The MUC16 C-terminal (MUC16c) level is associated with tumor serum CA-125 levels, however, the roles remain unclear in gallbladder carcinoma (GBC). In this study, we found that MUC16c promoted glucose uptake and glycolysis for GBC cell proliferation. Mass spectrometry analysis suggested that MUC16c could combine with aldolase. The ALDOC mRNA and protein are overexpressed in GBC tumors. The IHC results also showed the consistent up-regulation of.

ALDOC and MUC16c level in GBC tumor tissues than in peritumor tissues. We determined that MUC16c combining with ALDOC promoted ALDOC protein stability and disrupted the ability of ALDOC sensing glucose deficiency, which activated AMPK pathway and increased GBC cell proliferation. ALDOC knockdown significantly inhibited the glucose uptake and glycolysis induced by MUC16c. Our study established important roles of MUC16c promoting GBC cell glycolysis and proliferation and revealed the underlying mechanism of CA-125-related heavy tumor metabolic burden in GBC.

MUC16 C末端（MUC16c）水平与肿瘤血清CA-125水平相关，但是，在胆囊癌（GBC）中的作用仍不清楚。在这项研究中，我们发现MUC16c促进葡萄糖摄取和糖酵解，促进GBC细胞增殖。质谱分析表明MUC16c可以与醛缩酶结合。ALDOC mRNA和蛋白质在GBC肿瘤中过表达。IHC结果也显示出一致的上调。

GBC肿瘤组织中的ALDOC和MUC16c水平高于癌旁组织。我们确定，MUC16c与ALDOC结合可提高ALDOC蛋白的稳定性，并破坏ALDOC感知葡萄糖缺乏的能力，从而激活AMPK通路并增加GBC细胞增殖。ALDOC组合式大大抑制了MUC16c诱导的葡萄糖摄取和糖酵解。我们的研究确立了MUC16c促进GBC细胞糖酵解和增殖的重要作用，并揭示了CAC 125相关的重度肿瘤代谢负担在GBC中的潜在机制。