ArticleCell communication and signaling : CCS2014
INPP4B suppresses prostate cancer cell invasion.
Article in Cell communication and signaling : CCS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 42 citations in OpenAlex.
- The Role of the p21-Activated Kinase Family in Tumor Immunity.International journal of molecular sciences · 2025Review
- Inositol phosphatase INPP4B sustains ILC1s and intratumoral NK cells through an AKT-driven pathway.The Journal of experimental medicine · 2024Article
- Regulation of EZH2 Expression by INPP4B in Normal Prostate and Primary Prostate Cancer.Cancers · 2023Article
- Systematic Analysis of Cellular Signaling Pathways and Therapeutic Targets for SLC45A3:ERG Fusion-Positive Prostate Cancer.Journal of personalized medicine · 2022Article
- Expression patterns and the roles of phosphatidylinositol phosphatases in testis†.Biology of reproduction · 2022Article
- INPP4B protects from metabolic syndrome and associated disorders.Communications biology · 2021Article
- Estrogen receptor β regulates AKT activity through up-regulation of INPP4B and inhibits migration of prostate cancer cell line PC-3.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- AR-dependent phosphorylation and phospho-proteome targets in prostate cancer.Endocrine-related cancer · 2020Review
- Mitochondrial PAK6 inhibits prostate cancer cell apoptosisTheranostics · 2020Article
- Investigating the duality ofOncotarget · 2019Article
- Distinct transcriptional repertoire of the androgen receptor in ETS fusion-negative prostate cancer.Prostate cancer and prostatic diseases · 2019Article
- Inositol polyphosphate 4-phosphatase type II regulation of androgen receptor activity.Oncogene · 2019Article
- Nimesulide inhibits proliferation and induces apoptosis of pancreatic cancer cells by enhancing expression of PTEN.Experimental and therapeutic medicine · 2018Article
- Inositol polyphosphate-4-phosphatase type II plays critical roles in the modulation of cadherin-mediated adhesion dynamics of pancreatic ductal adenocarcinomas.Cell adhesion & migration · 2018Article
- Article
- Regulation of PI3K effector signalling in cancer by the phosphoinositide phosphatases.Bioscience reports · 2017Review
- Nuclear Receptor Corepressor 1 Expression and Output Declines with Prostate Cancer Progression.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Phosphatidylinositolphosphate phosphatase activities and cancer.Journal of lipid research · 2016Review
- Article
- Tumor Suppressive Function of p21-activated Kinase 6 in Hepatocellular Carcinoma.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundINPP4B and PTEN dual specificity phosphatases are frequently lost during progression of prostate cancer to metastatic disease. We and others have previously shown that loss of INPP4B expression correlates with poor prognosis in multiple malignancies and with metastatic spread in prostate cancer.
resultsWe demonstrate that de novo expression of INPP4B in highly invasive human prostate carcinoma PC-3 cells suppresses their invasion both in vitro and in vivo. Using global gene expression analysis, we found that INPP4B regulates a number of genes associated with cell adhesion, the extracellular matrix, and the cytoskeleton. Importantly, de novo expressed INPP4B suppressed the proinflammatory chemokine IL-8 and induced PAK6. These genes were regulated in a reciprocal manner following downregulation of INPP4B in the independently derived INPP4B-positive LNCaP prostate cancer cell line. Inhibition of PI3K/Akt pathway, which is highly active in both PC-3 and LNCaP cells, did not reproduce INPP4B mediated suppression of IL-8 mRNA expression in either cell type. In contrast, inhibition of PKC signaling phenocopied INPP4B-mediated inhibitory effect on IL-8 in either prostate cancer cell line. In PC-3 cells, INPP4B overexpression caused a decline in the level of metastases associated BIRC5 protein, phosphorylation of PKC, and expression of the common PKC and IL-8 downstream target, COX-2. Reciprocally, COX-2 expression was increased in LNCaP cells following depletion of endogenous INPP4B.
conclusionTaken together, we discovered that INPP4B is a novel suppressor of oncogenic PKC signaling, further emphasizing the role of INPP4B in maintaining normal physiology of the prostate epithelium and suppressing metastatic potential of prostate tumors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.