scholarly journals Iodine Promotes Tumorigenesis of Thyroid Cancer by Suppressing Mir-422a and Up-Regulating MAPK1

2017 ◽  
Vol 43 (4) ◽  
pp. 1325-1336 ◽  
Author(s):  
Junyi  Wang ◽  
Haiou Yang ◽  
Yiran Si ◽  
Dongzhi Hu ◽  
Yang Yu ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Thyroid Carcinoma ◽  
Cancer Cells ◽  
Mitogen Activated Protein Kinase ◽  
In Vivo Studies ◽  
Mitogen Activated Protein ◽  
And Migration ◽  
Cell Migration And Proliferation ◽  
Thyroid Cancer Cells

Background/Aims: Iodine may trigger tumorigenesis and development of thyroid carcinoma, but the mechanisms involved remained elusive. MicroRNA (MiRNAs) are known to be involved in each stage of cancer development; however, the role of miRNAs in iodine-induced tumorigenesis of thyroid carcinoma remained unknown. In this study, we aimed at investigating miRNA related signaling pathway in thyroid cancer cells. Methods: Levels of miRNAs and mRNAs were determined using RT-qPCR and proteins were quantified by western blotting. Cell migration and proliferation were checked using Transwell assay and CCK8 assay respectively. Tumor xenografts in nude mice were established by subcutaneous injection of cancer cells. Results: Mitogen activated protein kinase 1 (MAPK1) was significantly up-regulated, while miR-422a was down-regulated in thyroid cancer cells cultured with high iodine; miR-422a directly bound to the 3’UTR of MAPK1 mRNA. Moreover, miR-422a negatively regulated MAPK1 expression, and down-regulated miR-422a promoted proliferation and migration of TPC-1 cells. In vivo studies also confirmed that iodine promoted tumor growth by suppressing miR-422a and up-regulating MAPK1. Conclusions: Our study illustrates a new pathway comprising iodine, miRNA and MAPK1, and defines a novel mechanism in thyroid cancer.

scholarly journals Suppression of MIR31HG Affects the Functional Properties of Thyroid Cancer Cells Depending on miR-761/MAPK1 Axis

2021 ◽  
Author(s):  
Shuwang Peng ◽  
Luyang Chen ◽  
Zhengtai Yuan ◽  
Shanshan Duan
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Mitogen Activated Protein Kinase ◽  
Luciferase Reporter ◽  
Invasion And Migration ◽  
And Migration ◽  
Cancer Suppression ◽  
Thyroid Cancer Cells

Abstract Background: Long non-coding RNAs (lncRNAs) possess pivotal roles in human cancers, including thyroid cancer. In this study, we sought to elucidate the precise action of MIR31HG in the functional behaviors of thyroid cancer cells.Methods: MIR31HG, microRNA (miR)-761 and mitogen-activated protein kinase 1 (MAPK1) were quantified by quantitative real-time PCR (qRT-PCR) or immunoblotting analysis. Cell viability, proliferation, apoptosis, invasion, and migration abilities were evaluated by MTS, 5-Ethynyl-2’-Deoxyuridine (EdU), flow cytometry, transwell and wound-healing assays, respectively. Dual-luciferase reporter assays were performed to validate the relationship between miR-761 and MIR31HG or MAPK1. Mouse xenografts were formed to assess the effect of MIR31HG on tumor growth.Results: MIR31HG expression was at high levels in thyroid cancer. Suppression of MIR31HG impeded cell proliferation, invasion, and migration, as well as promoted cell apoptosis in vitro, and diminished the growth of xenograft tumors in vivo. Mechanistically, MIR31HG targeted and regulated miR-761. Moreover, the effects of MIR31HG suppression was partly dependent on increased abundance of miR-761. MAPK1 was established as a direct and functional target of miR-761. Furthermore, MIR31HG involved the modulation of MAPK1 expression through competitively binding to miR-761 by the shared binding sequence.Conclusion: Our findings demonstrate the workings of an undescribed regulatory network, in which MIR31HG targets miR-761 to regulate MAPK1 expression, leading to the alteration of the functional behaviors of thyroid cancer cells.

scholarly journals Local Anesthetics Induce Apoptosis in Human Thyroid Cancer Cells through the Mitogen-Activated Protein Kinase Pathway

PLoS ONE ◽  
2014 ◽  
Vol 9 (2) ◽  
pp. e89563 ◽  
Author(s):  
Yuan-Ching Chang ◽  
Yi-Chiung Hsu ◽  
Chien-Liang Liu ◽  
Shih-Yuan Huang ◽  
Meng-Chun Hu ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Local Anesthetics ◽  
Mitogen Activated Protein Kinase ◽  
Human Thyroid ◽  
Mitogen Activated Protein ◽  
Thyroid Cancer Cells ◽  
Kinase Pathway

scholarly journals AXL/GAS6 Inhibition Induces Apoptosis and Suppresses Cell Proliferation and Migration by Blocking the PI3K/AKT Signaling Pathways in Thyroid Cancer Cells in Vivo

2022 ◽  
Author(s):  
Zhenhua Zhang ◽  
Zijie Su ◽  
Ji Zhang
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Akt Pathway ◽  
Protein Expressions ◽  
And Migration ◽  
Thyroid Cancer Cells ◽  
Proliferation And Migration

Abstract Background: The Gas6/Axl-PI3K/Akt pathway is known as one of the most critical molecular signaling pathways involved in the regulation of key cellular processes. GAS6 has emerged as the perfect target for many malignancy treatments, but its role in thyroid cancer remains less described. This study aimed to evaluate both knockdown and overexpression effects of GAS6 on thyroid cancer cell proliferation, migration, and viability.Methods: Both RT-PCR and western blot analysis were performed to evaluate mRNA and protein expressions of GAS6; cell viability was assessed by MTT assay; then, TUNEL apoptosis, Transwell and migration assays were monitored to determine the effects of GAS6 knockdown or GAS6 overexpression on 850-5C and CAL62 thyroid cancer cells. Results: The mRNAs and protein expressions of GAS6 were the highest in CAL62 cancer cells. AXL/GAS6 knockdown through the application of siGAS6 and XL184, an AXL inhibitor, strongly diminished the proliferation and migration levels of CAL62 by inducing cell apoptosis. Meanwhile, overexpression of GAS6 produced the inversed effects, and the protein levels of PI3K, AKT, and p-AKT were significantly up and downregulated, accordingly. Conclusion: GAS6 inhibition promotes apoptosis and represses the proliferation of thyroid cancer cells by activating PI3K/AKT pathway; thus, provides a novel target for thyroid cancer therapy.

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