ArticleCancer science2021
LPAR5 promotes thyroid carcinoma cell proliferation and migration by activating class IA PI3K catalytic subunit p110β.
Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- PIK3CA mutations and PI3K isoform expression define prognostic signatures in ovarian clear cell carcinoma.Archives of gynecology and obstetrics · 2026Article
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- Decoding lysophosphatidic acid signaling in physiology and disease: mapping the multimodal and multinodal signaling networks.Signal transduction and targeted therapy · 2025Review
- Effects of dietary protein levels on genes related to subcutaneous fat deposition and lipid metabolism in Tibetan sheep.BMC genomics · 2025Article
- The Emerging Role of LPA as an Oncometabolite.Cells · 2024Review
- PARP1 modulates METTL3 promoter chromatin accessibility and associated LPAR5 RNA mMolecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Emerging roles of lysophosphatidic acid receptor subtype 5 (LPAR5) in inflammatory diseases and cancer.Pharmacology & therapeutics · 2023Review
- Potential role of LPAR5 gene in prognosis and immunity of thyroid papillary carcinoma and pan-cancer.Scientific reports · 2023Article
- Identifying and analyzing the key genes shared by papillary thyroid carcinoma and Hashimoto's thyroiditis using bioinformatics methods.Frontiers in endocrinology · 2023Article
- LPAR5 confers radioresistance to cancer cells associated with EMT activation via the ERK/Snail pathway.Journal of translational medicine · 2022Article
- Review
- Platelets involved tumor cell EMT during circulation: communications and interventions.Cell communication and signaling : CCS · 2022Review
- Review
- LPAR5 promotes thyroid carcinoma cell proliferation and migration by activating class IA PI3K catalytic subunit p110β.Cancer science · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Lysophosphatidic acid receptor 5 (LPAR5) is involved in mediating thyroid cancer progression, but the underlying mechanism needs to be further revealed. In this study, we confirmed that LPAR5 is upregulated in papillary thyroid carcinoma (PTC), especially in BRAF-like PTC, by analyzing The Cancer Genome Atlas (TCGA) database and performing immunohistochemistry assay in human thyroid cancer tissues. LPAR5-specific antagonist TC LPA5 4 treatment inhibited CGTH-W3, TPC-1, B-CPAP, and BHT-101 cell proliferation, CGTH-W3 and TPC-1 cell migration significantly. In vivo, TC LPA5 4 treatment could delay CGTH-W3 xenograft growth in nude mice. We also found that LPAR5-specific antagonist TC LPA5 4, PI3K inhibitor wortmannin, or mTOR inhibitor rapamycin pretreatment abrogated phosphorylation of Akt and p70S6K1 stimulated by LPA in CGTH-W3 and TPC-1 cells. Stimulating CGTH-W3 cells transfected with pEGFPC1-Grp1-PH fusion protein with LPA resulted in the generation of phosphatidylinositol (3,4,5)-triphosphate, which indicates that PI3K was activated by LPA directly. The p110β-siRNA instead of p110α-siRNA transfection abrogated the increase of levels of phosphorylated Akt and S6K1 stimulated by LPA. Furthermore, immunoprecipitation assay confirmed an interaction between LPAR5 and p110β. Overall, we provide new insights that the downregulation of LPAR5 decreased the proliferation and migration phenotype via the PI3K/Akt pathway. Inhibition of LPAR5 or the PI3K/Akt signal may be a novel therapeutic strategy for treating thyroid 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 Socratic graph.