ArticleAging2020
FHL3 promotes pancreatic cancer invasion and metastasis through preventing the ubiquitination degradation of EMT associated transcription factors.
Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 29 citations in OpenAlex.
- Activation of the FAK-MAPK/ERK1 pathway promotes intestinal epithelial cell sheet migration during fistula tract repair.Scientific reports · 2026Article
- The Hippo-YAP signaling pathway promotes hepatocellular carcinoma progression by inducing FHL3 expression.Cell death & disease · 2025Article
- Transcriptome-wide Mendelian randomization exploring dynamic CD4+ T cell gene expression in colorectal cancer development.Journal of leukocyte biology · 2025Article
- Twist1 Regulates the Immune Checkpoint VISTA and Promotes the Proliferation, Migration and Progression of Pancreatic Cancer Cells.Journal of cellular and molecular medicine · 2025Article
- Transcriptome-wide Mendelian randomisation exploring dynamic CD4+ T cell gene expression in colorectal cancer development.medRxiv : the preprint server for health sciences · 2025Article
- Overexpression of FHL1 suppresses papillary thyroid cancer proliferation and progression via inhibiting Wnt/β-catenin pathway.Endocrine · 2024Article
- Identification and clinical validation of diverse cell-death patterns-associated prognostic features among low-grade gliomas.Scientific reports · 2024Article
- Molecular profile of metastasis, cell plasticity and EMT in pancreatic cancer: a pre-clinical connection to aggressiveness and drug resistance.Cancer metastasis reviews · 2024Review
- Emerging horizons on molecular and circulating biomarkers in pancreatic adenocarcinoma.Frontiers in oncology · 2024Review
- Construction of an anaplastic thyroid cancer stratification signature to guide immune therapy selection and validation of the pivotal gene HLF throughFrontiers in immunology · 2024Article
- Article
- High-throughput proteomics profiling-derived signature associated with chemotherapy response and survival for stage II/III colorectal cancer.NPJ precision oncology · 2023Article
- Establishment and Analysis of an Individualized Immune-Related Gene Signature for the Prognosis of Gastric Cancer.Frontiers in surgery · 2022Article
- The Roles of FHL3 in Cancer.Frontiers in oncology · 2022Review
- LDexpress: an online tool for integrating population-specific linkage disequilibrium patterns with tissue-specific expression data.BMC bioinformatics · 2021Article
- Article
- Article
- KIN17 promotes tumor metastasis by activating EMT signaling in luminal-A breast cancer.Thoracic cancer · 2021Article
- FHL3 Contributes to EMT and Chemotherapy Resistance Through Up-Regulation of Slug and Activation of TGFFrontiers in oncology · 2021Article
- Microdissected pancreatic cancer proteomes reveal tumor heterogeneity and therapeutic targets.JCI insight · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is intractable due to its strong invasiveness and metastatic ability. Epithelial-mesenchymal transition (EMT) is the pivotal driver of tumor invasion and metastasis. The four-and-a-half LIM domain (FHL) family is involved in regulating transforming growth factor (TGF)-β and Ras signaling, which might control the EMT process. In this study, we found that higher expression of four-and-a-half LIM domains 3 (FHL3) predicted poor prognosis in PDAC. The decreasing of FHL3 changed the EMT phenotype by blocking the TGFβ/Atk/GSK3β/ubiquitin pathways. Interestingly, the GSK3β inhibitor could abrogate the role of FHL3 in the regulation of snail1 and twist1 expression, which implied that GSK3β plays a pivotal role in the FHL3-mediated EMT process. Furthermore, we found that FHL3 can directly bind to GSK3β, which weakened the interaction between GSK3β and snail1/twist1. We also found that the LIM-3 domain of FHL3 was required for the binding of FHL3 to GSK3β. Collectively, our study implied that FHL3, as a binding partner of GSK3β, promoted tumor metastasis in PDAC through inhibiting the ubiquitin-degradation of snail1 and twist1.
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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.