Lysophosphatidic Acid Receptor 5 (LPAR5) Plays a Significance Role in Papillary Thyroid Cancer via Phosphatidylinositol 3-Kinase/Akt/Mammalian Target of Rapamycin (mTOR) Pathway
Autor: | Xiaohua Zhang, Ru-Tian Hao, Ruida Quan, Chen Zheng, Erjie Xia, Cheng-Yong Wu, Jing Hu |
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Rok vydání: | 2020 |
Předmět: |
Adult
Male Proteomics endocrine system diseases Thyroid Gland Apoptosis 030204 cardiovascular system & hematology medicine.disease_cause Papillary thyroid cancer Thyroid carcinoma 03 medical and health sciences 0302 clinical medicine Cell Movement Lab/In Vitro Research Cell Line Tumor medicine Humans Thyroid Neoplasms Receptors Lysophosphatidic Acid Protein kinase B Thyroid cancer PI3K/AKT/mTOR pathway Aged Cell Proliferation Chemistry TOR Serine-Threonine Kinases LPAR5 General Medicine Middle Aged medicine.disease Oncogene Protein v-akt Thyroid Cancer Papillary 030220 oncology & carcinogenesis Cancer research Female Signal transduction Phosphatidylinositol 3-Kinase Carcinogenesis Proto-Oncogene Proteins c-akt Signal Transduction |
Zdroj: | Medical Science Monitor : International Medical Journal of Experimental and Clinical Research |
ISSN: | 1643-3750 |
Popis: | BACKGROUND Thyroid cancer is the most common endocrine system malignancy. Scientists have done considerable research into the molecular mechanisms involved, but many mechanisms remain undiscovered. MATERIAL AND METHODS We performed a comprehensive analysis of the whole-transcriptome resequencing derived from thyroid tissues and paired papillary thyroid cancer (PTC) and showed that lysophosphatidic acid receptor 5 (LPAR5) is strongly overexpressed in thyroid carcinoma. Then, we used TPC-1 and KTC-1 to explore the effect of LPAR5 knockdown on colony formation, migration, proliferation, invasion, and apoptosis of PTC cell line cells. AKT activator was used for the recovery test. Finally, we designed proteomic experiments to explore the role of LPAR5 in the AKT pathway and the EMT process. RESULTS Cell function experiments showed that LPAR5 knockdown can significantly induce apoptosis of KTC-1 and TPC-1 cells. Furthermore, LPAR5 can promote PTC metastasis and tumorigenesis by activating the PI3K/AKT pathway and decreasing its cancer-promoting effect when using AKT agonist. We also found that LPAR5 can regulate the expression of EMT-related proteins, which affect invasion and migration. CONCLUSIONS In summary, downregulation of LPAR5 expression can inhibit the physiological process of PTC, and this phenomenon is related to the PI3K/AKT pathway and EMT. |
Databáze: | OpenAIRE |
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