Authors: Noel A. Jacquet, Yunfeng Zhao
Published: 2025-04-21
DOI: 10.1158/1538-7445.am2025-4179
Source: Full article
The incidence of hepatocellular carcinoma (HCC) has steadily increased over the past few decades, with minimal progress in developing effective therapeutic agents. As the most common form of primary liver cancer, HCC is currently the third leading cause of cancer-related deaths. HCC originates from hepatocytes, the primary liver cell type responsible for vital metabolic functions, including the processing of amino acids, lipids, carbohydrates, and xenobiotics. Dysregulation of cellular metabolism can drive malignancies and lead to tumorigenesis. AarF Domain Containing Kinase 1 (ADCK1), a putative kinase, is implicated in regulating mitochondrial functions, which are essential for cellular metabolism. Defects in mitochondrial function are known to contribute to tumorigenesis. Although ADCK1 remains poorly studied in humans, early research suggests its involvement in the tumorigenesis of parathyroid, colon, and osteosarcoma cancers. Our lab aims to elucidate the role of ADCK1 in cellular metabolism and the behavior of HCC cells. Bioinformatics analysis conducted by our group revealed that high ADCK1 expression correlates with worse overall survival rates in HCC patients compared to those with low ADCK1 expression. To investigate the impact of ADCK1 loss, we generated ADCK1 knockout (KO) clones in HCC cells. Our findings indicate that the loss of ADCK1 modulates several malignant characteristics associated with HCC tumorigenesis, including alterations in cellular proliferation, cell cycle regulation, programmed cell death, colony formation, and mitochondrial respiration. Future studies will explore the mechanisms underlying these processes, to establish ADCK1 as a promising therapeutic target for HCC treatment. This abstract has been proofread and enhanced for clarity through the assistance of Grammarly and ChatGPT AI.