Department of Gastroenterology, Second Affiliated Hospital of General Hospital of PLA, 100091 Beijing, China.
Mol Biol Rep. 2010 Jul;37(6):2579-86. doi: 10.1007/s11033-009-9777-y. Epub 2009 Sep 2.
BTG2 (B cell translocation gene 2) is downregulated in several human tumors and has been known as a tumor suppressor in carcinogenesis of thymus, prostate, kidney, and liver. However, little is known about the role BTG2 plays in gastric adenocarcinoma. In the present study, we intended to investigate the influence of BTG2 on the growth, proliferation, apoptosis, invasion and cell cycle of the gastric cancer cell lines SGC7901 and MKN45. BTG2 cDNA was insected into a constitutive vector pcDNA3.1 followed by transfection in gastric cancer cell line MKN45 and SGC7901 by using liposome. Then stable transfectants were selected and appraised. The apoptosis and cell cycles of these transfectants were analyzed by using flow cytometric assay. The growth and proliferation were analyzed by cell growth curves and colony-forming assay, respectively. The invasion of these clones was analyzed by using cell migration assay. MKN-BTG2 (MKN45 with stable transfection of BTG2 gene) and SGC-BTG2 (SGC7901 with stable transfection of BTG2 gene) grew slower than their control groups, respectively. The cell counts of MKN-BTG2 in the fourth, fifth, sixth and seventh days were significantly fewer than those of control groups (P < 0.05). Those of SGC-BTG2 in the fourth fifth, sixth and seventh days were significantly fewer than those of control groups too (P < 0.05). Cell cycle analysis showed that proportions of MKN-BTG2 and SGC-BTG2 cells in G0-G1 and S were different significantly with those of their control groups, respectively (P < 0.05). The apoptosis rate of MKN-BTG2 was significantly higher than those of control groups (P < 0.05). Results of colony-forming assay showed that the colon formation rates of MKN-BTG2 and SGC-BTG2 were lower than those of their control groups (P < 0.05). The results of cell migration assay showed that the cell migration rates of MKN-BTG2 and SGC-BTG2 were not significantly different with those of their control groups (P > 0.05). BTG2 can restrain the growth and proliferation of gastric cancer cells powerfully. It can reduce some malignant phenotype of these tumor cells. But it could not impact the ability of invasion of gastric cancer cells, so could not restrain the metastasis of gastric cancer. In gastric cancer, BTG2 could be thought as a tumor-inhibiting gene in some distance, so the gene could be a potential target of gene therapy.
BTG2(B 细胞易位基因 2)在几种人类肿瘤中下调,并且已知在胸腺、前列腺、肾脏和肝脏的致癌作用中作为肿瘤抑制因子。然而,关于 BTG2 在胃腺癌中的作用知之甚少。在本研究中,我们旨在研究 BTG2 对胃癌细胞系 SGC7901 和 MKN45 的生长、增殖、凋亡、侵袭和细胞周期的影响。将 BTG2 cDNA 插入组成型载体 pcDNA3.1 中,然后通过脂质体转染胃癌细胞系 MKN45 和 SGC7901。然后选择并评估稳定转染体。通过流式细胞术分析这些转染体的凋亡和细胞周期。通过细胞生长曲线和集落形成测定分别分析生长和增殖。通过细胞迁移测定分析这些克隆的侵袭。MKN-BTG2(BTG2 基因稳定转染的 MKN45)和 SGC-BTG2(BTG2 基因稳定转染的 SGC7901)的生长速度均慢于其对照组。MKN-BTG2 细胞在第四天、第五天、第六天和第七天的细胞计数明显少于对照组(P <0.05)。SGC-BTG2 细胞在第四天、第五天、第六天和第七天的细胞计数也明显少于对照组(P <0.05)。细胞周期分析表明,MKN-BTG2 和 SGC-BTG2 细胞的 G0-G1 和 S 期比例与对照组相比有显著差异(P <0.05)。MKN-BTG2 的细胞凋亡率明显高于对照组(P <0.05)。集落形成试验结果表明,MKN-BTG2 和 SGC-BTG2 的集落形成率低于对照组(P <0.05)。细胞迁移试验结果表明,MKN-BTG2 和 SGC-BTG2 的细胞迁移率与对照组相比无显著差异(P >0.05)。BTG2 可强力抑制胃癌细胞的生长和增殖。它可以降低这些肿瘤细胞的一些恶性表型。但它不能影响胃癌细胞侵袭的能力,因此不能抑制胃癌的转移。在胃癌中,BTG2 可以在一定程度上被认为是一种肿瘤抑制基因,因此该基因可能是基因治疗的潜在靶点。