ArticleCancer science2019
Loss of PTPN4 activates STAT3 to promote the tumor growth in rectal cancer.
Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Altered microRNA profiles and associated pathways in canine mammary adenocarcinoma.Scientific reports · 2025Article
- Centromere protein A knockdown inhibits rectal cancer through O6-methylguanine DNA methyltransferase/protein tyrosine phosphatase nonreceptor type 4 axis.World journal of gastrointestinal oncology · 2025Article
- KPNA5 Suppresses Malignant Progression of Ovarian Cancer Through Importing the PTPN4 Into the Nucleus.Cancer medicine · 2025Article
- Exosomal miR-106a-5p derived from intermittently hypoxic non-small-cell lung cancer increases tumor malignancy.Physiological reports · 2024Article
- Fetal growth restriction and placental defects in obese mice are associated with impaired decidualisation: the role of increased leptin signalling modulators SOCS3 and PTPN2.Cellular and molecular life sciences : CMLS · 2024Article
- Plasma circulating microRNAs associated with blood-based immune markers: a population-based study.Clinical and experimental immunology · 2024Article
- Review
- Modulation of rectal cancer stemness, patient outcome and therapy response by adipokines.Journal of physiology and biochemistry · 2023Article
- Novel Potential Therapeutic Targets of PTPN Families for Lung Cancer.Journal of personalized medicine · 2022Article
- A two-stage genome-wide association study to identify novel genetic loci associated with acute radiotherapy toxicity in nasopharyngeal carcinoma.Molecular cancer · 2022Article
- MicroRNA-375 is a therapeutic target for castration-resistant prostate cancer through the PTPN4/STAT3 axis.Experimental & molecular medicine · 2022Article
- Structural and biochemical analysis of the PTPN4 PDZ domain bound to the C-terminal tail of the human papillomavirus E6 oncoprotein.Journal of microbiology (Seoul, Korea) · 2022Article
- Critical roles of PTPN family members regulated by non-coding RNAs in tumorigenesis and immunotherapy.Frontiers in oncology · 2022Review
- Article
- PTPN18 promotes colorectal cancer progression by regulating the c-MYC-CDK4 axis.Genes & diseases · 2021Article
- Identification of a 5-Gene-Based Scoring System by WGCNA and LASSO to Predict Prognosis for Rectal Cancer Patients.Analytical cellular pathology (Amsterdam) · 2021Article
- Automatic Bayesian Weighting for SAXS Data.Frontiers in molecular biosciences · 2021Article
- Inhibition of microRNA-15b-5p Attenuates the Progression of Oral Squamous Cell Carcinoma via Modulating theCancer management and research · 2020Article
- Loss of PTPN4 activates STAT3 to promote the tumor growth in rectal cancer.Cancer science · 2019Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Colorectal cancer (CRC) is one of the most common types of malignant tumor. Many genetic factors have been proved to show high association with the occurrence and development of CRC and many mutations are detected in CRC. PTPN4/PTP-MEG1 is a widely expressed non-receptor protein tyrosine phosphatase. Over the past three decades, PTPN4 has been demonstrated in the literature to participate in many biological processes. In this study, we identified a nonsense mutation of PTPN4 with a mutation ratio of 90.90% from 1 case of rectal cancer, leading to loss of function in PTPN4 gene. Several somatic mutations occurred in 5/137 rectal cancer samples from The Cancer Genome Atlas Rectum Adenocarcinoma (TCGA READ) database. Interestingly, we found that PTPN4 negative cytoplasm staining was more prone to lymphatic metastasis (N = 50, P = 0.0153) and low expression of PTPN4 in rectal cancer was highly associated with poor prognosis. Overexpression of PTPN4 suppressed the cell growth, and moreover, the loss of PTPN4 accelerated cell growth and boosted clonogenicity of CRC cells. Furthermore, we revealed that the deletion of PTPN4 promoted the tumor formation of NCM460 cells in vivo. In terms of the molecular mechanism, we demonstrated that PTPN4 dephosphorylates pSTAT3 at the Tyr705 residue with a direct interaction and suppresses the transcriptional activity of STAT3. In summary, our study revealed a novel mechanism that the tumorigenesis of colorectal cancer might be caused by the loss of PTPN4 through activating STAT3, which will broaden the therapy strategy for anti-rectal cancer in the future.
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