Zhang H, Zhou X, Xu C, Yang J, Xiang J, Tao M, Xie Y
Department of General Surgery, the First Affiliated Hospital of Soochow University, Suzhou, China.
Department of Oncology, the First Affiliated Hospital of Soochow University, Suzhou, China.
Cancer Gene Ther. 2016 Jan;23(1):13-23. doi: 10.1038/cgt.2015.59. Epub 2015 Nov 13.
Both inhibitor of growth 4 (ING4) and phosphatase and tensin homolog (PTEN) have been shown to be strong candidate tumor suppressors. However, the combined efficacy of ING4 and PTEN for human gastric cancer remains to be determined. In this report, we constructed a multiple promoter expression cassette-based recombinant adenovirus coexpressing ING4 and PTEN (AdVING4/PTEN), assessed the combined effects of AdVING4/PTEN on gastric cancer using wild-type p53 AGS and SNU-1 human gastric cancer cell lines, and elucidated its underlying mechanisms. We found that AdVING4/PTEN-induced synergistic growth inhibition and apoptosis in vitro AGS or SNU-1 tumor cells and in vivo AGS xenografted tumors subcutaneously inoculated in athymic BALB/c nude mice. Mechanistically, AdVING4/PTEN exhibited an enhanced effect on upregulation of p53, Ac-p53 (K382), P21, Bax, PUMA, Noxa, cleaved Caspase-9, cleaved Caspase-3 and cleaved PARP as well as downregulation of Bcl-2 in vitro and in vivo. In addition, AdVING4/PTEN synergistically downregulated tumor vessel CD34 expression and reduced microvessel density, and additively inhibited vascular endothelial growth factor (VEGF) expression in vivo. The synergistic tumor suppression elicited by AdVING4/PTEN was closely associated with the synergistic induction of apoptosis possibly via enhancement of endogenous p53 responses through cooperatively facilitating p53's stability and acetylation, and the synergistic inhibition of tumor angiogenesis probably via overlapping reduction of VEGF through cooperatively downregulating hypoxia inducible factor-1α's level and transcription activity. Thus, our results indicate that cancer gene therapy combining ING4 and PTEN may constitute a novel and effective therapeutic modality for human gastric cancer and other cancers.
生长抑制因子4(ING4)和磷酸酶及张力蛋白同源物(PTEN)均已被证明是强大的候选肿瘤抑制因子。然而,ING4和PTEN对人类胃癌的联合疗效仍有待确定。在本报告中,我们构建了一种基于多启动子表达盒的重组腺病毒,其共表达ING4和PTEN(AdVING4/PTEN),使用野生型p53的AGS和SNU-1人胃癌细胞系评估AdVING4/PTEN对胃癌的联合作用,并阐明其潜在机制。我们发现AdVING4/PTEN在体外的AGS或SNU-1肿瘤细胞以及体内接种于无胸腺BALB/c裸鼠皮下的AGS异种移植瘤中诱导协同生长抑制和凋亡。机制上,AdVING4/PTEN在体外和体内对p53、乙酰化p53(K382)、P21、Bax、PUMA、Noxa、裂解的半胱天冬酶-9、裂解的半胱天冬酶-3和裂解的PARP的上调以及Bcl-2的下调表现出增强作用。此外,AdVING4/PTEN在体内协同下调肿瘤血管CD34表达并降低微血管密度,并累加抑制血管内皮生长因子(VEGF)表达。AdVING4/PTEN引发的协同肿瘤抑制可能与协同诱导凋亡密切相关,这可能是通过协同促进p53的稳定性和乙酰化来增强内源性p53反应实现的,并且可能与通过协同下调缺氧诱导因子-1α的水平和转录活性来重叠降低VEGF从而协同抑制肿瘤血管生成有关。因此,我们的结果表明,联合ING4和PTEN的癌症基因治疗可能构成一种针对人类胃癌和其他癌症的新型有效治疗方式。