ArticleJournal of experimental & clinical cancer research : CR2022
INPP5F translocates into cytoplasm and interacts with ASPH to promote tumor growth in hepatocellular carcinoma.
Article in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Targeting the Notch signaling pathway in digestive system cancers: from bench to bedside.Cancer cell international · 2026Review
- Hypoxia-induced upregulation of lncRNA SLC9A3-AS1 promotes lung adenocarcinoma progression through the miR-506-5p/ASPH/NOTCH1 pathway.Scientific reports · 2026Article
- Comprehensive transcriptomics and proteome analysis to identify prognostic risk factors for MYCN non-amplified high-risk neuroblastoma.Human genomics · 2026Article
- EIF1AX Nucleolar Condensates Enhance Susceptibilities for the Management of Endometrial Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Putative Imprinting Control Regions with Aberrant Blood-Based DNA Methylation are Associated with Hepatocellular Carcinoma Risk.Journal of hepatocellular carcinoma · 2026Article
- HRASLS2 promotes the growth and glycolysis of pancreatic cancer by enhancing the stability of ASPH.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- ASPH interacts with RUVBL2 to promote tumor metastasis in lung adenocarcinoma via MAPK and Notch signaling pathways.Frontiers of medicine · 2025Article
- Exploration of prognosis and immune infiltration characteristics in glioblastoma multiforme based on lipid metabolism related genes.Discover oncology · 2025Article
- Current research of the Notch pathway in hepatocellular carcinoma.European journal of medical research · 2025Review
- Exploring the genetic profiles linked to senescence in thyroid tumors: insights on predicting disease progression and immune responses.Frontiers in oncology · 2025Article
- SMYD4 monomethylates PRMT5 and forms a positive feedback loop to promote hepatocellular carcinoma progression.Cancer science · 2024Article
- Heterogeneous Response of Tumor Cell Lines to Inhibition of Aspartate β-hydroxylase.Journal of Cancer · 2024Article
- Exploration of prognosis and immunometabolism landscapes in ER+ breast cancer based on a novel lipid metabolism-related signature.Frontiers in immunology · 2023Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIncreasing evidence has suggested inositol polyphosphate 5-phosphatase family contributes to tumorigenesis and tumor progression. However, the role of INPP5F in hepatocellular carcinoma (HCC) and its underlying mechanisms is unclear.
methodsThe expression of INPP5F in HCC was analyzed in public databases and our clinical specimens. The biological functions of INPP5F were investigated in vitro and vivo. The molecular mechanism of INPP5F in regulating tumor growth were studied by transcriptome-sequencing analysis, mass spectrometry analysis, immunoprecipitation assay and immunofluorescence assay.
resultsHigh expression of INPP5F was found in HCC tissues and was associated with poor prognosis in HCC patients. Overexpression of INPP5F promoted HCC cell proliferation, and vice versa. Knockdown of INPP5F suppressed tumor growth in vivo. Results from transcriptome-sequencing analysis showed INPP5F not only regulated a series of cell cycle related genes expression (c-MYC and cyclin E1), but also promoted many aerobic glycolysis related genes expression. Further studies confirmed that INPP5F could enhance lactate production and glucose consumption in HCC cell. Mechanistically, INPP5F activated Notch signaling pathway and upregulated c-MYC and cyclin E1 in HCC via interacting with ASPH. Interestingly, INPP5F was commonly nuclear-located in cells of adjacent non-tumor tissues, while in HCC, cytoplasm-located was more common. LMB (nuclear export inhibitor) treatment restricted INPP5F in nucleus and was associated with inhibition of Notch signaling and cell proliferation. Sequence of nuclear localization signals (NLSs) and nuclear export signals (NESs) in INPP5F aminoacidic sequence were then identified. Alteration of the NLSs or NESs influenced the localization of INPP5F and the expression of its downstream molecules. Furthermore, we found INPP5F interacted with both exportin and importin through NESs and NLSs, respectively, but the interaction with exportin was stronger, leading to cytoplasmic localization of INPP5F in HCC.
conclusionThese findings indicate that INPP5F functions as an oncogene in HCC via a translocation mechanism and activating ASPH-mediated Notch signaling pathway. INPP5F may serve as a potential therapeutic target for HCC patients.
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