Interplay of TGFβ signaling and microRNA in thyroid cell loss of differentiation and cancer progression

Fuziwara, César Seigi; Saito, Kelly Cristina; Kimura, Edna Teruko

doi:10.20945/2359-3997000000172

Cited by 7 publications

(5 citation statements)

References 66 publications

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“…Further, metastasis-related cytokines were positively regulated by UHRF1. According to our previous and present results in thyroid cancer, UHRF1 should be an essential gene in dedi erentiation and metastasis [7,[26][27][28]. roughout cancer development, the main published downstream targets of UHRF1 were tumor suppressor genes.…”

Section: Discussionsupporting

confidence: 54%

UHRF1 Induces Metastasis in Thyroid Cancer

Kuang

Lin

Liu

et al. 2022

Journal of Oncology

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Background. Ubiquitin-like with PHD and ring-finger domain 1 (UHRF1) has been defined as an oncogene in tumor cells. However, the role of UHRF1 in mediating metastasis in thyroid cancer remains unexplored. In this study, we aimed to investigate the metastatic function and the potential mechanisms of UHRF1 in thyroid cancer. Methods. Transwell assays were used to detect the metastatic capability of thyroid cancer. Dual-luciferase reporter assays were applied to examine the activation of transcription factors. Coimmunoprecipitation assays and immunofluorescence staining assays were used to elucidate the potential mechanisms of UHRF1 in promoting the metastasis of thyroid cancer. Results. In this study, we found that overexpression of UHRF1 promoted the metastasis of papillary thyroid cancer cells, and suppression of UHRF1 decreased the metastasis of anaplastic thyroid cancer cells. Regarding the signaling pathway in regulating metastasis, UHRF1 directly combined and activated the transcription factor c-Jun/AP-1 in the nucleus, subsequently increasing the transcription of IL-6 and MIF. Conclusion. Our results suggest that UHRF1 could induce the metastasis of thyroid cancer, and the potential signaling pathway might be that UHRF1 activates c-Jun/AP-1 to increase the expression of IL-6 and MIF. These findings provide a novel mechanism of UHRF1 and illustrate that UHRF1/AP-1 complex could be a potential therapeutic target for patients with thyroid cancer.

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Section: Discussionsupporting

confidence: 54%

UHRF1 Induces Metastasis in Thyroid Cancer

Kuang

Lin

Liu

et al. 2022

Journal of Oncology

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“…As elucidated by Fuziwara and cols. in a recent review, a series of different microRNAs can target mRNA related with the TGF-β1 signaling pathway, and its deregulation is frequently seen in thyroid neoplasia (43).…”

Section: Discussionmentioning

confidence: 99%

Clinical utility of TGFB1 and its receptors (TGFBR1 and TGFBR2) in thyroid nodules: evaluation based on single nucleotide polymorphisms and mRNA analysis

Peres¹,

Teodoro²,

Amaral³

et al. 2021

Archives of Endocrinology and Metabolism

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Objective: Abnormalities involving the TGFB1 gene and its receptors are common in several types of cancer and often related to tumor progression. We investigated the role of single nucleotide polymorphisms (SNP) in the susceptibility to cancer, their impact on its features, as well as the role of mRNA expression of these genes in thyroid malignancy. Materials and methods: We genotyped TGFB1, TGFBR1, and TGFBR2 SNPs in 157 papillary thyroid cancer (PTC) patients and 200 healthy controls. Further, we investigated RNA samples of 47 PTC and 80 benign nodules, searching for differential mRNA expression. Results: SNPs rs1800472 and rs1800469 were associated with characteristics of PTC aggressiveness. Effect predictor software analysis of nonsynonymous SNP rs1800472 indicated increasing protein stability and post-translational changes. TGFB1 mRNA expression was upregulated in PTC and downregulated in benign samples, differentiating malignant from benign nodules (p<0.0001); PTC from goiter (p<0.0001); and PTC from FA (p<0.0001). TGFBR1 mRNA expression was upregulated in goiter and PTC, but downregulated in FA, distinguishing PTC from goiter (p=0.0049); PTC from FA (p<0.0001); and goiter from FA (p=0.0267). On the other hand, TGFBR2 was downregulated in all histological types analyzed and was not able to differentiate thyroid nodules. Conclusion: TGFB1 polymorphism rs1800472 may confer greater activity to TGF-β1 in the tumor microenvironment, favoring PTC aggressiveness. Evaluation of TGFB1 and TGFBR1 mRNA levels may be useful to identify malignancy in thyroid nodules.

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“…Therefore, exploring the pathological mechanism of thyroid cancer is of great clinical significance for the diagnosis and treatment of patients with thyroid cancer. miRNAs are non-coding microRNAs, which mainly influence the biological function of cells through mRNA matching with downstream target genes (5). Studies have shown that miRNAs play a vital part in the occurrence and development of thyroid cancer.…”

Section: Introductionmentioning

confidence: 99%

Effects of CDK6 regulated by miR‑298 on proliferation and apoptosis of thyroid cancer cells

Li¹,

Liu²,

Zhao

et al. 2020

Oncol Lett

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Effects of CDK6 regulated by miR-298 on proliferation and apoptosis of thyroid cancer cells were explored. Seventy-five cases of thyroid carcinoma and adjacent tissues were collected. The expression levels of miR-298 and CDK6 mRNA in tissues and cells were detected by RT-PCR. In addition, thyroid cancer cells and human normal thyroid cells Nthy-ori3-1 were purchased, with the former transfected with miR-298-mimics, miR-298-inhibitor, miR-NC, si-CDK6, si-NC, Sh-CDK6, Sh-NC to build cell models. Then the expression levels of miR-298 and CDK6 in thyroid cancer tissues and cells were detected by qRT-PCR, and the expression of CDK6, Bax, Bcl-2 and caspase-3 by WB. CCK-8 and flow cytometry were employed to detect cell proliferation and apoptosis, and dual luciferase report was adopted to determine the relationship between miR-298 and CDK6. miR-298 was underexpressed in thyroid cancer, and CDK6 was highly expressed in thyroid cancer. Cell experiments revealed that overexpression of miR-298 or inhibition of CDK6 expression could suppress cell proliferation, promote apoptosis, and significantly increase the expression levels of Bax and caspase-3 proteins, decrease Bcl-2 protein expression, which was contrary to the biological phenotype of cells after inhibition of miR-298 or further overexpression of CDK6. Dual luciferase report confirmed that miR-298 was a targeting site of CDK6. miR-298 can inhibit the proliferation of thyroid cells and promote apoptosis of thyroid cancer cells by regulating the expression of CDK6, which is expected to be a potential target for clinical application.

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Interplay of TGFβ signaling and microRNA in thyroid cell loss of differentiation and cancer progression

Cited by 7 publications

References 66 publications

UHRF1 Induces Metastasis in Thyroid Cancer

UHRF1 Induces Metastasis in Thyroid Cancer

Clinical utility of TGFB1 and its receptors (TGFBR1 and TGFBR2) in thyroid nodules: evaluation based on single nucleotide polymorphisms and mRNA analysis

Effects of CDK6 regulated by miR‑298 on proliferation and apoptosis of thyroid cancer cells

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