ArticleBioscience reports2017
Folic acid inhibits nasopharyngeal cancer cell proliferation and invasion via activation of FRα/ERK1/2/TSLC1 pathway.
Article in Bioscience reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Folate receptor 1 is a stemness trait-associated diagnostic and prognostic marker for hepatocellular carcinoma.Biomarker research · 2025Article
- Folic acid depletion as well as oversupplementation helps in the progression of hepatocarcinogenesis in HepG2 cells.Scientific reports · 2022Article
- Article
- Development of a novel multi-functional integrated bioconjugate effectively targeting K-Ras mutant pancreatic cancer.Journal of pharmaceutical analysis · 2022Article
- Emerging roles for folate receptor FOLR1 in signaling and cancer.Trends in endocrinology and metabolism: TEM · 2022Review
- Article
- Folic Acid-Doxorubicin-Double-Functionalized-Lipid-Core Nanocapsules: Synthesis, Chemical Structure Elucidation, and Cytotoxicity Evaluation on Ovarian (OVCAR-3) and Bladder (T24) Cancer Cell Lines.Pharmaceutical research · 2021Article
- Functional and Clinical Characteristics of Cell Adhesion Molecule CADM1 in Cancer.Frontiers in cell and developmental biology · 2021Review
- Effects of folic acid withdrawal on transcriptomic profiles in murine triple-negative breast cancer cell lines.Biochimie · 2020Article
- Tripartite Motif Containing 11 Interacts with DUSP6 to Promote the Growth of Human Osteosarcoma Cells through Regulating ERK1/2 Pathway.BioMed research international · 2019Article
- Functionalized Folic Acid-Conjugated Amphiphilic Alternating Copolymer Actively Targets 3D Multicellular Tumour Spheroids and Delivers the Hydrophobic Drug to the Inner Core.Nanomaterials (Basel, Switzerland) · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Folic acid (FA), which is necessary for normal cell division of mammals, has been implicated to be involved in many tumors. Dietary FA intake has been reported to be associated with a lower risk of nasopharyngeal cancer (NPC). However, the molecular mechanisms of FA in NPC cells remain unclear. In the present study, we found that FA treatment dose dependently inhibited the proliferation, invasion and migration of NPC cells, via folate receptor α (FRα). We further found that FA, bound to FRα, induced the activation of MEK/ERK1/2, and increased the expressions of TSLC1 and E-cadherin. Moreover, blocking of ERK1/2 activation attenuated FA-mediated increase in TSLC1 expression. In addition, knockdown of TSLC1 abolished the FA-mediated inhibition of cell proliferation, invasion and migration, and suppressed the FA-mediated increase oinE-cadherin expression in NPC cells. Taken together, our data suggest that FA treatment inhibits NPC cell proliferation and invasion via activation of FRα/ERK1/2/ TSLC1 signaling pathway. Therefore, FA could be explored as a therapeutic drug for the treatment of NPC, and TSLC1 may act as a tumor suppressor in NPC.
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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.