ArticleCancer letters2016
Expression of transforming growth factor β1 promotes cholangiocarcinoma development and progression.
Article in Cancer letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Cross-Talk Between Tumor Cells and Stellate Cells Promotes Oncolytic VSV Activity in Intrahepatic Cholangiocarcinoma.Cancers · 2025Article
- Targeting the tumor microenvironment in cholangiocarcinoma to improve immune checkpoint blockade: potential strategies and translational pre-clinical models.Clinical & translational immunology · 2025Review
- The Tumor Immune Microenvironment plays a Key Role in Driving the Progression of Cholangiocarcinoma.Current cancer drug targets · 2024Review
- Assessment of the TGFB1 gene expression and methylation status of the promoter region in patients with colorectal cancer.Scientific reports · 2022Article
- Targeting Aspartate Beta-Hydroxylase with the Small Molecule Inhibitor MO-I-1182 Suppresses Cholangiocarcinoma Metastasis.Digestive diseases and sciences · 2021Article
- Intrahepatic cholangiocarcinoma: Morpho-molecular pathology, tumor reactive microenvironment, and malignant progression.Advances in cancer research · 2021Review
- Emerging roles of long noncoding RNAs in cholangiocarcinoma: Advances and challenges.Cancer communications (London, England) · 2020Review
- Article
- Phase I study of bintrafusp alfa, a bifunctional fusion protein targeting TGF-β and PD-L1, in patients with pretreated biliary tract cancer.Journal for immunotherapy of cancer · 2020Article
- Metformin and Biliary Tract Cancer in Patients With Type 2 Diabetes.Frontiers in oncology · 2020Article
- Ski mediates TGF-β1-induced fibrosarcoma cell proliferation and promotes tumor growth.Journal of Cancer · 2020Article
- Construction of a model to predict the prognosis of patients with cholangiocarcinoma using alternative splicing events.Oncology letters · 2019Article
- Review
- Intrahepatic Cholangiocarcinoma: Continuing Challenges and Translational Advances.Hepatology (Baltimore, Md.) · 2019Review
- Expression of FOXP1 and FOXO3a in extrahepatic cholangiocarcinoma and the implications in clinicopathological significance and prognosis.OncoTargets and therapy · 2019Article
- Extracellular vesicle-encapsulated miR-30e suppresses cholangiocarcinoma cell invasion and migration via inhibiting epithelial-mesenchymal transition.Oncotarget · 2018Article
- Molecular Mechanisms Driving Cholangiocarcinoma Invasiveness: An Overview.Gene expression · 2018Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimsThe role of transforming growth factor beta 1 (TGFβ1) in cholangiocarcinoma (CCA) initiation and growth requires further definition.
methodsWe employed pharmacological and genetic approaches to inhibit or enhance TGFβ1 signaling, respectively, and determine the cellular mechanisms involved.
resultsIt was observed that inhibiting TGFβ1 activity with short hairpin RNA (shRNA) or pharmaceutical agents suppressed CCA development and growth, whereas overexpression of TGFβ1 enhanced CCA tumor size and promoted intrahepatic metastasis in a rat model. Suppression of TGFβ1 activity inhibits downstream target gene expression mediated by miR-34a that includes cyclin D1, CDK6, and c-Met. In addition, "knockdown" of TGFβ1 expression revealed a miR-34a positive feedback mechanism for enhanced p21 expression in CCAs. A miR-34a inhibitor reversed the effects of "knocking down" TGFβ1 on cell growth, migration, cyclin D1, CDK6 and c-Met expression, suggesting that TGFβ1 mediated effects occur, in part, through this miR-34a signaling pathway. Overexpression of TGFβ1 was associated with CCA tumor progression.
conclusionsThis study suggests that TGFβ1 is involved in CCA tumor progression and participates through miR-34a mediated downstream cascades, and is a target to inhibit CCA development and growth.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.