Explore the vast range of titles available.

[This retracts the article DOI: 10.1155/2021/1736819.].

The journal retracts the publication \"Wogonin Suppresses the Activity of Matrix Metalloproteinase-9 and Inhibits Migration and Invasion in Human Hepatocellular Carcinoma\" [...].The journal retracts the publication \"Wogonin Suppresses the Activity of Matrix Metalloproteinase-9 and Inhibits Migration and Invasion in Human Hepatocellular Carcinoma\" [...].

The Journal retracts the article \"Chlorogenic Acid Improves the Regorafenib Effects in Human Hepatocellular Carcinoma Cells\" [...].The Journal retracts the article \"Chlorogenic Acid Improves the Regorafenib Effects in Human Hepatocellular Carcinoma Cells\" [...].

Background The pathogenesis of hepatocellular carcinoma (HCC) emphasizes metabolic disorders. HCC patients showed abnormally low expression of Acyl-CoA dehydrogenase short chain (ACADS). Objectives This study aimed to elucidate the clinical significance and mechanistic role of ACADS in HCC. Methods We investigated the expression patterns and significance of ACADS in HCC by analyzing multiple public databases and clinical samples (Chip data). Immunohistochemistry was employed to observe the expression levels of ACADS in HCC tissues. In vitro experiments involved silencing or overexpressing ACADS in HCC cell lines, with protein expression levels determined by Western blotting. Functional validation included CCK-8, Transwell, and scratch wound healing assays. TOPFlash and FOPFlash reporter gene assays, co-immunoprecipitation, and immunofluorescence were used to explore the interaction between ACADS and -catenin. Results ACADS was low expressed in HCC and was clinically associated with vascular invasion, TNM stage, and AFP levels. The low ACADS expression in HCC patients was negatively correlated with their survival. Overexpression of ACADS significantly suppressed the viability, migration, and invasive capacity of HCC cells, whereas silencing ACADS had the opposite effect. Mechanistically, co-immunoprecipitation experiments indicated that there was an interaction between ACADS and -catenin. Overexpression of ACADS inhibited -catenin activity and resulted in decreased nuclear -catenin translocation and increased its cytoplasmic level. Immunofluorescence results also showed a decrease in -catenin nuclear import following ACADS overexpression, whereas silencing ACADS led to an enhancement of its nuclear translocation. Conclusion ACADS emerges as a potentially valuable biomarker for HCC prognosis, exhibiting tumor-suppressive functions in HCC by participating in the regulation of -catenin activity.