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

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.

Models considering hepatocellular carcinoma (HCC) complexity cannot be accurately replicated in routine cell lines or animal models. We aimed to evaluate the practicality of tissue slice culture by combining it with a cryopreservation technique. We prepared 0.3-mm-thick tissue slices by a microtome and maintained their cell viability using a cryopreservation technique. Slices were cultured individually in the presence or absence of regorafenib (REG) for 72 h. Alterations in morphology and gene expression were assessed by histological and genetic analysis. Overall viability was also analyzed in tissue slices by CCK-8 quantification assay and fluorescent staining. Tissue morphology and cell viability were evaluated to quantify drug effects. Histological and genetic analyses showed that no significant alterations in morphology and gene expression were induced by the vitrification-based cryopreservation method. The viability of warmed HCC tissues was up to 90% of the fresh tissues. The viability and proliferation could be retained for at least four days in the filter culture system. The positive drug responses in precision-cut slice culture in vitro were evaluated by tissue morphology and cell viability. In summary, the successful application of precision-cut HCC slice culture combined with a cryopreservation technique in a systematic drug screening demonstrates the feasibility and utility of slice culture method for assessing drug response.