ArticleOncology reports2016
Suppression of STAT5b in pancreatic cancer cells leads to attenuated gemcitabine chemoresistance, adhesion and invasion.
Article in Oncology reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- STAT5: Understanding the Biology of KRASJournal of cellular and molecular medicine · 2024Article
- Pancreatic cancer-derived exosomal miR-510 promotes macrophage M2 polarization and facilitates cancer cell aggressive phenotypes.Human cell · 2024Article
- B3GNT5 is a novel marker correlated with malignant phenotype and poor outcome in pancreatic cancer.iScience · 2024Article
- Article
- Growth Hormone Receptor Antagonist Markedly Improves Gemcitabine Response in a Mouse Xenograft Model of Human Pancreatic Cancer.International journal of molecular sciences · 2024Article
- Integrative proteomics and n-glycoproteomics reveal the synergistic anti-tumor effects of aspirin- and gemcitabine-based chemotherapy on pancreatic cancer cells.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- STAT5B Suppresses Ferroptosis by Promoting DCAF13 Transcription to Regulate p53/xCT Pathway to Promote Mantle Cell Lymphoma Progression.Biologics : targets & therapy · 2024Article
- γ-Synuclein promotes proliferation and inhibits apoptosis of oral squamous cell carcinoma via JAK2/STAT5b signaling pathway.American journal of cancer research · 2024Article
- Interplay between signal transducers and activators of transcription (STAT) proteins and cancer: involvement, therapeutic and prognostic perspective.Clinical and experimental medicine · 2023Review
- The predictive value of prognosis and therapeutic response for STAT family in pancreatic cancer.Heliyon · 2023Article
- Immune cells and immune cell-targeted therapy in chronic pancreatitis.Frontiers in oncology · 2023Review
- DOT1L promotes cell proliferation and invasion by epigenetically regulating STAT5B in renal cell carcinoma.American journal of cancer research · 2023Article
- Porphyromonas gingivalis Activation of Tumor-Associated Macrophages via DOK3 Promotes Recurrence of Oral Squamous Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2022Article
- Identification of a novel IL-5 signaling pathway in chronic pancreatitis and crosstalk with pancreatic tumor cells.Cell communication and signaling : CCS · 2020Article
- Prognostic value of key genes of the JAK-STAT signaling pathway in patients with cutaneous melanoma.Oncology letters · 2020Article
- SRPX2 boosts pancreatic cancer chemoresistance by activating PI3K/AKT axis.Open medicine (Warsaw, Poland) · 2020Article
- The Signal Transducer and Activator of Transcription 5B (STAT5B) Gene Promotes Proliferation and Drug Resistance of Human Mantle Cell Lymphoma Cells by Activating the Akt Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- 17Journal of the Endocrine Society · 2018Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal solid malignancies, and there is an urgent need for new therapeutic strategies based on the molecular biology of PDAC. Signal transducers and activators of transcription 5 (STAT5) are known to be activated in a variety of malignancies and involved in tumor proliferation, apoptosis, and invasion, whereas the expression and biological role of STAT5b in PDAC are less clearly defined. In the present study, we examined the expression and role of STAT5b in human pancreatic cancer cell lines. Expressions of STAT5b mRNA and protein were detected in eight kinds of pancreatic cancer cells. Confocal microscopy and western blot analysis indicated that STAT5b is localized in both cytoplasm and nuclei. Immunoprecipitation analysis revealed tyrosine phosphorylation of STAT5b in pancreatic cancer cells. These results indicate that STAT5b in pancreatic cancer cells is constitutively activated. STAT5b shRNA clones in PANC-1 cells, which express relatively high levels of STAT5b, exhibited reduced chemoresistance against gemcitabine, adhesion and invasion compared to sham. On the other hand, AsPC-1 and BxPC3 cells, which express relatively low levels of STAT5b, exhibited reduced chemoresistance compared to PANC-1 cells. Moreover, STAT5b overexpression clones in AsPC-1 cells exhibited increased chemoresistance compared to sham. STAT5b shRNA clones in PANC-1 cells were more sensitive to the proapoptotic actions of gemcitabine, as evidenced by PARP and cleaved caspase-3 activation. Gemcitabine also significantly reduced Bcl-xL levels in the STAT5b shRNA-expressing cells. We also investigated the clinicopathological characteristics of STAT5b expression of PDAC. Although a significant correlation between STAT5b expression and overall survival rates was not observed, a significant correlation with main pancreatic duct invasion was observed. These findings suggest that STAT5b confers gemcitabine chemoresistance and promotes cell adherence and invasiveness in pancreatic cancer cells. Targeting STAT5b may lead to novel therapeutic strategies for PDAC.
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