Liyuan Hao,1,2,* Shenghao Li,1,2,* Qing Peng,1,2 Junli Zhang,3 Jiali Deng,1,2 Xiaoyu Hu2 

1School of Clinical Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan Province, People’s Republic of China; 2Department of Infectious Diseases, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan Province, People’s Republic of China; 3Department of Infectious Diseases, Jiangsu Province Hospital of Chinese Medicine, Nanjing, Jiangsu Province, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Xiaoyu Hu, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan Province, People’s Republic of China, Email xiaoyuhu202206@163.com

Abstract: Cholangiocarcinoma (CCA) is a highly aggressive and poorly prognostic tumor. Due to the lack of early symptoms, diagnosing CCA remains challenging, often occurring at an advanced stage. Therefore, exploring the underlying mechanisms of CCA development and identifying potential biomarkers and therapeutic targets is crucial. Recently, metabolic reprogramming in cancer cells has emerged as a hallmark of the disease. Glycolysis has been identified as a central component of metabolic reprogramming in CCA, with multiple signaling pathways and key enzymes playing significant roles. Additionally, non-coding RNAs (ncRNAs) and post-translational modifications of proteins are also involved in regulating glycolysis in CCA. In this review, we provide a comprehensive summary of the alterations in cancer metabolism and the diverse signaling pathways involved, as they might exert an impact on the development of CCA. Overall, targeting glycolysis holds considerable promise as a crucial strategy for enhancing the therapeutic outcomes of CCA. In addition, we performed a bioinformatic analysis of the relationship between CCA and glycolysis to identify and investigate potential targets. The purpose of this study is to provide a theoretical basis for the development of CCA targets.

Keywords: cholangiocarcinoma, glycolysis, HK2, PKM2, mechanisms