Dataset Information

Kiss1 Inhibits the Proliferation of Nasopharyngeal Carcinoma Cells Via Activation of the LKB1/AMPK Pathway.

ABSTRACT: Nasopharyngeal carcinoma (NPC) is a cancer that occurs in the nasopharynx. Infinite proliferation and distant metastasis are the main characteristics of NPC cells, and the main reason for the current failure of malignant tumor treatment. In this study, by integrating the immunohistochemical, cell transfection, western blot and real-time reverse transcriptase polymerase chain reaction (RT-PCR) analysis, we observed that the expression of KISS1 and its receptor gene (KISS1R) negatively related with the proliferation of NPC cells. Overexpression of the KISS1 genes in cells reduced cell proliferation, slow down the cell cycle, and increased apoptosis. Additionally, overexpression of these genes significantly increased Liver Kinase B1 (LKB1), phosphorylation of LKB1 and AMPK, indicated by Western blotting. Together, all of these results suggested for the first time that KISS1 and KISS1R suppress the proliferation of NPC cells by activating the LKB1/AMPK pathway, thus revealing a viable indicator for diagnosis of NPC in clinical practice.

SUBMITTER: Li T

PROVIDER: S-EPMC8804215 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature

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Kiss1 Inhibits the Proliferation of Nasopharyngeal Carcinoma Cells <i>Via</i> Activation of the LKB1/AMPK Pathway.

Li Tingting T Tian Yong Y Wang Yixuan Y Cui Zhen Z He Zelai Z Wu Xiao X Zhang Yajun Y Jiang Hao H

Frontiers in oncology 20220118

Nasopharyngeal carcinoma (NPC) is a cancer that occurs in the nasopharynx. Infinite proliferation and distant metastasis are the main characteristics of NPC cells, and the main reason for the current failure of malignant tumor treatment. In this study, by integrating the immunohistochemical, cell transfection, western blot and real-time reverse transcriptase polymerase chain reaction (RT-PCR) analysis, we observed that the expression of KISS1 and its receptor gene (KISS1R) negatively related wit ...[more]

PMID: 35117986

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Project description:BackgroundCircular RNAs (circRNAs) are widely expressed in human cells and are closely associated with cancer development. However, they have rarely been investigated in the context of nasopharyngeal carcinoma (NPC).MethodsWe screened a new circRNA, circRNF13, in NPC cells using next-generation sequencing of mRNA. Reverse transcription polymerase chain reaction and RNA fluorescence in situ hybridization were used to detect circRNF13 expression in 12 non-tumor nasopharyngeal epithelial (NPE) tissues and 36 NPC samples. Cell proliferation was detected using MTT and flow cytometry assays, and colony formation capability was detected using colony formation assays. Cell migration and invasion were analyzed using wound-healing and Transwell assays, respectively. Cell glycolysis was analyzed using the Seahorse glycolytic stress test. Glucose transporter type 1 (GLUT1) ubiquitination and SUMOylation modifications were analyzed using co-immunoprecipitation and western blotting. CircRNF13 and Small Ubiquitin-like Modifier 2 (SUMO2) interactions were analyzed using RNA pull-down and luciferase reporter assays. Finally, to test whether circRNF13 inhibited NPC proliferation and metastasis in vivo, we used a xenograft nude mouse model generated by means of subcutaneous or tail vein injection.ResultsWe found that circRNF13 was stably expressed at low levels in NPC clinical tissues and NPC cells. In vitro and in vivo experiments showed that circRNF13 inhibited NPC proliferation and metastasis. Moreover, circRNF13 activated the SUMO2 protein by binding to the 3'- Untranslated Region (3'-UTR) of the SUMO2 gene and prolonging the half-life of SUMO2 mRNA. Upregulation of SUMO2 promotes GLUT1 degradation through SUMOylation and ubiquitination of GLUT1, which regulates the AMPK-mTOR pathway by inhibiting glycolysis, ultimately resulting in the proliferation and metastasis of NPC.ConclusionsOur results revealed that a novel circRNF13 plays an important role in the development of NPC through the circRNF13-SUMO2-GLUT1 axis. This study implies that circRNF13 mediates glycolysis in NPC by binding to SUMO2 and provides an important theoretical basis for further elucidating the pathogenesis of NPC and targeted therapy.

Project description:BackgroundUrsolic acid (UA) is a triterpenoid compound with multiple biological functions. This compound has recently been reported to possess an anti-obesity effect; however, the mechanisms are less understood.ObjectiveAs adipogenesis plays a critical role in obesity, the present study was conducted to investigate the effect of UA on adipogenesis and mechanisms of action in 3T3-L1 preadipocytes.Methods and resultsThe 3T3-L1 preadipocytes were induced to differentiate in the presence or absence of UA for 6 days. The cells were determined for proliferation, differentiation, fat accumulation as well as the protein expressions of molecular targets that regulate or are involved in fatty acid synthesis and oxidation. The results demonstrated that ursolic acid at concentrations ranging from 2.5 µM to 10 µM dose-dependently attenuated adipogenesis, accompanied by reduced protein expression of CCAAT element binding protein ? (C/EBP?), peroxisome proliferator-activated receptor ? (PPAR?), CCAAT element binding protein ? (C/EBP?) and sterol regulatory element binding protein 1c (SREBP-1c), respectively. Ursolic acid increased the phosphorylation of acetyl-CoA carboxylase (ACC) and protein expression of carnitine palmitoyltransferase 1 (CPT1), but decreased protein expression of fatty acid synthase (FAS) and fatty acid-binding protein 4 (FABP4). Ursolic acid increased the phosphorylation of AMP-activated protein kinase (AMPK) and protein expression of (silent mating type information regulation 2, homolog) 1 (Sirt1). Further studies demonstrated that the anti-adipogenic effect of UA was reversed by the AMPK siRNA, but not by the Sirt1 inhibitor nicotinamide. Liver kinase B1 (LKB1), the upstream kinase of AMPK, was upregulated by UA. When LKB1 was silenced with siRNA or the inhibitor radicicol, the effect of UA on AMPK activation was diminished.ConclusionsUrsolic acid inhibited 3T3-L1 preadipocyte differentiation and adipogenesis through the LKB1/AMPK pathway. There is potential to develop UA into a therapeutic agent for the prevention or treatment of obesity.

Dataset Information

Kiss1 Inhibits the Proliferation of Nasopharyngeal Carcinoma Cells Via Activation of the LKB1/AMPK Pathway.

Publications

Kiss1 Inhibits the Proliferation of Nasopharyngeal Carcinoma Cells <i>Via</i> Activation of the LKB1/AMPK Pathway.

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