■线粒体肌酸激酶(MtCK)在细胞能量代谢中起关键作用,在各种肿瘤中表现出增强的表达,包括结直肠癌(CRC)。肌酸激酶线粒体2(CKMT2)是MtCK的一种亚型;然而,其临床意义,生物学功能,CRC的潜在分子机制仍然难以捉摸。
■我们采用免疫组织化学染色来辨别CKMT2在CRC和邻近患者的非肿瘤组织中的表达。评估CKMT2水平与临床病理因素之间的相关性。此外,我们使用Kaplan-Meier生存曲线和Cox回归分析评估了CKMT2与CRC患者预后之间的相关性.同时,采用定量逆转录聚合酶链反应(qRT-PCR)检测不同CRC细胞系中CKMT2的表达水平。最后,我们通过各种技术探索CKMT2在CRC细胞中的生物学功能和潜在的分子机制,包括qRT-PCR,细胞培养,细胞转染,westernblot,Transwell腔室分析,流式细胞术,和免疫共沉淀。
■我们发现,与邻近的非肿瘤组织相比,CKMT2在CRC组织中显著过表达。CKMT2的表达与病理类型有关,肿瘤大小,远处转移,和CRC患者的生存率。重要的是,通过Cox回归分析,CKMT2成为独立的预后因素。CRC细胞系中CKMT2表达的实验性下调抑制了这些细胞的迁移并促进了细胞凋亡。此外,我们发现CKMT2通过与乳酸脱氢酶B(LDHB)相互作用促进CRC细胞有氧糖酵解的新作用.
■在这项研究中,我们发现CKMT2在CRC中的表达升高,它是CRC患者的可靠预后指标。CKMT2通过与LDHB相互作用放大Warburg效应来调节葡萄糖代谢,促进了CRC的发展。这些见解揭示了CKMT2影响CRC的新调控机制,并为未来的CRC治疗干预提供了有希望的目标。
UNASSIGNED: Mitochondrial creatine kinase (MtCK) plays a pivotal role in cellular energy metabolism, exhibiting enhanced expression in various tumors, including colorectal cancer (CRC). Creatine kinase mitochondrial 2 (CKMT2) is a subtype of MtCK; however, its clinical significance, biological functions, and underlying molecular mechanisms in CRC remain elusive.
UNASSIGNED: We employed immunohistochemical staining to discern the expression of CKMT2 in CRC and adjacent nontumor tissues of patients. The correlation between CKMT2 levels and clinical pathological factors was assessed. Additionally, we evaluated the association between CKMT2 and the prognosis of CRC patients using Kaplan-Meier survival curves and Cox regression analysis. Meanwhile, quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expression levels of CKMT2 in different CRC cell lines. Finally, we explored the biological functions and potential molecular mechanisms of CKMT2 in CRC cells through various techniques, including qRT-PCR, cell culture, cell transfection, western blot, Transwell chamber assays, flow cytometry, and co-immunoprecipitation.
UNASSIGNED: We found that CKMT2 was significantly overexpressed in CRC tissues compared with adjacent nontumor tissues. The expression of CKMT2 is correlated with pathological types, tumor size, distant metastasis, and survival in CRC patients. Importantly, CKMT2 emerged as an independent prognostic factor through Cox regression analysis. Experimental downregulation of CKMT2 expression in CRC cell lines inhibited the migration and promoted apoptosis of these cells. Furthermore, we identified a novel role for CKMT2 in promoting aerobic glycolysis in CRC cells through interaction with lactate dehydrogenase B (LDHB).
UNASSIGNED: In this study, we found the elevated expression of CKMT2 in CRC, and it was a robust prognostic indicator in CRC patients. CKMT2 regulates glucose metabolism via amplifying the Warburg effect through interaction with LDHB, which promotes the growth and progression of CRC. These insights unveil a novel regulatory mechanism by which CKMT2 influences CRC and provide promising targets for future CRC therapeutic interventions.