Epithelial-to-mesenchymal transition in thyroid cancer: a comprehensive review

Shakib, Heewa; Rajabi, Sadegh; Dehghan, Mohammad Hossien; Mashayekhi, Farideh Jalali; Safari-Alighiarloo, Nahid; Hedayati, Mehdi

doi:10.1007/s12020-019-02030-8

Cited by 63 publications

(59 citation statements)

References 195 publications

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“…Epithelial-mesenchymal transition (EMT) is a process that cancer cells lose their cell-cell adhesion and obtain mesenchymal characteristics, which plays an important role in the metastasis of various human tumors including PTC (28)(29)(30). To investigate whether SHCBP1 induces EMT, the expression of EMT markers was evaluated.…”

Section: Knockdown Of Shcbp1 Suppresses Ptc Cell Migration and Invasionmentioning

confidence: 99%

RETRACTED: SHCBP1 Promotes Papillary Thyroid Carcinoma Carcinogenesis and Progression Through Promoting Formation of Integrin and Collagen and Maintaining Cell Stemness

Geng

Guo

et al. 2021

Front. Endocrinol.

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Papillary thyroid carcinoma (PTC) is the most common thyroid cancer with a rapidly increasing incidence globally. Bioinformatics analyses suggested that SHCBP1 (SHC SH2 Domain-Binding Protein 1) was significantly up-regulated in PTC tumor tissues, which was further confirmed by immunohistochemical staining and qPCR analyses in Xuzhou cohort. Moreover, the results indicated that the mRNA level of SHCBP1 was negatively associated with patients’ disease-free survival rate, and further analysis reveals that patients with high SHCBP1 expression tend to have more lymph node metastasis. Afterward, MTT, colony formation, cell-cycle assay, FACS apoptosis assay, invasion, migration, as well as scratch assay were performed to study the phenotypes change of PTC cells after knocking down SHCBP1. The in vivo subcutaneous tumor model was developed to study the proliferation ability of PTC cells after SHCBP1 knockdown. We show that knock down of SHCBP1 significantly inhibits PTC cell proliferation, cell cycle, invasion and migration in vivo and in vitro. Western blot and qRT-PCR showed that knockdown of SHCBP1 could significantly reduce MYC, KLF4, CD44, ITGA6, ITGB1, ITGB5, and COL4A2 expression at both RNA and protein levels, which indicated that SHCBP1 might be involved in PTC carcinogenesis and progression through targeting formation of integrin and collagen and cell stemness pathways, and can be a potential diagnosis biomarker and therapeutic target for PTC.

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Section: Knockdown Of Shcbp1 Suppresses Ptc Cell Migration and Invasionmentioning

confidence: 99%

RETRACTED: SHCBP1 Promotes Papillary Thyroid Carcinoma Carcinogenesis and Progression Through Promoting Formation of Integrin and Collagen and Maintaining Cell Stemness

Geng

Guo

et al. 2021

Front. Endocrinol.

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“…EMT is involved in the metastatic progression of various malignancies. [20][21][22] We measured the expression of EMTassociated factors to determine the EMT process after knocking-down the expression of CMTM2. As compared to Huh-7-NC cells, the epithelial markers E-cadherin and…”

Section: Down-regulated Cmtm2 Promotes Hcc Metastasis Through Inducinmentioning

confidence: 99%

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

Zhang¹,

Tian²,

Bei³

et al. 2020

OTT

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Background: Our recent study identified that human chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family member 2 (CMTM2) was deregulated in hepatocellular carcinoma (HCC) tissues and posed as a potential tumor suppressor. However, the mechanism of CMTM2 in HCC occurrence and development has not been well elaborated. Materials and Methods: The expression of CMTM2 was knocked-down by RNA interruption in Huh-7 and SMMC7721 cells. Cell proliferation ability was detected by CCK8 test and colony formation assay. The cell invasion and migration were measured by wound healing and Transwell assay. Results: We found that the cell proliferation was significantly increased by interruption of CMTM2 expression, both in Huh-7 and SMMC7721 cells. Moreover, down-regulated CMTM2 could promote the invasion and migration ability of HCC cells through inducing the epithelial-mesenchymal transition (EMT) process. We further discovered that both the expression of CMTM2 and the EMT-associated marker E-cadherin were decreased in the same thirty cases of HCC tissues compared with the corresponding adjacent non-tumor tissues. Pearson correlation test showed that there was a significantly positive correlation between CMTM2 and E-cadherin in HCC tissues (P<0.05). Conclusion: Based on the results of cell model and HCC tissues, our study suggests that down-regulated CMTM2 promotes HCC metastasis through inducing the EMT process.

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“…This process results from the induction of transcription factors that change gene expression, therefore promoting the loss of cell-cell adhesion, modifying cytoskeletal dynamics and leading to a change from epithelial morphology and physiology to the mesenchymal phenotype. EMT can be induced by various signaling pathways, for example mediated by transforming growth factor β (TGFβ), Wnt-β-catenin, Notch, Hedgehog receptor tyrosine kinases (RTK) [4,5].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, it was discovered both in vitro and in vivo that thyroid tumour cells from PTCs and anaplastic cancer (ATCs) may constitutively display an active EMT process when compared to normal thyrocytes. This results in the loss of cells' polarity, decreased expression of particular epithelial markers and increased expression of mesenchymal markers [5,6].…”

Section: Introductionmentioning

confidence: 99%

Snail-1 Overexpression Correlates with Metastatic Phenotype in BRAFV600E Positive Papillary Thyroid Carcinoma

Wieczorek-Szukała

Kopczyński

Kowalska

et al. 2020

JCM

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The ability of cancer to metastasize is regulated by various signaling pathways, including transforming growth factor β (TGFβ), also implicated in the upregulation of Snail-1 transcription factor in malignant neoplasms. B-type Raf kinase gene (BRAF)V600E, the most common driving mutation in papillary thyroid carcinoma (PTC), induces epithelial to mesenchymal transition (EMT) in thyroid cancer cells through changes in the Snail-1 level, increasing cell migration and invasion. However, little is known about the mechanism of Snail-1 and BRAFV600E relations in humans. Our study included 61 PTC patients with evaluated BRAFV600E mutation status. A total of 18 of those patients had lymph node metastases—of whom 10 were BRAFV600E positive, and 8 negative. Our findings indicate that the expression of Snail-1, but not TGFβ1, correlates with the metastatic phenotype in PTC. This is the first piece of evidence that the upregulation of Snail-1 corresponds with the presence of BRAFV600E mutation and increased expression of Snail-1 in metastatic PTC samples is dependent on BRAFV600E mutation status.

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Epithelial-to-mesenchymal transition in thyroid cancer: a comprehensive review

Cited by 63 publications

References 195 publications

RETRACTED: SHCBP1 Promotes Papillary Thyroid Carcinoma Carcinogenesis and Progression Through Promoting Formation of Integrin and Collagen and Maintaining Cell Stemness

RETRACTED: SHCBP1 Promotes Papillary Thyroid Carcinoma Carcinogenesis and Progression Through Promoting Formation of Integrin and Collagen and Maintaining Cell Stemness

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

Snail-1 Overexpression Correlates with Metastatic Phenotype in BRAFV600E Positive Papillary Thyroid Carcinoma

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