ArticleBMC cancer2022
The expression characteristics and clinical significance of ACP6, a potential target of nitidine chloride, in hepatocellular carcinoma.
Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 11 citations in OpenAlex.
- Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study.Frontiers in oncology · 2026Article
- Nitidine chloride inhibits colorectal cancer by targeting BUB1: mechanistic insights from molecular dynamics simulation, spatial transcriptomics, and single-cell RNA sequencing.BMC gastroenterology · 2025Article
- Acid phosphatase type 6 promotes endometrial cancer progression via activating PI3K/AKT pathway.Molecular biology reports · 2025Article
- Exploring the potential function of high expression ofWorld journal of gastrointestinal oncology · 2025Article
- High expression of stearoyl-coenzyme A desaturase in colorectal cancer oncogenic functions and its potential as a therapeutic target.World journal of gastrointestinal surgery · 2025Article
- Nitidine chloride inhibits the progression of hepatocellular carcinoma by suppressing IGF2BP3 and modulates metabolic pathways in an mMolecular medicine (Cambridge, Mass.) · 2025Article
- Article
- Plasma protein changes reflect colorectal cancer development and associated inflammation.Frontiers in oncology · 2023Article
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15 authors at 3 institutions in 1 country.
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Abstract
backgroundAcid phosphatase type 6 (ACP6) is a mitochondrial lipid phosphate phosphatase that played a role in regulating lipid metabolism and there is still blank in the clinico-pathological significance and functional roles of ACP6 in human cancers. No investigations have been conducted on ACP6 in hepatocellular carcinoma (HCC) up to date.
methodsHerein, we appraised the clinico-pathological significance of ACP6 in HCC via organizing expression profiles from globally multi-center microarrays and RNA-seq datasets. The molecular basis of ACP6 in HCC was explored through multidimensional analysis. We also carried out in vitro and in vivo experiment on nude mice to investigate the effect of knocking down ACP6 expression on biological functions of HCC cells, and to evaluate the expression variance of ACP6 in xenograft of HCC tissues before and after the treatment of NC.
resultsACP6 displayed significant overexpression in HCC samples (standard mean difference (SMD) = 0.69, 95% confidence interval (CI) = 0.56-0.83) and up-regulated ACP6 performed well in screening HCC samples from non-cancer liver samples. ACP6 expression was also remarkably correlated with clinical progression and worse overall survival of HCC patients. There were close links between ACP6 expression and immune cells including B cells, CD8 + T cells and naive CD4 + T cells. Co-expressed genes of ACP6 mainly participated in pathways including cytokine-cytokine receptor interaction, glucocorticoid receptor pathway and NABA proteoglycans. The proliferation and migration rate of HCC cells transfected with ACP6 siRNA was significantly suppressed compared with those transfected with negative control siRNA. ACP6 expression was significantly inhibited by nitidine chloride (NC) in xenograft HCC tissues.
conclusionsACP6 expression may serve as novel clinical biomarker indicating the clinical development of HCC and ACP6 might be potential target of anti-cancer effect by NC in HCC.
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