC tumor progression. METHODS: Clinical NSCLC tissues and common cell lines were collected. Real-time PCR was performed to quantify the miR-498 expression. In addition, the association of miR-498 expression with clinical pathological factors and prognosis was statistically analyzed. Furthermore, cell proliferation was measured after miR-498 was overexpressed transiently in cells. RESULTS: We found that miR-498 was significantly decreased in NSCLC tumors as well as cell lines, when compared with their separated controls. Decreased miR-498 expression was associated with sex, tumor type and tumor size. Functionally, ectopic expression of miR-498 in A549 and H661 cells inhibited cell proliferation. CONCLUSION: Our data indicated that miR-498 is downregulated and correlated with tumor progression, which might be a putitive therapeutic target in NSCLC treatment.