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Abstract：
UNASSIGNED: To analyze the expression of mitochondrial translational initiation factor 2 (MTIF2) and the biological functions of the gene in hepatocellular carcinoma (HCC).
UNASSIGNED: The treatment of HCC treatment and its prognostic prediction are limited by a lack of comprehensive understanding of the molecular mechanisms in HCC. OBJECTIVE: To determine the cells expressing MTIF2 in HCC and the function of the MTIF2+ cell subpopulation.
UNASSIGNED: Gene expression analysis on TIMER 2.0, UALCAN, and GEPIA databases was performed to measure the expression of MTIF2 in HCC tissues. Cell clustering subgroups and annotation were conducted based on the single-cell sequencing data of HCC and paracancerous tissues in the Gene Expression Omnibus (GEO) database. MTIF2 expression in different cell types was analyzed. Further, biological pathways potentially regulated by MTIF2 in each cell type were identified. In addition, protein-protein interaction (PPI) networks of MTIF2 with genes in its regulated biological pathways were developed. The cell function assay was performed to verify the effects of superoxide dismutase-2 (SOD2) and MTIF2 on HCC cells. Finally, we screened virtual drugs targeting MTIF2 and SOD2 employing database screening, molecular docking and molecular dynamics.
UNASSIGNED: MTIF2 showed a remarkably high expression in HCC tissues. We identified a total of 10 cell types between HCC tissues and paracancerous tissues. MTIF2 expression was upregulated in epithelial cells, macrophages, and hepatocytes. More importantly, high-expressed MTIF2 in HCC tissues was mainly derived from epithelial cells and hepatocytes, in which the reactive oxygen species (ROS) pathway was significantly positively correlated with MTIF2. In the PPI network, there was a unique interaction pair between SOD2 and MTIF2 in the ROS pathway. Cell function experiments showed that overexpression of MTIF2 enhanced the proliferative and invasive capacities of HCC, which could synergize with SOD2 to co-promote the development of HCC. Finally, molecular dynamics simulations showed that DB00183 maintained a high structural stability with MTIF2 and SOD2 proteins during the simulation process.
UNASSIGNED: Our study confirmed that the high-expressed MTIF2 in HCC tissues was derived from epithelial cells and hepatocytes. MTIF2 might act on SOD2 to regulate the ROS pathway, thereby affective the progression of HCC.
UNASSIGNED: The treatment of HCC treatment and its prognostic prediction are limited by a lack of comprehensive understanding of the molecular mechanisms in HCC. OBJECTIVE: To determine the cells expressing MTIF2 in HCC and the function of the MTIF2+ cell subpopulation.
UNASSIGNED: Gene expression analysis on TIMER 2.0, UALCAN, and GEPIA databases was performed to measure the expression of MTIF2 in HCC tissues. Cell clustering subgroups and annotation were conducted based on the single-cell sequencing data of HCC and paracancerous tissues in the Gene Expression Omnibus (GEO) database. MTIF2 expression in different cell types was analyzed. Further, biological pathways potentially regulated by MTIF2 in each cell type were identified. In addition, protein-protein interaction (PPI) networks of MTIF2 with genes in its regulated biological pathways were developed. The cell function assay was performed to verify the effects of superoxide dismutase-2 (SOD2) and MTIF2 on HCC cells. Finally, we screened virtual drugs targeting MTIF2 and SOD2 employing database screening, molecular docking and molecular dynamics.
UNASSIGNED: MTIF2 showed a remarkably high expression in HCC tissues. We identified a total of 10 cell types between HCC tissues and paracancerous tissues. MTIF2 expression was upregulated in epithelial cells, macrophages, and hepatocytes. More importantly, high-expressed MTIF2 in HCC tissues was mainly derived from epithelial cells and hepatocytes, in which the reactive oxygen species (ROS) pathway was significantly positively correlated with MTIF2. In the PPI network, there was a unique interaction pair between SOD2 and MTIF2 in the ROS pathway. Cell function experiments showed that overexpression of MTIF2 enhanced the proliferative and invasive capacities of HCC, which could synergize with SOD2 to co-promote the development of HCC. Finally, molecular dynamics simulations showed that DB00183 maintained a high structural stability with MTIF2 and SOD2 proteins during the simulation process.
UNASSIGNED: Our study confirmed that the high-expressed MTIF2 in HCC tissues was derived from epithelial cells and hepatocytes. MTIF2 might act on SOD2 to regulate the ROS pathway, thereby affective the progression of HCC.
摘要：
■分析线粒体翻译起始因子2（MTIF2）在肝细胞癌（HCC）中的表达和该基因的生物学功能。
■由于缺乏对HCC分子机制的全面了解，HCC的治疗及其预后预测受到限制。目的：确定肝癌中表达MTIF2的细胞和MTIF2细胞亚群的功能。
■TIMER2.0、UALCAN、和GEPIA数据库用于测量MTIF2在HCC组织中的表达。基于基因表达综合（GEO）数据库中HCC和癌旁组织的单细胞测序数据进行细胞聚类亚组和注释。分析不同细胞类型中的MTIF2表达。Further,确定了每种细胞类型中可能受MTIF2调节的生物学途径。此外,建立了MTIF2与其调节生物学途径中的基因的蛋白质-蛋白质相互作用（PPI）网络。进行细胞功能测定以验证超氧化物歧化酶2（SOD2）和MTIF2对HCC细胞的影响。最后,我们通过数据库筛选筛选了针对MTIF2和SOD2的虚拟药物，分子对接和分子动力学。
■MTIF2在HCC组织中显示出极高的表达。我们在HCC组织和癌旁组织之间总共鉴定了10种细胞类型。MTIF2在上皮细胞中表达上调,巨噬细胞，和肝细胞。更重要的是,MTIF2在肝癌组织中的高表达主要来源于上皮细胞和肝细胞,其中活性氧（ROS）途径与MTIF2呈显著正相关。在PPI网络中，在ROS通路中，SOD2和MTIF2之间存在独特的相互作用对。细胞功能实验表明，MTIF2的过表达增强了肝癌的增殖和侵袭能力，与SOD2协同作用共同促进HCC的发展。最后,分子动力学模拟表明，DB00183在模拟过程中与MTIF2和SOD2蛋白保持了较高的结构稳定性。
■我们的研究证实，肝癌组织中的MTIF2高表达来源于上皮细胞和肝细胞。MTIF2可能作用于SOD2调节ROS通路,从而影响HCC的进展。
■由于缺乏对HCC分子机制的全面了解，HCC的治疗及其预后预测受到限制。目的：确定肝癌中表达MTIF2的细胞和MTIF2细胞亚群的功能。
■TIMER2.0、UALCAN、和GEPIA数据库用于测量MTIF2在HCC组织中的表达。基于基因表达综合（GEO）数据库中HCC和癌旁组织的单细胞测序数据进行细胞聚类亚组和注释。分析不同细胞类型中的MTIF2表达。Further,确定了每种细胞类型中可能受MTIF2调节的生物学途径。此外,建立了MTIF2与其调节生物学途径中的基因的蛋白质-蛋白质相互作用（PPI）网络。进行细胞功能测定以验证超氧化物歧化酶2（SOD2）和MTIF2对HCC细胞的影响。最后,我们通过数据库筛选筛选了针对MTIF2和SOD2的虚拟药物，分子对接和分子动力学。
■MTIF2在HCC组织中显示出极高的表达。我们在HCC组织和癌旁组织之间总共鉴定了10种细胞类型。MTIF2在上皮细胞中表达上调,巨噬细胞，和肝细胞。更重要的是,MTIF2在肝癌组织中的高表达主要来源于上皮细胞和肝细胞,其中活性氧（ROS）途径与MTIF2呈显著正相关。在PPI网络中，在ROS通路中，SOD2和MTIF2之间存在独特的相互作用对。细胞功能实验表明，MTIF2的过表达增强了肝癌的增殖和侵袭能力，与SOD2协同作用共同促进HCC的发展。最后,分子动力学模拟表明，DB00183在模拟过程中与MTIF2和SOD2蛋白保持了较高的结构稳定性。
■我们的研究证实，肝癌组织中的MTIF2高表达来源于上皮细胞和肝细胞。MTIF2可能作用于SOD2调节ROS通路,从而影响HCC的进展。
