Reduction in the hepatocellular carcinoma antioncogene SLC39A14 during the malignant progression of hepatocellular carcinoma
Year: 2025
Type: article
Abstract: BACKGROUND Hepatocellular carcinoma (HCC) is characterized by high morbidity and mortality owing to its mechanistic complexity and individual heterogeneity, making early diagnosis challenging. The role of SLC39A14 , a biomarker for multiple tumors, in HCC remains to be elucidated. AIM To determine the tumor-suppressive role of SLC39A14 in HCC and its underlying molecular mechanisms. METHODS The expression pattern of SLC39A14 in HCC was evaluated using quantitative reverse transcriptase PCR and western blotting, and its association with tumor malignancy was further validated in C57BL/6J mouse HCC model. A series of functional assays, including cell counting kit-8, colony formation, apoptosis, scratch, and invasion tests, were conducted to assess how alterations in the SLC39A14 expression affect the oncological behavior of HCC cells. In addition, bioinformatics analysis was performed to investigate the potential regulatory mechanism underlying SLC39A14 expression in HCC. RESULTS The protein expression and RNA abundance of SLC39A14 in human HCC tissues were significantly lower than those in paracancerous tissues (P < 0.01). In HCC model mice, the SLC39A14 expression decreased gradually as the disease progressed. The overexpression of SLC39A14 significantly inhibited the proliferation, migration, and invasion of Huh7 HCC cells while promoting their apoptosis. The knockdown of SLC39A14 exerted the opposite effect. Bioinformatics analysis suggested the involvement of the transcription factor STAT3 in regulating the SLC39A14 expression. CONCLUSION SLC39A14 dysregulation promotes HCC progression through BCL-2/BAX/Caspase-3 apoptotic axis and epithelial–mesenchymal transition transformation axis, suggesting potential therapeutic targets.
Language: English
Subfield: Hepatology
Field: Medicine
Domain: Health Sciences
Open Access status: diamond
OpenAlex ID: W4415465251