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背景与目的肺癌位居全球癌症相关死亡率的首位,其中肿瘤转移是导致肺癌患者死亡的主要原因,研究表明mi R-373与多种肿瘤细胞的侵袭转移有密切关系。本研究旨在探讨mi R-373-3p在非小细胞肺癌(non-small cell lung cancer,NSCLC)中的表达情况及其对肺腺癌细胞侵袭转移能力的影响。方法利用q RTPCR法检测mi R-373-3p在NSCLC组织和肺腺癌细胞株中的表达。瞬时转染hsa-mi R-373-3p的mimics和inhibitor至肺腺癌H1299和A549细胞株中,利用Transwell小室检测转染后肺腺癌细胞侵袭转移能力的改变,Western blot检测转染后肺腺癌细胞中基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)及MMP-14蛋白水平的改变。结果mi R-373-3p在51例NSCLC组织和5种肺腺癌细胞株中均明显高表达。在mi R-373-3p低表达的H1299细胞中过表达mi R-373-3p,细胞的侵袭转移能力明显提高,同时MMP-9及MMP-14的表达上调;在mi R-373-3p高表达的A549细胞中抑制mi R-373-3p表达,细胞的侵袭转移能力下降,并且下调MMP-9和MMP-14的表达。结论 mi R-373-3p可能通过正向调节MMP-9、MMP-14的表达而促进肺腺癌细胞的侵袭转移能力。
BACKGROUND & OBJECTIVE: Lung cancer ranks the top of the global cancer-related deaths. Tumor metastasis is the leading cause of death in lung cancer patients. Studies have shown that mi R-373 is closely related to the invasion and metastasis of a variety of tumor cells. This study aimed to investigate the expression of mi R-373-3p in non-small cell lung cancer (NSCLC) and its effect on the invasion and metastasis of lung adenocarcinoma. Methods q RTPCR was used to detect the expression of mi R-373-3p in NSCLC tissues and lung adenocarcinoma cell lines. The mimics and inhibitor of hsa-mi R-373-3p were transiently transfected into lung adenocarcinoma H1299 and A549 cell lines. Transwell chamber was used to detect the invasion and metastasis of transfected lung adenocarcinoma cells. Alteration of matrix metalloproteinase-9 (MMP-9) and MMP-14 protein levels in adenocarcinoma cells. Results mi R-373-3p was highly expressed in 51 NSCLC tissues and 5 lung adenocarcinoma cell lines. The overexpression of mi R-373-3p in mi R-373-3p-overexpressing H1299 cells significantly enhanced the invasion and metastasis of cells, meanwhile, the expressions of MMP-9 and MMP-14 were up-regulated. In mi R-373-3p The expression of mi R-373-3p was inhibited in A549 cells. The invasion and metastasis of cells were decreased and the expressions of MMP-9 and MMP-14 were down-regulated. Conclusion mi R-373-3p may promote the invasion and metastasis of lung adenocarcinoma cells by up-regulating the expressions of MMP-9 and MMP-14.