ArticleSaudi journal of biological sciences2018
DUSP1 is involved in the progression of small cell carcinoma of the prostate.
Article in Saudi journal of biological sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- SPAG6 Promotes Multiple Myeloma Through Activation of the MAPK/ERK Signaling Pathway.Frontiers in pharmacology · 2025Article
- piRNA PROPER Suppresses DUSP1 Translation by Targeting NAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Upregulation of hsa-miR-141-3p promotes uterine cervical carcinoma progression via targeting dual-specificity protein phosphatase 1.Functional & integrative genomics · 2024Article
- Engrailed-1 Promotes Pancreatic Cancer Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- A mechanism study of DUSP1 in inhibiting malignant progression of endometrial carcinoma by regulating ERK/AP-1 axis and dephosphorylation of EPHA2.Journal of Cancer · 2023Article
- Transcriptomic Network Regulation of Rat Tooth Germ from Bell Differentiation Stage to Secretory Stage: MAPK Signaling Pathway Is Crucial to Extracellular Matrix Remodeling.BioMed research international · 2023Article
- Small-cell carcinoma of the prostate with negative CD56, NSE, Syn, and CgA indicators: A case report.World journal of clinical cases · 2022Article
- MiR-34a-3p suppresses pulmonary vascular proliferation in acute pulmonary embolism rat by targeting DUSP1.Bioscience reports · 2022Article
- Downregulated Dual-Specificity Protein Phosphatase 1 in Ovarian Carcinoma: A Comprehensive Study With Multiple Methods.Pathology oncology research : POR · 2022Article
- Hypaphorine exerts anti-inflammatory effects in sepsis induced acute lung injury via modulating DUSP1/p38/JNK pathway.The Kaohsiung journal of medical sciences · 2021Article
- CD105 expression is associated with invasive capacity in ovarian cancer and promotes invasiveness by inhibiting NDRG1 and regulating the epithelial-mesenchymal transition.American journal of translational research · 2021Article
- Exosome-transmitted microRNA-133b inhibited bladder cancer proliferation by upregulating dual-specificity protein phosphatase 1.Cancer medicine · 2020Article
- Expression of Dual-Specificity Phosphatase 2 (DUSP2) in Patients with Serous Ovarian Carcinoma and in SKOV3 and OVCAR3 Cells In Vitro.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Identification and interaction analysis of key miRNAs in medullary thyroid carcinoma by bioinformatics analysis.Molecular medicine reports · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Small cell carcinoma of the prostate (SCCP) is a rare and the most aggressive variant of prostate cancer. There is no effective cure or treatment for SCCP. Therefore, there is an urgent need for new therapy to improve the prognosis of patients with SCCP. DUSP1 is a dual specific phosphatase with an increasingly recognized in tumor biology. Altered expression of DUSP1 induced changes in the expression of genes involved in various biological pathways, including cell-cell signaling and angiogenesis. To understand more about the role of DUSP1 in SCCP, we evaluated the biological function and associated regulatory mechanism of DUSP1. In this study, DUSP1 was significantly down-regulated in human SCCP compared with the non-carcinoma tissues (P < 0.05). Overexpression of DUSP1 was found to suppress MAPK signaling and cell proliferation in PC-3 cells. Additionally, silencing of DUSP1 enhanced MAPK signaling and PC-3 cell proliferation. Moreover, it was observed that DUSP1 blocked the phosphorylation of p38 MAPK induced by anisomycin. Taken together, this investigation suggests that DUSP1 is involved in the progression of SCCP and may provide a new therapeutic target for SCCP treatment.
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