目的：探讨过氧化物酶体膜蛋白4（PXMP4）对肝细胞癌（HCC）细胞迁移和侵袭及上皮间质转化（EMT）进程的影响。 方法:采用生物信息学和免疫组织化学方法分析 HCC 组织中 PXMP4 的表达，分析其与患者临床病理特征的相关性。在 HCCLM3和MHCC97H细胞中干扰PXMP4，在Huh7和MHCC97L细胞中过表达PXMP4，利用WB和qPCR法验证干扰/过表达 效率。利用CCK-8、划痕愈合实验和Transwell侵袭实验检测干扰/过表达PXMP4对HCC细胞增殖、迁移和侵袭能力的影响，采用 WB法检测干扰/过表达PXMP4或0、5、10和20 μmol/L U0126处理对HCC细胞中N-cadherin、E-cadherin、vimentin、细胞外信号调 节激酶（ERK）、p-ERK表达的影响。结果：生物信息学和免疫组织化学分析显示，HCC组织中PXMP4呈高表达（P<0.05）。临床 病理分析发现，PXMP4的表达与肿瘤分化程度有关联（P<0.05）。在HCC细胞中，干扰PXMP4后抑制细胞增殖、侵袭和EMT进 程（P<0.05）；反之，过表达PXMP4后促进HCC细胞增殖、侵袭及EMT进程（P<0.05）。此外，PXMP4通过激活ERK1/2信号通路 促进HCC细胞EMT进程，U0126处理同样能够抑制HCC细胞EMT进程。结论：PXMP4在HCC组织中呈高表达且与HCC细胞 分化有关联，PXMP4通过激活ERK1/2信号通路促进HCC细胞EMT进程。

Objective: To investigate the impact of peroxisomal membrane protein 4 (PXMP4) on the migration, invasion, and epithelial-mesenchymal transition (EMT) of hepatocellular carcinoma (HCC) cells. Methods: A total of 38 pairs of HCC and paracancerous tissue samples were collected from the Department of Pathology, the Third Affiliated Hospital of Xinxiang Medical College from January 2018 to December 2022. Bioinformatics and immunohistochemistry were used to analyze PXMP4 expression in HCC tissues and its correlation with clinicopathological features of HCC patients. PXMP4 was silenced in HCCLM3 and MHCC97H cells and overexpressed in Huh7 and MHCC97L cells. The silencing/overexpression efficiency was verified by WB assay and qPCR. CCK-8 assay, wound healing assay, and Transwell invasion assay were used to detect the effects of PXMP4 interference or overexpression on the proliferation, migration, and invasion abilities of HCC cells. WB assay was used to detect the protein expression of N-cadherin, E-cadherin, vimentin, extracellular signal-regulated kinase (ERK), and p-ERK in HCC cells with PXMP4 interference/ overexpression or 0, 5, 10, and 20 μmol/L U0126 treatment. Results: Bioinformatics and immunohistochemistry showed that PXMP4 was highly expressed in HCC tissues (PPPPConclusion: PXMP4 is highly expressed in HCC tissues and is closely related to HCC cell differentiation. PXMP4 promotes EMT in HCC cells by activating the ERK1/2 signaling pathway.

河南省高等学校重点科研项目（No. 23B310002）；河南省大学生创新创业训练计划（No.202310472007）