ArticleJournal of experimental & clinical cancer research : CR2018
Transgelin-2 is a novel target of KRAS-ERK signaling involved in the development of pancreatic cancer.
Article in Journal of experimental & clinical cancer research : CR, 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, 17 citations in OpenAlex.
- B3GNT6 suppresses colorectal cancer progression by inhibiting the KRAS/ERK signaling pathway.BMC biotechnology · 2026Article
- Mass Spectrometry-Driven Proteomic Biomarkers for Serum-Based Detection of Pancreatic Ductal Adenocarcinoma and Intraductal Papillary Mucinous Neoplasm-Associated Invasive Carcinoma.Cancer medicine · 2026Article
- Endometrial mesonephric-like adenocarcinoma: Clinicopathologic features, treatment, and outcomes.Biomolecules & biomedicine · 2025Article
- Mapping the Proteomic Landscape of Pancreatic Cancer: Prognostic Insights and Subtype Stratification.Cancer research communications · 2025Article
- Single-cell RNA sequencing reveals the lineage of malignant epithelial cells and upregulation of TAGLN2 promotes peritoneal metastasis in gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- Gene-Expression Profiling of Mucinous Ovarian Tumors and Comparison with Upper and Lower Gastrointestinal Tumors Identifies Markers Associated with Adverse Outcomes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Chrysin-Induced G Protein-Coupled Estrogen Receptor Activation Suppresses Pancreatic Cancer.International journal of molecular sciences · 2022Article
- The Effects of a Transgelin-2 Agonist Administered at Different Times in a Mouse Model of Airway Hyperresponsiveness.Frontiers in pharmacology · 2022Article
- TAGLN2 promotes the proliferation, invasion, migration and epithelial-mesenchymal transition of colorectal cancer cells by activating STAT3 signaling through ANXA2.Oncology letters · 2021Article
- Transgelin-2: A Double-Edged Sword in Immunity and Cancer Metastasis.Frontiers in cell and developmental biology · 2021Review
- KIF23 enhances cell proliferation in pancreatic ductal adenocarcinoma and is a potent therapeutic target.Annals of translational medicine · 2020Article
- KRAS wild-type pancreatic ductal adenocarcinoma: molecular pathology and therapeutic opportunities.Journal of experimental & clinical cancer research : CR · 2020Review
- Transgelins: Cytoskeletal Associated Proteins Implicated in the Metastasis of Colorectal Cancer.Frontiers in cell and developmental biology · 2020Review
- Actin and Actin-Associated Proteins in Extracellular Vesicles Shed by Osteoclasts.International journal of molecular sciences · 2019Review
- Transgelin-2: Biochemical and Clinical Implications in Cancer and Asthma.Trends in biochemical sciences · 2019Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe KRAS mutation is the driving force of pancreatic ductal adenocarcinoma (PDAC). Downstream effectors of KRAS signal pathways are crucial to the development of PDAC. The purpose of this study was to investigate the relationship between KRAS mutation and transgelin-2. Transgelin-2 is highly expressed in PDAC tissues compared with adjacent normal tissues. The underlying mechanism for upregulating transgelin-2 is largely unknown.
methodsExpression of transgelin-2 was analyzed by microarray data and qRT-PCR. The effect of KRAS signaling on transgelin-2 expression was examined in PDAC cells in the presence or absence of the ERK inhibitor. The interaction of transgelin-2 with ERK was confirmed by immunoprecipitation. ERK-mediated Phosphorylation of transglein-2 was detected by in vivo and in vitro kinase assays. The gain-of-function and loss-of-function approaches were used to examine the role of phosphorylation of transgelin-2 on cell proliferation. Phosphorylation of transgelin-2 was detected by immunohistochemistry in PDAC tissues.
resultsHere we found transgelin-2 expression was induced by KRAS mutation. In the case of KRAS mutation, ERK2 interacted with 29-31 amino acids of transgelin-2 and subsequently phosphorylated the S145 residue of transgelin-2. S145 phosphorylation of transgelin-2 played important roles in cell proliferation and tumorigenesis of PDAC. In addition, S145 phosphorylation of transgelin-2 was associated with a poor prognosis in patients with PDAC.
conclusionsThis study indicated that KRAS-ERK-mediated transeglin-2 phosphorylation played an important role in the development of PDAC. Inhibition of transgelin-2 phosphorylation may be a potential therapeutic strategy for targeting PDAC with KRAS mutation.
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