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( 13 ). When IGF-1 binds to its corresponding receptor, it triggers downstream signaling pathways, of which the most important is the phosphatidylinositol-3-kinase (PI3K)/Akt pathway ( 14 ). The PI3K/Akt pathway has been implicated in the regulation of
Radboud Institute for Molecular Life Sciences (RIMLS), Radboud University Medical Center, Nijmegen, The Netherlands
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Division of Endocrinology, Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands
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Department of Nuclear Medicine and Endocrine Tumors, Institute of Oncology ‘Prof. Dr. Ion Chiricuta’, Cluj-Napoca, Romania
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Department of Nuclear Medicine and Endocrine Tumors, Institute of Oncology ‘Prof. Dr. Ion Chiricuta’, Cluj-Napoca, Romania
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Endocrinology Clinic, Cluj County Emergency Hospital, Cluj-Napoca, Romania
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Department of Nuclear Medicine and Endocrine Tumors, Institute of Oncology ‘Prof. Dr. Ion Chiricuta’, Cluj-Napoca, Romania
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disease is confronted with long-term disease and increased risk of death as no curative treatment options are available ( 5 , 6 , 7 ). The intracellular proteins PI3K, Akt and mTOR are part of a central signaling pathway in NMTC tumorigenesis by
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, 15 , 16 ). Moreover, FFAR1 and FFAR4 are expressed in MDA-MB-231 and MCF-7 breast cancer cells and mammary non-tumorigenic epithelial cells MCF10A ( 9 , 11 , 17 ). The PI3K/AKT/mTOR pathway has been involved in growth, proliferation, survival
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Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China
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Signaling Technology), anti-FAK (Cell Signaling Technology), anti-Akt (Cell Signaling Technology), anti-p-Akt (Cell Signaling Technology), and anti-β-catenin (ProteinTech Group). After incubation with secondary antibodies (Epizime, China) for 2 h at room
Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China
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Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China
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Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China
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Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China
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Nanchang University, Nanchang, Jiangxi Province, China
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Department of Urology, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China
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Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China
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found that SLC7A11 functions as an invasive biomarker and was highly expressed in invasive PitNETs. In addition, knockdown of SLC7A11 inhibited epithelial–mesenchymal transition (EMT) through the PI3K/AKT signaling pathway. Materials and methods
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Background: Transforming growth factor beta receptor III (TGFBR3) has been shown to play a tumor suppressive role in a variety of cancers. However, its role in papillary thyroid cancer (PTC) remains unknown.
Method: TGFBR3 expression levels in PTC were analyzed utilizing TCGA and GEO database. Edu, wounding healing and Transwell assays were used to evaluate cell proliferation, migration and invasion. Transcriptome sequencing, qRT-PCR and Western blotting were used to detect the underlying mechanism of TGFBR3 in PTC progression.
Result: This study demonstrated that TGFBR3 expression was significantly down-regulated in PTC compared to normal thyroid tissues. Low expression of TGFBR3 was associated with poor prognosis of patients with PTC. Furthermore, TGFBR3 expression positively correlated with thyroid differentiation score. In investigating the biological impact of TGFBR3 over-expression in PTC cell lines, we found that the proliferation, migration and invasion of PTC cells were significantly inhibited in response to TGFBR3 overexpression. Moreover, we also demonstrated that overexpression of TGFBR3 inhibited PI3K/AKT pathway and epithelial mesenchymal transformation processes. Lastly, TGFBR3 expression was found to be involved in tumor immune infiltration, highlighting its potential influence on immune dynamics within the tumor microenvironment in PTC.
Conclusion: TGFBR3 plays a tumor suppressive role in PTC progression by inhibiting PI3K/AKT pathway and EMT.
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insulin binding, its receptor is auto-phosphorylated and activates several downstream targets such as IRS1 and kinases such as PI3K, and AKT, which are critical nodes in the insulin signaling pathway ( 18 ). PI3K/AKT pathway regulates glucose uptake
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Department of Cardiology, Yanbian University Hospital, Yanji, China
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), the bands were processed with Image J software (National Institutes of Health, Bethesda, MD, USA). The following antibodies were used in this experiment: Anti-GLP1-1R Antibody (ab218532, Abcam), AKT (phospho-S473) polyclonal antibody(80455
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. Gottlob ( 28 ) and Majewski ( 29 ) found that AKT, also known as protein kinase B, increases the basal levels of HK units bound to mitochondria. A few years later, it was demonstrated that this interaction was a consequence of direct phosphorylation of HK
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Department of General Surgery, Xiangya Hospital, Central South University, Changsha, China
Department of Burns and Plastic Surgery, The Third Xiangya Hospital, Central South University, Changsha, China
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), anti-total-ERK, anti-phospho-ERK (Thr202/Tyr204), anti-total-AKT and anti-phosho-AKT (Ser473) (all Cell Signaling). The secondary antibody used was goat anti-rabbit (R&D Systems). Quantification of protein expression was performed using ImageJ (EHD