The Transcription Factor ETV5 Mediates BRAFV600E-Induced Proliferation and TWIST1 Expression in Papillary Thyroid Cancer Cells

Puli, Oorvashi Roy; Danysh, Brian P.; McBeath, Elena; Sinha, Deepankar; Hoang, Nguyet M.; Powell, Reid T.; Danysh, Heather E.; Cabanillas, Maria E.; Cote, Gilbert J.; Hofmann, Marie‐Claude

doi:10.1016/j.neo.2018.09.003

Cited by 36 publications

(30 citation statements)

References 76 publications

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“…Furthermore, the signaling activation of MAPK using BRAF V600E induces the ETV5 TF, which subsequently modulates TWIST1 expression transcriptionally to promote EMT in thyroid-cancer cells (47). Conversely, in a human PTC cell line, ETV5 knockdown attenuated this phenotype and reduced cell migration, invasion, and proliferation.…”

Section: Tgfβ and Mirnas In Emt Regulationmentioning

confidence: 99%

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

Fuziwara

Saito

Kimura

2019

Archives of Endocrinology and Metabolism

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Thyroid cancer has been rapidly increasing in prevalence among humans in last 2 decades and is the most prevalent endocrine malignancy. Overall, thyroid-cancer patients have good rates of long-term survival, but a small percentage present poor outcome. Thyroid cancer aggressiveness is essentially related with thyroid follicular cell loss of differentiation and metastasis. The discovery of oncogenes that drive thyroid cancer (such as RET, RAS, and BRAF), and are aligned in the MAPK/ERK pathway has led to a new perspective of thyroid oncogenesis. The uncovering of additional oncogenemodulated signaling pathways revealed an intricate and active signaling cross-talk. Among these, microRNAs, which are a class of small, noncoding RNAs, expanded this cross-talk by modulating several components of the oncogenic network-thus establishing a new layer of regulation. In this context, TGFβ signaling plays an important role in cancer as a dual factor: it can exert an antimitogenic effect in normal thyroid follicular cells, and promote epithelial-to-mesenchymal transition (EMT), cell migration, and invasion in cancer cells. In this review, we explore how microRNAs influence the loss of thyroid differentiation and the increase in aggressiveness of thyroid cancers by regulating the dual function of TGFβ. This review provides directions for future research to encourage the development of new strategies and molecular approaches that can improve the treatment of aggressive thyroid cancer.

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Section: Tgfβ and Mirnas In Emt Regulationmentioning

confidence: 99%

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

Fuziwara

Saito

Kimura

2019

Archives of Endocrinology and Metabolism

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“…For instance, SDC4 gene silencing inhibited thyroid cancer cell EMT via the Wnt/β-catenin pathway (14). Puli et al showed that the transcription factor ETV5 decreased BRAFV600E-induced TWIST1 expression in thyroid cancer cells (15). In addition, microRNA-150-5p affected EMT by regulating the BRAFV600E mutation in thyroid cancer cells (16).…”

Section: Introductionmentioning

confidence: 99%

LRG‑1 enhances the migration of thyroid carcinoma cells through promotion of the epithelial‑mesenchymal transition by activating MAPK/p38 signaling

Ban

Tang

et al. 2019

Oncol Rep

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Leucine-rich-alpha-2-glycoprotein 1 (LRG-1) has been reported to be associated with multiple malignancies. However, its participation in thyroid carcinoma progression remains unclear. In the present study, the biological function and underlying molecular mechanisms of LRG-1 in thyroid carcinoma were investigated. It was found that LRG-1 was overexpressed in thyroid carcinoma tissues, and high LRG-1 expression predicted poor patient survival and late tumor stage. As shown in the mouse xenograft study, knockdown of LRG-1 significantly attenuated thyroid cancer growth in vivo . Based on wound healing, Transwell, proliferation and apoptosis assays, it was found that the knockdown of LRG-1, using shLRG-1, inhibited cell migration and invasion, but did not affect proliferation and apoptosis in thyroid cancer cells . Furthermore, LRG-1 also induced epithelial-mesenchymal transition (EMT) in thyroid carcinoma cells. Western blot analysis revealed that this tumor-promoting bioactivity of LRG-1 was attributed to its selective activation of MAPK/p38 signaling. All of these findings indicate that LRG-1 plays a deleterious role in the progression of thyroid carcinoma. LRG-1 may serve as a promising biomarker for predicting prognosis in thyroid carcinoma patients, and LRG-1-based therapy may be developed into a novel strategy for the treatment of thyroid carcinoma.

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“…Presently, the use of these molecules as markers in the diagnostic and prognostic management of PTC is increasing 8,9. Puli provided evidence suggesting that ETV5 and its putative target CCND1/2 may be proliferative markers of advanced PTC 10. Chen suggested that SDC4 affects PTC cells apoptosis via the Wnt/β-catenin pathways 11.…”

Section: Introductionmentioning

confidence: 99%

<p>JAZF1 Suppresses Papillary Thyroid Carcinoma Cell Proliferation and Facilitates Apoptosis via Regulating TAK1/NF-κB Pathways</p>

Huang¹,

Cai²,

Luo³

et al. 2019

OTT

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PurposeJuxtaposed with another zinc finger gene 1 (JAZF1) is involved in gluconeogenesis, insulin sensitivity, cell differentiation, lipid metabolism and inflammation, but its role in carcinoma remains inexplicit.Patients and methodsWe explored the JAZF1 expression in human papillary thyroid cancer (PTC) tissues, adjacent normal thyroid tissues and nodular goitre tissues, as well as Ki67 expression in PTC tissues, using immunohistochemistry staining. Western blotting and RT-qPCR were performed to explore the JAZF1 expression levels in Nthy-ori 3–1, BCPAP and TPC-1 cells. BCPAP cells overexpressing JAZF1 were constructed using an Adv-JAZF1-GFP recombinant adenovirus vector. Next, the cell proliferation assay, colony formation assay, cell cycle analysis, apoptosis and immunofluorescence were performed. The mRNA expression level of nuclear factor-κB p65 (NF-κB p65) was examined using RT-qPCR. The expression of Bcl-2, Bax, transforming growth factor beta-activated kinase 1 (TAK1), NF-κB p65 and NF-κB p-p65 were examined using Western blotting.ResultsThe expression of JAZF1 in human PTC tissues was downregulated compared with adjacent thyroid tissues or nodular goitre. Additionally, JAZF1 expression was associated with the location and lymph node metastasis of PTC. The expression level of JAZF1 had a negative correlation with Ki67 labelling index (LI). Compared to Nthy-ori 3–1 cells and TPC-1 cells, BCPAP cells expressed the lowest JAZF1. JAZF1 overexpressed significantly inhibited proliferation, caused G0/G1 cell cycle arrest and promoted apoptosis in BCPAP cells. Furthermore, JAZF1 overexpressed in BCPAP cells clearly upregulated the expression level of Bax protein, whereas decreased the expression of Bcl-2, TAK1, NF-κB but did not affect the mRNA or protein expression level of NF-κB p65.ConclusionJAZF1 inhibits proliferation and induces apoptosis in BCPAP cells by suppressing the activation of TAK1/NF-κB signalling pathways, suggesting that JAZF1 may serve as a reliable molecular marker in PTC.

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The Transcription Factor ETV5 Mediates BRAFV600E-Induced Proliferation and TWIST1 Expression in Papillary Thyroid Cancer Cells

Cited by 36 publications

References 76 publications

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

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

LRG‑1 enhances the migration of thyroid carcinoma cells through promotion of the epithelial‑mesenchymal transition by activating MAPK/p38 signaling

<p>JAZF1 Suppresses Papillary Thyroid Carcinoma Cell Proliferation and Facilitates Apoptosis via Regulating TAK1/NF-κB Pathways</p>

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