ArticleJournal of nanobiotechnology2024
ACYP2 functions as an innovative nano-therapeutic target to impede the progression of hepatocellular carcinoma by inhibiting the activity of TERT and the KCNN4/ERK pathway.
Article in Journal of nanobiotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- OTUD1-mediated deubiquitination stabilizes SLC7A11 to suppress ferroptosis in hepatocellular carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Integrated ICD-based subtyping and prognostic model reveal KCNN4 as a novel therapeutic target in NSCLC.Discover oncology · 2026Article
- The Participation of Acetyl Phosphate, a Microbial and Host Metabolite, in the Regulation of the Calcium Balance in Mitochondria and Cells.International journal of molecular sciences · 2026Article
- ACYP2 Induces Temozolomide Resistance in Glioblastoma by Promoting PARP1-Mediated DNA Damage Repair.Molecular cancer research : MCR · 2026Article
- Nanomaterials in the diagnosis and treatment of gastrointestinal tumors: New clinical choices and treatment strategies.Materials today. Bio · 2025Review
- NCAPG-mediated CDK1 promotes malignant progression of non-small cell lung cancer via ERK signaling activation.American journal of cancer research · 2024Article
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Authors and funding
9 authors.
Funding
Abstract
An increasing body of evidence suggests that acylphosphatase-2 (ACYP2) polymorphisms are correlated with an increased susceptibility to a range of malignancies. Nevertheless, its potential functions, molecular mechanisms in hepatocellular carcinoma (HCC) and whether it can be act as a therapeutic target remain uninvestigated. Herein, ACYP2 was found to be lowly expressed in HCC and was negatively correlated with tumor size, tumor differentiation, microvascular invasion and the prognosis of HCC patients. Functional investigations revealed that overexpression of ACYP2 inhibited the proliferation and metastasis of HCC cells while promoting apoptosis; knockdown of ACYP2 had the exact opposite effect. Additionally, it was observed that ACYP2 was distributed in both the cytoplasm and nucleus of HCC cells. According to the mechanistic studies, the expression of potassium calcium-activated channel subfamily N member 4 (KCNN4) was negatively regulated by cytoplasmic ACYP2, resulting in the inhibition of K
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