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目的观察长链非编码RNA-肺腺癌转移相关转录因子1(MALAT1)对结直肠癌细胞介导的血管形成的影响,并初步探索其中可能的机理。方法在结直肠癌细胞株SW48中通过转染质粒过表达MALAT1经常规培养或乏氧培养后,收集培养液上清利用酶联免疫吸附试验(ELISA)检测其中血管内皮生长因子(VEGF)的含量,并利用此培养液上清孵育脐静脉内皮细胞(HUVEC),检测其对HUVEC形成血管微管能力的影响;同时收集SW48细胞通过蛋白质免疫印迹(Western blot)法检测其中缺氧诱导因子-1α(HIF-1α)的表达。结果在SW48中过表达MALAT1后,常规培养条件下其培养液上清中的VEGF含量为(514±32)mg/L,较对照组的(110±14)mg/L明显增高(P<0.05),乏氧培养条件下MALAT1组VEGF含量为(928±18)mg/L,较对照组的(230±21)mg/L也有明显增高(P<0.05);利用上述培养液上清孵育HUVEC,过表达MALAT1可促进其体外的成管能力;同时Western blot法证实过表达MALAT1可促进HIF-1α蛋白的表达。结论过表达MALAT1可促进结直肠癌细胞介导的血管形成,其可能作为结直肠癌新的药物治疗靶点。
Objective To investigate the effect of long chain nontranscriptional transcription factor 1 (MALAT1) on colorectal cancer cell mediated angiogenesis and to explore the possible mechanism. Methods The colorectal cancer cell line SW48 was transfected with plasmid MALAT1 by routine or hypoxic culture. The supernatant of the culture supernatants was collected and the content of vascular endothelial growth factor (VEGF) was detected by enzyme - linked immunosorbent assay (ELISA) The HUVECs were incubated with the culture supernatant to detect the effect of HUVECs on the formation of vascular microtubules. Simultaneously, SW48 cells were collected for detection of hypoxia-inducible factor-1α by Western blot (HIF-1α) expression. Results After MALAT1 was overexpressed in SW48, the level of VEGF in supernatant of culture medium was (514 ± 32) mg / L, which was significantly higher than that of control group (110 ± 14) mg / L ), The level of VEGF in MALAT1 group was (928 ± 18) mg / L, which was significantly higher than that in control group (230 ± 21) mg / L , Overexpression of MALAT1 can promote its in vitro tube capacity; Western blot confirmed that overexpression of MALAT1 can promote the expression of HIF-1αprotein. Conclusion Overexpression of MALAT1 can promote colorectal cancer cell-mediated angiogenesis, which may serve as a new drug target for colorectal cancer.