TG-interacting factor 1 (TGIF1) exerts inhibitory effects on transforming growth factor-beta (TGF-β) signaling by suppressing Smad signaling pathway at multiple levels. TGIF1 activity is important for normal embryogenesis and organogenesis, yet its dysregulation can culminate in tumorigenesis. For instance, increased expression of TGIF1 correlates with poor prognosis in triple-negative breast cancer patients, and enforced expression of TGIF1 facilitates Wnt-driven mammary tumorigenesis, suggesting that TGIF1 might function as an oncoprotein. Quite surprisingly, TGIF1 has recently been shown to function as a tumor suppressor in pancreatic ductal adenocarcinoma (PDAC), possibly owing to its ability to antagonize the pro-malignant transcription factor Twist1. In this article, we will briefly elaborate on the biological and clinical significance of the unique tumor-suppressive function of TGIF1 and its functional interaction with Twist1 in the context of PDAC pathogenesis and progression.
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http://dx.doi.org/10.1016/j.csbj.2020.09.023 | DOI Listing |
United European Gastroenterol J
January 2025
"Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania.
The rising incidence of pancreatic diseases, including acute and chronic pancreatitis and various pancreatic neoplasms, poses a significant global health challenge. Pancreatic ductal adenocarcinoma (PDAC) for example, has a high mortality rate due to late-stage diagnosis and its inaccessible location. Advances in imaging technologies, though improving diagnostic capabilities, still necessitate biopsy confirmation.
View Article and Find Full Text PDFJ Exp Clin Cancer Res
January 2025
Department of Hepato-Biliary-Pancreatic Surgery, General Surgery, Huadong Hospital, Fudan University, Shanghai, 200040, PR China.
Purpose: Glucose starvation induces the accumulation of disulfides and F-actin collapse in cells with high expression of SLC7A11, a phenomenon termed disulfidptosis. This study aimed to confirm the existence of disulfidptosis in pancreatic ductal adenocarcinoma (PDAC) and elucidate the role of Cancer Susceptibility 8 (CASC8) in this process.
Methods: The existence of disulfidptosis in PDAC was assessed using flow cytometry and F-actin staining.
Br J Cancer
January 2025
Department of Visceral, Thoracic and Vascular Surgery, University Hospital and Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Background: Pancreatic ductal adenocarcinoma (PDAC) exhibits a high frequency of neural invasion (NI). Schwann cells (SCs) have been shown to be reprogrammed to facilitate cancer cell migration and invasion into nerves. Since extracellular vesicles (EVs) affect the tumour microenvironment and promote metastasis, the present study analysed the involvement of EVs from pancreatic cancer cells and their microenvironment in altering SC phenotype as part of the early events in the process of NI.
View Article and Find Full Text PDFSemin Cancer Biol
January 2025
Biomedical Research Center, Slovak Academy of Sciences, Dubravska Cesta 9, 84505 Bratislava, Slovakia. Electronic address:
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy characterized by late detection and poor prognosis. Recent research highlights the pivotal role of epigenetic alter- ations in driving PDAC development and progression. These changes, in conjunction with genetic mutations, contribute to the intricate molecular landscape of the disease.
View Article and Find Full Text PDFPharmaceutics
December 2024
Division of Functional Imaging, Exploratory Oncology Research & Clinical Trial Center, National Cancer Center, Kashiwa 277-8577, Japan.
: Alpha radionuclide therapy has emerged as a promising novel strategy for cancer treatment; however, the therapeutic potential of Ac-labeled peptides in pancreatic cancer remains uninvestigated. : In the cytotoxicity study, tumor cells were incubated with Ac-DOTA-RGD. DNA damage responses (γH2AX and 53BP1) were detected using flowcytometry or immunohistochemistry analysis.
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