MiR-345-5p inhibits tumorigenesis of papillary thyroid carcinoma by targeting SETD7

Zhao, Ming; Wang, Kejing; Shang, Jing; Zhong, Liang; Zheng, Weihui; Gu, Jialei

doi:10.5114/aoms.2019.83823

Cited by 10 publications

(15 citation statements)

References 33 publications

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“…Here, we monitored a regulatory effect of circRPS28 on miR-125a-5p, miR-345-5p, miR-542-3p and miR-589-5p in PTC cells. MiR-125a-5p and miR-345-5p could suppress cell malignancy and glucose metabolism of PTC cells [19,24]; miR-589-5p could target thyroid receptor interacting protein 6 to play as a tumor suppressor in endometrial carcinoma [25]. Yet, expression and role of miR-589-5p and miR-542-3p remained unstudied in PTC tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

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circRPS28 (hsa_circ_0049055) is a novel contributor for papillary thyroid carcinoma by regulating cell growth and motility <i>via</i> functioning as ceRNA for miR-345-5p to regulate frizzled family receptor 8 (FZD8)

Mao

Huo

et al. 2021

Endocr J

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Circular RNA 40S ribosomal protein S28 (circRPS28; hsa_circ_0049055) is upregulated in papillary thyroid carcinoma (PTC) patients. However, its role remained uncovered in the progression of PTC. Above all, expression of circRPS28 was determined in PTC samples by real-time quantitative PCR and circRPS28 was highly expressed in tumor tissues and cells. Besides, circRPS28 was predominantly distributed in the cytoplasm. Functional experiments were launched using colony formation assay, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, 5-ethynyl-2-deoxyuridine (EdU) assay, transwell assays, scratch wound assay, and flow cytometry. As a result, blocking circRPS28 restrained PTC cell viability, EdU positive cell rate, colony formation number, wounding healing rate, and numbers of migration and invasion cells, accompanied with apoptosis rate promotion. These effects paralleled with low B-cell lymphoma (Bcl)-2 level and high Bcl-2-associated X protein (Bax), matrix metalloproteinase-2 (MMP2), and MMP9 levels, as analyzed by western blotting. Overexpressing microRNA (miR)-345-5p exerted similar roles to circRPS28 silencing. Notably, dual-luciferase reporter assay and RNA immunoprecipitation confirmed the target relationship between circRPS28 and miR-345-5p, miR-345-5p and frizzled family receptor 8 (FZD8). Downregulating miR-345-5p abrogated effects of circRPS28 blockage in PTC cells, and restoring FZD8 counteracted miR-345-5p roles, either. Furthermore, xenograft tumor model was established in mice, and exhausting circRPS28 delayed the growth of PTC cells in vivo by regulating miR-345-5p and FZD8. In conclusion, we demonstrated that blocking circRPS28 and/or promoting miR-345-5p suppressed PTC cell growth and motility via regulating FZD8. This study might suggest a novel circRPS28/miR-345-5p/FZD8 competing endogenous RNA pathway in PTC.

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Section: Discussionmentioning

confidence: 99%

“…MiRNA (miR)-345-5p is versatile in human cancers [17,18], and it has been proposed as a tumor suppressor in PTC [19]. Frizzled family receptor 8 (FZD8) is Wnt receptor in canonical Wnt signaling pathway that is therapeutic target to antagonize human cancers [20].…”

mentioning

confidence: 99%

circRPS28 (hsa_circ_0049055) is a novel contributor for papillary thyroid carcinoma by regulating cell growth and motility <i>via</i> functioning as ceRNA for miR-345-5p to regulate frizzled family receptor 8 (FZD8)

Mao

Huo

et al. 2021

Endocr J

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“…BC is one of the malignant tumors affecting human life with high morbidity and incidence rates, imposing a heavy social and economic burden [20][21][22]. The current mainstream therapy of BC has major toxic and side effects, and the problems are still unresolved.…”

Section: Discussionmentioning

confidence: 99%

Anti-tumor effects of isoliquiritigenin in Bcl-2/Bax and PCNA expression of T24 human bladder cancer cells

Huang

Wang

2020

Arch Med Sci

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IntroductionThe aim of this study was to investigate the proliferation and apoptosis of T24 after treatment with isoliquiritigenin (ISL) and to explore the underlying mechanism.Material and methodsT24 cells were divided into 6 groups and cultured. The five experimental groups were seeded into medium with 10, 20, 40, 80, and 160 µM ISL and the control group was administered with 0.01% DMSO. The cell morphology was observed using an optical microscope. The proliferation of cells and half maximal inhibitory concentration (IC50) were determined and calculated by MTS. Cell cycle and apoptosis were evaluated by flow cytometry. The migration ability of cells was detected by wound healing assay. The expression of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), and proliferating cell nuclear antigen (PCNA) was determined by RT-qPCR and western blot.ResultsAt 24 h after treatment with ISL, morphology revealed that cell number diminished and the cell volume shrank with increasing concentration. According to the results of MTS, ISL significantly inhibited the T24 cell proliferation in a dose- and time-dependent manner. Flow cytometry showed that ISL could block the replication of T24 cell DNA from S phase to G2, therefore promoting cell apoptosis. Wound healing assay showed that at 48 h after treatment with ISL, the migration of T24 cells was remarkably inhibited. The results of RT-qPCR and Western blot revealed that after 24 h of treatment, the expression levels of Bcl-2 and PCNA were down-regulated, and the expression level of Bax was increased in the different dose of the ISL treated group.ConclusionsISL possesses detrimental effects on the viability of BC cell T24 in a dose-dependent manner via blocking the cell cycle and inducing apoptosis by down-regulation of PCNA and Bcl-2 expression and up-regulation of Bax expression.

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“…Realtime PCR was performed by SYBR Master Mix on the ABI 7500 Realtime PCR system (Applied Biosystems, USA) as previously described [39]. The relative mRNA expression of target genes to endogenous control glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was calculated using the 2 -ΔΔCT method.…”

Section: Realtime Pcrmentioning

confidence: 99%

Lipotoxicity induced pancreatic beta cell damage is associated with GPR119/MST1/FoxO1 Pathway

Song

et al. 2021

Arch Med Sci

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IntroductionG-protein-coupled receptor 119 (GPR119) is emerging as a potential therapeutic target against type 2 diabetes with beneficial effects on glucose homeostasis. However, the function of GRP119 in lipotoxicity induced pancreatic beta cell apoptosis and the molecular mechanism remains largely unknown.Material and methodsImpact of GPR119 on pancreatic islet beta cell apoptosis was evaluated in INS-1 cells treated with palmitate. The subsequent modulation of the MST1-FOXO1-Pdx1 signaling pathway and pro-apoptotic caspase-3 system were determined by measuring the target protein and mRNA expression. Dyslipidemia mice with gain and loss of GPR119 function by the application of specific lenti-viral vector was utilized to evaluate the impact of GPR119 on pancreas function in vivo. Lipid metabolism, glucose and insulin response, morphological changes as well as activation/inhibition of MST1-FOXO1-Pdx1 signaling pathway in pancreas were analyzed systematically.ResultsPalmitate treatment stimulated pro-apoptotic response in INS-1 cells, accompanied by inhibition of GPR119 expression and the subsequent activation of the MST1-FOXO1 combined with inhibition of Pdx1 signaling cascade. Activation of GPR119 by MBX prevents INS-1 cell from lipotoxicity induced apoptosis by targeting the MST1-FOXO1-Pdx1 pathway. Moreover, overexpression of GPR119 significantly attenuates the dyslipidemia and dysfunction of the pancreas. In contrast, inactivation of GPR119 by lentiviral vector in mice results in accelerated pancreas apoptosis and malfunction. The protective effects of GRP119 on lipotoxicity induced pancreas dysfunction are associated with modulating the MST1-FOXO1-Pdx1 signaling cascade.ConclusionsGPR119 alleviates lipotoxicity induced pancreatic beta cell apoptosis and malfunction through regulating MST1-FOXO1-Pdx1 signaling pathway.

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MiR-345-5p inhibits tumorigenesis of papillary thyroid carcinoma by targeting SETD7

Cited by 10 publications

References 33 publications

circRPS28 (hsa_circ_0049055) is a novel contributor for papillary thyroid carcinoma by regulating cell growth and motility <i>via</i> functioning as ceRNA for miR-345-5p to regulate frizzled family receptor 8 (FZD8)

circRPS28 (hsa_circ_0049055) is a novel contributor for papillary thyroid carcinoma by regulating cell growth and motility <i>via</i> functioning as ceRNA for miR-345-5p to regulate frizzled family receptor 8 (FZD8)

Anti-tumor effects of isoliquiritigenin in Bcl-2/Bax and PCNA expression of T24 human bladder cancer cells

Lipotoxicity induced pancreatic beta cell damage is associated with GPR119/MST1/FoxO1 Pathway

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