Impact of BTG2 expression on proliferation and invasion of gastric cancer cells in vitro
Impact of BTG2 expression on proliferation and invasion of gastric cancer cells in vitro
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DOI：
10.1007/s11033-009-9777-y
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发表时间：
2010-07-01
影响因子：
2.8
通讯作者：
Wu, Benyan
中科院分区：
文献类型：
--
作者：
Zhang, Lin;Huang, Haili;Wu, Benyan
BTG 2（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、肾和肝的致癌作用中是肿瘤抑制因子。然而，关于BTG 2在胃腺癌中的作用知之甚少。本研究旨在探讨BTG 2对胃癌细胞株SGC 7901和MKN 45生长、增殖、凋亡、侵袭和细胞周期的影响。将BTG 2 cDNA构建成真核表达载体pcDNA3.1，脂质体介导转染胃癌细胞株MKN 45和SGC 7901。筛选稳定的转化子并进行鉴定。流式细胞仪检测转染细胞凋亡和细胞周期的变化。通过细胞生长曲线和集落形成实验分析细胞生长和增殖情况。采用细胞迁移实验分析这些克隆的侵袭能力。MKN-BTG 2（稳定转染BTG 2基因的MKN 45）和SGC-BTG 2（稳定转染BTG 2基因的SGC 7901）的生长分别比其对照组慢。MKN-BTG 2细胞在第4、5、6、7天的计数均明显低于对照组（P < 0.05）。SGC-BTG 2组在第4、5、6、7天的细胞凋亡率也明显低于对照组（P < 0.05）。细胞周期分析显示，MKN-BTG 2和SGC-BTG 2细胞分别处于G 0-G1期和S期，与对照组比较差异有统计学意义（P < 0.05）。MKN-BTG 2细胞凋亡率明显高于对照组（P < 0.05）。集落形成实验结果显示，MKN-BTG 2和SGC-BTG 2的结肠形成率均低于其对照组（P < 0.05）。细胞迁移实验结果显示，MKN-BTG 2和SGC-BTG 2的细胞迁移率与其对照组相比无显著性差异（P > 0.05）。BTG 2对胃癌细胞的生长和增殖有较强的抑制作用。它可以降低这些肿瘤细胞的某些恶性表型。但对胃癌细胞的侵袭能力无影响，因此不能抑制胃癌的转移。在胃癌中，BTG 2可能是一个具有一定抑癌作用的基因，因此该基因可能是一个潜在的基因治疗靶点。
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.