ArticlePloS one2010
pp32 (ANP32A) expression inhibits pancreatic cancer cell growth and induces gemcitabine resistance by disrupting HuR binding to mRNAs.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
- Acidic nuclear phosphoprotein 32A (ANP32A): structure, function, and its role in disease pathogenesis.Molecular biology reports · 2026Review
- Targeting the RNA-Binding Protein HuR in Cancer.Cancer research · 2023Review
- [Silenced ANP32A inhibits the growth, invasion and migration of colorectal cancerNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- ANP32A Knockdown Attenuates the Malignant Biological Behavior of Colorectal Cancer Cells by Suppressing Epithelial-mesenchymal Transition and ERK Activation.Journal of Cancer · 2023Article
- Article
- ANP32 Family as Diagnostic, Prognostic, and Therapeutic Biomarker Related to Immune Infiltrates in Hepatocellular Carcinoma.Disease markers · 2022Article
- Gga-miR-181a modulates ANP32A expression and inhibits MDCC-MSB-1 cell.In vitro cellular & developmental biology. Animal · 2021Article
- Understanding and targeting the disease-related RNA binding protein human antigen R (HuR).Wiley interdisciplinary reviews. RNA · 2020Review
- The RNA-Binding Protein HuR in Digestive System Tumors.BioMed research international · 2020Review
- Human antigen R and drug resistance in tumors.Investigational new drugs · 2019Review
- The HuR CMLD-2 inhibitor exhibits antitumor effects via MAD2 downregulation in thyroid cancer cells.Scientific reports · 2019Article
- PHAP1 promotes glioma cell proliferation by regulating the Akt/p27/stathmin pathway.Journal of cellular and molecular medicine · 2018Article
- Paclitaxel Treatment and Proprotein Convertase 1/3 (PC1/3) Knockdown in Macrophages is a Promising Antiglioma Strategy as Revealed by Proteomics and Cytotoxicity Studies.Molecular & cellular proteomics : MCP · 2018Article
- Complex HuR function in pancreatic cancer cells.Wiley interdisciplinary reviews. RNA · 2018Review
- Downregulation of HuR Inhibits the Progression of Esophageal Cancer through Interleukin-18.Cancer research and treatment · 2018Article
- Pancreatic Cancer Chemoresistance to Gemcitabine.Cancers · 2017Review
- HuR-targeted small molecule inhibitor exhibits cytotoxicity towards human lung cancer cells.Scientific reports · 2017Article
- Article
- Human antigen R as a predictive marker for response to gemcitabine-based chemotherapy in advanced cisplatin-resistant urothelial cancer.Oncology letters · 2017Article
- HuR Contributes to TRAIL Resistance by Restricting Death Receptor 4 Expression in Pancreatic Cancer Cells.Molecular cancer research : MCR · 2016Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
The expression of protein phosphatase 32 (PP32, ANP32A) is low in poorly differentiated pancreatic cancers and is linked to the levels of HuR (ELAV1), a predictive marker for gemcitabine response. In pancreatic cancer cells, exogenous overexpression of pp32 inhibited cell growth, supporting its long-recognized role as a tumor suppressor in pancreatic cancer. In chemotherapeutic sensitivity screening assays, cells overexpressing pp32 were selectively resistant to the nucleoside analogs gemcitabine and cytarabine (ARA-C), but were sensitized to 5-fluorouracil; conversely, silencing pp32 in pancreatic cancer cells enhanced gemcitabine sensitivity. The cytoplasmic levels of pp32 increased after cancer cells are treated with certain stressors, including gemcitabine. pp32 overexpression reduced the association of HuR with the mRNA encoding the gemcitabine-metabolizing enzyme deoxycytidine kinase (dCK), causing a significant reduction in dCK protein levels. Similarly, ectopic pp32 expression caused a reduction in HuR binding of mRNAs encoding tumor-promoting proteins (e.g., VEGF and HuR), while silencing pp32 dramatically enhanced the binding of these mRNA targets. Low pp32 nuclear expression correlated with high-grade tumors and the presence of lymph node metastasis, as compared to patients' tumors with high nuclear pp32 expression. Although pp32 expression levels did not enhance the predictive power of cytoplasmic HuR status, nuclear pp32 levels and cytoplasmic HuR levels associated significantly in patient samples. Thus, we provide novel evidence that the tumor suppressor function of pp32 can be attributed to its ability to disrupt HuR binding to target mRNAs encoding key proteins for cancer cell survival and drug efficacy.
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