The Role of Chemokines in Thyroid Carcinoma

Yapa, Sharinie; Mulla, Omar; Green, Victoria; England, James; Greenman, John

doi:10.1089/thy.2016.0660

Cited by 39 publications

(40 citation statements)

References 98 publications

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“…Similar to other human malignancies, thyroid cancer microenvironment is composed of a mixture of immune cells (macrophages, mast cells, neutrophils, and lymphocytes) and soluble mediators (chemokines, cytokines, and growth factors), which are present within and nearby the primary thyroid tumor ( 21 – 23 ). Chemokines, which attract specific subpopulations of immune cell into the tumor site, are active immune mediators playing a role in thyroid tumor progression.…”

Section: Thyroid Cancermentioning

confidence: 99%

Role of Chemokines in Thyroid Cancer Microenvironment: Is CXCL8 the Main Player?

et al. 2018

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Tumor-related inflammation does influence the biological behavior of neoplastic cells and ultimately the patient’s outcome. With specific regard to thyroid cancer, the issue of tumor-associated inflammation has been extensively studied and recently reviewed. However, the role of chemokines, which play a crucial role in determining the immuno-phenotype of tumor-related inflammation, was not addressed in previous reviews on the topic. Experimental evidence shows that thyroid cancer cells actively secrete a wide spectrum of chemokines and, at least for some of them, solid scientific data support a role for these immune-active molecules in the aggressive behavior of the tumor. Our proposal for a review article on chemokines and thyroid cancer stems from the notion that chemokines, besides having the ability to attract and maintain immune cells at the tumor site, also produce several pro-tumorigenic actions, which include proangiogenetic, cytoproliferative, and pro-metastatic effects. Studies taking into account the role of CCL15, C–X–C motif ligand 12, CXCL16, CXCL1, CCL20, and CCL2 in the context of thyroid cancer will be reviewed with particular emphasis on CXCL8. The reason for focusing on CXCL8 is that this chemokine is the most studied one in human malignancies, displaying multifaceted pro-tumorigenic effects. These include enhancement of tumor cells growth, metastatization, and angiogenesis overall contributing to the progression of several cancers including thyroid cancer. We aim at reviewing current knowledge on the (i) ability of both normal and tumor thyroid cells to secrete CXCL8; (ii) direct/indirect pro-tumorigenic effects of CXCL8 demonstrated by in vitro and in vivo studies specifically performed on thyroid cancer cells; and (iii) pharmacologic strategies proven to be effective for lowering CXCL8 secretion and/or its effects on thyroid cancer cells.

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Section: Thyroid Cancermentioning

confidence: 99%

Role of Chemokines in Thyroid Cancer Microenvironment: Is CXCL8 the Main Player?

et al. 2018

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“…The mechanisms by which these DCs are recruited into and/or proliferate in thyroid cancers in this model has yet to be determined. Cancer cells secret growth factors, chemokines, cytokines, and exosome to inhibit tumor immunity 58 , 65 – 67 . Akt signaling has been shown by our group to regulate transcription and release of several of these factors, including exosomes 65 , but the isoform dependency of these effects has not been explored.…”

Section: Discussionmentioning

confidence: 99%

Akt isoform-specific effects on thyroid cancer development and progression in a murine thyroid cancer model

Saji

Kim

Wang

et al. 2020

Sci Rep

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The Akt family is comprised of three unique homologous proteins with isoform-specific effects, but isoform-specific in vivo data are limited in follicular thyroid cancer (FTC), a PI3 kinase-driven tumor. Prior studies demonstrated that PI3K/Akt signaling is important in thyroid hormone receptor βPV/PV knock-in (PV) mice that develop metastatic thyroid cancer that most closely resembles FTC. To determine the roles of Akt isoforms in this model we crossed Akt1−/−, Akt2−/−, and Akt3−/− mice with PV mice. Over 12 months, thyroid size was reduced for the Akt null crosses (p < 0.001). Thyroid cancer development and local invasion were delayed in only the PVPV-Akt1 knock out (KO) mice in association with increased apoptosis with no change in proliferation. Primary-cultured PVPV-Akt1KO thyrocytes uniquely displayed a reduced cell motility. In contrast, loss of any Akt isoform reduced lung metastasis while vascular invasion was reduced with Akt1 or 3 loss. Microarray of thyroid RNA displayed incomplete overlap between the Akt KO models. The most upregulated gene was the dendritic cell (DC) marker CD209a only in PVPV-Akt1KO thyroids. Immunohistochemistry demonstrated an increase in CD209a-expressing cells in the PVPV-Akt1KO thyroids. In summary, Akt isoforms exhibit common and differential functions that regulate local and metastatic progression in this model of thyroid cancer.

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“…Thyroid cancer is one of the fastest growing cancers worldwide. 1,2 It has two outstanding features. The first is the high rate of metastasis to lymph nodes or other organs, which is as high as 30% to 59.1%.…”

Section: Introductionmentioning

confidence: 99%

Nevirapine inhibits migration and invasion in dedifferentiated thyroid cancer cells

et al. 2019

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BackgroundMetastatic or recurrent thyroid cancer often behaves aggressively, and approximately two‐thirds of patients present with radioiodine resistance. Effective therapies to suppress thyroid cancer metastasis are urgently needed. Nevirapine has been proved to suppress tumor growth and induce differentiation in several tumor cells, but has not previously been evaluated in metastasis of thyroid cancer. The present study aimed to investigate the effect of nevirapine on migration and invasion in dedifferentiated thyroid cancer cells.MethodsHuman dedifferentiated thyroid cancer cell line (WRO 82‐1) was subject to real‐time quantitative PCR, western blot and transwell migration/invasion assays. The liver metastasis in tumor xenografts of nude mice was subject to hematoxylin‐eosin (HE) staining.ResultsNevirapine significantly repressed cell migration and invasion in WRO 82‐1 cells, and surprisingly significantly decreased liver metastatic tumor in the nude mouse model of dedifferentiated thyroid cancer compared with that of the control. Moreover, nevirapine significantly decreased the expression of IL‐6 mRNA and phosphorylation of JAK2 (Y1007+Y1008) and STAT3 (Tyr 705) in WRO 82‐1 cells compared with those in control cells.ConclusionOur findings suggest that nevirapine significantly repressed migration and invasion/metastasis in WRO 82‐1 cells and tumor xenografts, which may be related to inhibition of IL‐6/STAT3 signaling pathway. It promises great potential as a novel therapy for thyroid cancer, especially for those patients with metastasis.

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The Role of Chemokines in Thyroid Carcinoma

Cited by 39 publications

References 98 publications

Role of Chemokines in Thyroid Cancer Microenvironment: Is CXCL8 the Main Player?

Role of Chemokines in Thyroid Cancer Microenvironment: Is CXCL8 the Main Player?

Akt isoform-specific effects on thyroid cancer development and progression in a murine thyroid cancer model

Nevirapine inhibits migration and invasion in dedifferentiated thyroid cancer cells

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