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Abstract：
UNASSIGNED: The objective of this study is to elucidate the influence of MCU on the clinical pathological features of GC patients, to investigate the function and mechanism of the mitochondrial calcium uptake transporter MCU in the initiation and progression of GC, and to explore its impact on the metabolic pathways and biosynthesis of mitochondria. The ultimate goal is to identify novel targets and strategies for the clinical management of GC patients.
UNASSIGNED: Tumor and adjacent tissue specimens were obtained from 205 patients with gastric cancer, and immunohistochemical tests were performed to assess the expression of MCU and its correlation with clinical pathological characteristics and prognosis. Data from TCGA, GTEx and GEO databases were retrieved for gastric cancer patients, and bioinformatics analysis was utilized to investigate the association between MCU expression and clinical pathological features. Furthermore, we conducted an in-depth analysis of the role of MCU in GC patients. We investigated the correlation between MCU expression in GC and its impact on mitochondrial function, metabolism, biosynthesis, and immune cells. Additionally, we studied the proteins or molecules that interact with MCU.
UNASSIGNED: Our research revealed high expression of MCU in the GC tissues. This high expression was associated with poorer T and N staging, and indicated a worse disease-free survival period. MCU expression was positively correlated with mitochondrial function, mitochondrial metabolism, nucleotide, amino acid, and fatty acid synthesis metabolism, and negatively correlated with nicotinate and nicotinamide metabolism. Furthermore, the MCU also regulates the function of the mitochondrial oxidative respiratory chain. The MCU influences the immune cells of GC patients and regulates ROS generation, cell proliferation, apoptosis, and resistance to platinum-based drugs in gastric cancer cells.
UNASSIGNED: High expression of MCU in GC indicates poorer clinical outcomes. The expression of the MCU are affected through impacts the function of mitochondria, energy metabolism, and cellular biosynthesis in gastric cancer cells, thereby influencing the growth and metastasis of gastric cancer cells. Therefore, the mitochondrial changes regulated by MCU could be a new focus for research and treatment of GC.
UNASSIGNED: Tumor and adjacent tissue specimens were obtained from 205 patients with gastric cancer, and immunohistochemical tests were performed to assess the expression of MCU and its correlation with clinical pathological characteristics and prognosis. Data from TCGA, GTEx and GEO databases were retrieved for gastric cancer patients, and bioinformatics analysis was utilized to investigate the association between MCU expression and clinical pathological features. Furthermore, we conducted an in-depth analysis of the role of MCU in GC patients. We investigated the correlation between MCU expression in GC and its impact on mitochondrial function, metabolism, biosynthesis, and immune cells. Additionally, we studied the proteins or molecules that interact with MCU.
UNASSIGNED: Our research revealed high expression of MCU in the GC tissues. This high expression was associated with poorer T and N staging, and indicated a worse disease-free survival period. MCU expression was positively correlated with mitochondrial function, mitochondrial metabolism, nucleotide, amino acid, and fatty acid synthesis metabolism, and negatively correlated with nicotinate and nicotinamide metabolism. Furthermore, the MCU also regulates the function of the mitochondrial oxidative respiratory chain. The MCU influences the immune cells of GC patients and regulates ROS generation, cell proliferation, apoptosis, and resistance to platinum-based drugs in gastric cancer cells.
UNASSIGNED: High expression of MCU in GC indicates poorer clinical outcomes. The expression of the MCU are affected through impacts the function of mitochondria, energy metabolism, and cellular biosynthesis in gastric cancer cells, thereby influencing the growth and metastasis of gastric cancer cells. Therefore, the mitochondrial changes regulated by MCU could be a new focus for research and treatment of GC.
摘要：
■本研究的目的是阐明MCU对GC患者临床病理特征的影响，探讨线粒体钙摄取转运蛋白MCU在GC的发生和发展过程中的作用及机制,并探讨其对线粒体代谢途径和生物合成的影响。最终目标是确定GC患者临床管理的新目标和策略。
■肿瘤和邻近组织标本取自205例胃癌患者，并进行免疫组织化学检查，以评估MCU的表达及其与临床病理特征和预后的关系。数据来自TCGA，检索了胃癌患者的GTEx和GEO数据库，生物信息学分析用于研究MCU表达与临床病理特征之间的关联。此外，我们对单片机在GC患者中的作用进行了深入分析。我们研究了GC中MCU表达及其对线粒体功能的影响之间的相关性，新陈代谢，生物合成，和免疫细胞。此外,我们研究了与MCU相互作用的蛋白质或分子。
■我们的研究揭示了MCU在GC组织中的高表达。这种高表达与较差的T和N分期相关，并表明无病生存期较差。MCU表达与线粒体功能呈正相关,线粒体代谢，核苷酸，氨基酸,和脂肪酸合成代谢，与烟酸和烟酰胺代谢呈负相关。此外，MCU还调节线粒体氧化呼吸链的功能。MCU影响GC患者的免疫细胞并调节ROS的产生，细胞增殖，凋亡，以及胃癌细胞对铂类药物的耐药性。
■GC中MCU的高表达表明临床结果较差。单片机的表达通过影响线粒体的功能而受到影响,能量代谢，和胃癌细胞中的细胞生物合成，从而影响胃癌细胞的生长和转移。因此,MCU调控的线粒体变化可能成为GC研究和治疗的新热点。
■肿瘤和邻近组织标本取自205例胃癌患者，并进行免疫组织化学检查，以评估MCU的表达及其与临床病理特征和预后的关系。数据来自TCGA，检索了胃癌患者的GTEx和GEO数据库，生物信息学分析用于研究MCU表达与临床病理特征之间的关联。此外，我们对单片机在GC患者中的作用进行了深入分析。我们研究了GC中MCU表达及其对线粒体功能的影响之间的相关性，新陈代谢，生物合成，和免疫细胞。此外,我们研究了与MCU相互作用的蛋白质或分子。
■我们的研究揭示了MCU在GC组织中的高表达。这种高表达与较差的T和N分期相关，并表明无病生存期较差。MCU表达与线粒体功能呈正相关,线粒体代谢，核苷酸，氨基酸,和脂肪酸合成代谢，与烟酸和烟酰胺代谢呈负相关。此外，MCU还调节线粒体氧化呼吸链的功能。MCU影响GC患者的免疫细胞并调节ROS的产生，细胞增殖，凋亡，以及胃癌细胞对铂类药物的耐药性。
■GC中MCU的高表达表明临床结果较差。单片机的表达通过影响线粒体的功能而受到影响,能量代谢，和胃癌细胞中的细胞生物合成，从而影响胃癌细胞的生长和转移。因此,MCU调控的线粒体变化可能成为GC研究和治疗的新热点。
