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.

中文翻译：

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miR-101-3p介导的PDZK1在肝细胞癌进展中的作用及其潜在的PI3K/Akt信号传导机制

肝细胞癌（HCC）的分子靶点和相关机制已被广泛研究，但PDZK1在HCC中的作用尚不清楚。因此，本研究的目的是探讨PDZK1在HCC中的作用及相关机制。结果发现，PDZK1在HCC组织中的表达高于配对的癌旁组织。 PDZK1的高表达与淋巴结转移、分化程度和临床分期相关。 HCC 细胞中 PDZK1 的上调影响其增殖、迁移、侵袭、凋亡和细胞周期，并诱导 PI3K/AKT 激活。 PDZK1 是 miR-101-3p 的下游靶基因。因此，miR-101-3p表达的增加逆转了PDZK1在HCC中的促进作用。此外，PDZK1被发现可以通过PI3K/AKT途径加速细胞增殖并促进HCC的恶性进展。我们的研究表明，miR-101-3p/PDZK1 轴在 HCC 进展中发挥作用，可能有利于作为 HCC 治疗的新型生物标志物和新治疗靶点。