ArticlePLoS genetics2014
FHIT suppresses epithelial-mesenchymal transition (EMT) and metastasis in lung cancer through modulation of microRNAs.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 67 citations in OpenAlex.
- Non-small cell lung cancer map and analysis: exploring interconnected oncogenic signal integrators.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Inhibition of GSK3β is synthetic lethal with FHIT loss in lung cancer by blocking homologous recombination repair.Experimental & molecular medicine · 2025Article
- Non-coding RNAs as potential mediators of resistance to lung cancer immunotherapy and chemotherapy.Oncology research · 2025Review
- Extracellular vesicle-encapsulated miR-30c-5p reduces aging-related liver fibrosis.Aging cell · 2024Article
- Article
- Significance and implications of FHIT gene expression and promoter hypermethylation in acute lymphoblastic leukemia (ALL).Discover oncology · 2024Article
- HMGA2 promotes cancer metastasis by regulating epithelial-mesenchymal transition.Frontiers in oncology · 2024Review
- Expression of Tumor SuppressorInternational journal of molecular sciences · 2023Article
- Comprehensive analysis of suppressor of cytokine signaling 2 protein in the malignant transformation of NSCLC.Experimental and therapeutic medicine · 2023Article
- Review
- Discovery and functional characterization of novel cotton promoters with potential application to pest control.Plant cell reports · 2022Article
- Transcriptomic FHITFrontiers in immunology · 2022Article
- EMT changes actin cortex rheology in a cell-cycle-dependent manner.Biophysical journal · 2021Article
- Tanshinones induce tumor cell apoptosis via directly targeting FHIT.Scientific reports · 2021Article
- Fhit induces the reciprocal suppressions between Lin28/Let-7 and miR-17/92miR.International journal of medical sciences · 2021Article
- A Novel Six Metastasis-Related Prognostic Gene Signature for Patients With Osteosarcoma.Frontiers in cell and developmental biology · 2021Article
- Cancer-Associated Fibroblasts Differentiated by Exosomes Isolated from Cancer Cells Promote Cancer Cell Invasion.International journal of molecular sciences · 2020Article
- The fission yeast FHIT homolog affects checkpoint control of proliferation and is regulated by mitochondrial electron transport.Cell biology international · 2020Article
- Role of MicroRNA-30c in cancer progression.Journal of Cancer · 2020Review
- Upregulation of miR-130b Contributes to Risk of Poor Prognosis and Racial Disparity in African-American Prostate Cancer.Cancer prevention research (Philadelphia, Pa.) · 2019Article
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Metastasis is the principal cause of cancer death and occurs through multiple, complex processes that involve the concerted action of many genes. A number of studies have indicated that the Fragile Histidine Triad (FHIT) gene product, FHIT, functions as a tumor suppressor in a variety of common human cancers. Although there are suggestions of a role for FHIT loss in progression of various cancers, a role for such loss in metastasis has not been defined. Here, via in vivo and in vitro assays, we reveal that the enforced expression of FHIT significantly suppresses metastasis, accompanied by inhibition of the epithelial-mesenchymal transition (EMT), a process involved in metastasis through coordinate modulation of EMT-related genes. Specifically, miR-30c, a FHIT-upregulated microRNA, contributes to FHIT function in suppression of EMT and metastasis by directly targeting metastasis genes Metadherin (MTDH), High-mobility group AT-hook 2 (HMGA2), and the mesenchymal markers, Vimentin (VIM) and Fibronectin (FN1), in human lung cancer. Finally, we demonstrate that the expression pattern of FHIT and miR-30c is inversely correlated with that of MTDH and HMGA2 in normal tissue, non-metastatic and metastatic tumors, serving as a potential biomarker for metastasis in lung cancer.
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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.