Experimental validation shows HK2 enhances proliferation and invasion in esophageal cancer, indicating a mechanism involving VDAC1 and apoptosis resistance.
Abstract Background: Esophageal cancer is becoming increasingly common worldwide, and esophageal squamous cell carcinoma is the most predominant type, for which there is no very effective treatment. Hexokinase 2 (HK2) has carcinogenic effects in a variety of tumours, and it has been found that HK2 is highly expressed in esophageal squamous cell carcinoma through bioinformatics methods and clinical sample observations, but whether HK2 promotes the development of esophageal squamous cell carcinoma and its mechanism of action is still unclear. Results: In this study, we verified that HK2 promoted the proliferation, migration and invasion of esophageal cancer by CCK8, wound healing assay, Transwell; flow cytometry detected ROS and apoptosis to explore the level of apoptosis, as well as the mitochondrial function detected by JC-1 and UCP2 protein expression. The role of HK2 was verified in an in vivo subcutaneous xenograft tumour model, and changes in tumour size and immunohistochemical indices were observed.Highly expressed HK2 inhibited the expression of type 1 voltage-dependent anion channel (VDAC1) to resist apoptosis, which in turn promoted the proliferation, migration and invasion of esophageal squamous cell carcinoma, whereas knockdown of HK2 attenuated the malignant features of ESCC. Conclusions: Overall, HK2 plays an important role as an oncogene in ESCC and accelerates cancer progression by affecting the mitochondrial apoptotic pathway, and it may serve as a potential target for ESCC therapy.
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Dai et al. (2025) studied this question.
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