LINC01296/miR-1255b-5p促进非小细胞肺癌进展的研究

目的 探究下调LINC01296的表达对非小细胞肺癌（non-small cell lung cancer，NSCLC）进展的影响，以及LINC01296调控miR-1255b-5p在NSCLC发生发展中的分子机制。方法 培养6种NSCLC细胞系；实时荧光定量聚合酶链反应法检测LINC01296在NSCLC细胞系以及在48例患者样本中表达水平的高低；细胞计数试剂盒-8法检测稳转细胞株的细胞增殖情况；克隆形成实验检测细胞的生长以及增殖状况；划痕实验检测细胞的迁移情况；FITC-Annexin-V法检测细胞凋亡；动物实验，包括裸鼠尾静脉和皮下瘤注射，观察癌细胞的转移以及成瘤情况；双荧光素酶报告基因实验验证LINC01296与miR-1255b-5p之间存在靶向结合关系。 结果 LINC01296在NSCLC中高表达；LINC01296基因敲低抑制NSCLC细胞生长、迁移；LINC01296敲低抑制体内瘤体的生长和转移；LINC01296与miR-1255b-5p的之间存在海绵吸附作用；LINC01296与miR-1255b-5p的表达呈负相关。结论 LINC01296作为NSCLC的促癌分子，通过抑制miR-1255b-5p的表达水平，促进了NSCLC的发展。

Research on the promotion of non-small cell lung cancer progression by LINC01296/miR-1255b-5p

Objective To explore the influence of down-regulation of LINC01296 expression on the progression of non-small cell lung cancer and the molecular mechanism of LINC01296 regulating miR-1255b-5p in the occurrence and development of non-small cell lung cancer. Methods Six NSCLC cell lines were cultured to test the expression level of LINC01296. The expression level of LINC01296 in NSCLC cell lines and 48 patient samples was detected by quantitative real time-polymerase chain reaction (qRT-PCR). Cell counting kit-8 (CCK-8) was used to detect the cell proliferation of stably transformed cell lines. Clone Formation test was used to detect the growth and proliferation of cells. The migration of cells was detected by Wound Healing test. FITC-Annexin-V was used to detect apoptosis. Animal experiments, including tail vein and subcutaneous tumor injection in nude mice, observed the metastasis and tumorigenesis of cancer cells. The experiment of double luciferase reporter gene verified that there was a targeted binding relationship between LINC01296 and mir-1255a-5p. Results LINC01296 was highly expressed in NSCLC. Knockdown of the LINC01296 gene inhibited the growth and migration of non-small cell lung cancer cells. Knockdown of the LINC01296inhibited the growth and migration of tumor in vivo. There was Sponge adsorption between LINC01296 and miR-1255b-5p existing. The expression level of LINC01296 was negatively correlated with the expression level of mir-1255a-5p.Conclusion LINC01296, as a cancer-promoting molecule of NSCLC, promoted the development of NSCLC by inhibiting the expression level of miR-1255b-5p.