miR-101-3p-mediated role of PDZK1 in hepatocellular carcinoma progression and the underlying PI3K/Akt signaling mechanism

• Published in: Cell division Vol. 19; no. 1; p. 9
• Main Authors: Gao, Huihui, Gao, Zhaofeng, Liu, Xiaobei, Sun, Xu, Hu, Zhonghui, Song, Zhengwei, Zhang, Cheng, Fei, Jianguo, Wang, Xiaoguang
• Format: Journal Article
• Language: English
• Published: England BioMed Central 26.03.2024; BMC
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Apoptosis; Cell cycle; Cell growth; Cell migration; Cell proliferation; Experiments; Hepatocellular carcinoma; Liver cancer; Lymph nodes; Metastases; Metastasis; MicroRNAs; miR-101-3p; PDZK1; Phosphorylation; PI3K/AKT; Proteins; Signal transduction; Therapeutic targets; Tumors; Viral infections; Cell proliferation; Hepatocellular carcinoma; PDZK1; miR-101-3p; PI3K/AKT
• ISSN: 1747-1028; 1747-1028
• DOI: 10.1186/s13008-023-00106-6

The molecular targets and associated mechanisms of hepatocellular carcinoma (HCC) have been widely studied, but the roles of PDZK1 in HCC are unclear. Therefore, the aim of this study is to explore the role and associated mechanisms of PDZK1 in HCC. It was found that the expression of PDZK1 in HCC tissues was higher than that in paired paracancerous tissues. High expression of PDZK1 was associated with lymph node metastasis, degree of differentiation, and clinical stage. Upregulation of PDZK1 in HCC cells affected their proliferation, migration, invasion, apoptosis, and cell cycle, and also induced PI3K/AKT activation. PDZK1 is a downstream target gene of miR-101-3p. Accordingly, increase in the expression of miR-101-3p reversed the promotive effect of PDZK1 in HCC. Moreover, PDZK1 was found to accelerate cell proliferation and promote the malignant progression of HCC via the PI3K/AKT pathway. Our study indicated that the miR-101-3p/PDZK1 axis plays a role in HCC progression and could be beneficial as a novel biomarker and new therapeutic target for HCC treatment.