Pathak Subhajit, Singh Vijayata, Kumar G Narendra, Jayandharan Giridhara R
Laurus Center for Gene Therapy, Department of Biological Sciences and Bioengineering and Mehta Family Center for Engineering in Medicine and Gangwal School of Medical Sciences and Technology, Indian Institute of Technology Kanpur, Uttar Pradesh, Kanpur, 208016, India.
Cancer Gene Ther. 2024 Dec;31(12):1796-1803. doi: 10.1038/s41417-024-00844-x. Epub 2024 Oct 9.
Advanced-stage hepatocellular carcinoma (HCC) remains an untreatable disease with an overall survival of less than one year. One of the critical molecular mediators contributing to increased resistance to therapy and relapse, is increased hypoxia-inducible factor 1α (HIF-1α) levels, leading to metastasis of tumor cells. Several microRNAs are known to be dysregulated and impact HIF-1α expression in HCC. An in silico analysis demonstrated that hsa-miR-199a-5p is downregulated at various stages of HCC and is known to repress HIF-1α expression. Based on this analysis, we developed a combinatorial suicide gene therapy by employing hepatotropic Adeno-associated virus-based vectors encoding an inducible caspase 9 (iCasp9) and miR-199a. The overexpression of miR-199a-5p alone significantly decreased ( ~ 2-fold vs. Mock treated cells, p < 0.05) HIF-1α mRNA levels, with a concomitant increase in cancer cell cytotoxicity in Huh7 cells in vitro and in xenograft models in vivo. To further enhance the efficacy of gene therapy, we evaluated the synergistic therapeutic effect of AAV8-miR-199a and AAV6-iCasp9 in a xenograft model of HCC. Our data revealed that mice receiving combination suicide gene therapy exhibited reduced expression of HIF-1α ( ~ 4-fold vs. Mock, p < 0.001), with a significant reduction in tumor growth when compared to mock-treated animals. These findings underscore the therapeutic potential of downregulating HIF-1α during suicide gene therapy for HCC.
晚期肝细胞癌(HCC)仍然是一种无法治愈的疾病,总体生存期不到一年。导致治疗耐药性增加和复发的关键分子介质之一是缺氧诱导因子1α(HIF-1α)水平升高,这会导致肿瘤细胞转移。已知几种微小RNA在HCC中表达失调并影响HIF-1α的表达。一项计算机分析表明,hsa-miR-199a-5p在HCC的各个阶段均下调,并且已知其可抑制HIF-1α的表达。基于此分析,我们通过使用编码诱导型半胱天冬酶9(iCasp9)和miR-199a的嗜肝腺相关病毒载体开发了一种联合自杀基因疗法。单独过表达miR-199a-5p可显著降低(与模拟处理的细胞相比约2倍,p<0.05)HIF-1α mRNA水平,同时在体外Huh7细胞和体内异种移植模型中癌细胞的细胞毒性增加。为了进一步提高基因治疗的疗效,我们在HCC异种移植模型中评估了AAV8-miR-199a和AAV6-iCasp9的协同治疗效果。我们的数据显示,接受联合自杀基因治疗的小鼠HIF-1α表达降低(与模拟组相比约4倍,p<0.001),与模拟处理的动物相比,肿瘤生长显著减少。这些发现强调了在HCC自杀基因治疗过程中下调HIF-1α的治疗潜力。