Biological role of epithelial–mesenchymal-transition-inducing transcription factors in head and neck squamous cell carcinoma: A systematic review

Morais, Everton Freitas de; Rolim, Larissa Santos Amaral; Almeida, Dennys Ramon de Melo Fernandes; Morais, Hannah Gil de Farias; Souza, Lélia Batista de; Freitas, Roseana de Almeida

doi:10.1016/j.archoralbio.2020.104904

Cited by 20 publications

(16 citation statements)

References 47 publications

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“…Our data showed that SLUG directly or indirectly affects the expression levels of SNAIL and vimentin, which is consistent with previous reports 4,20 . On the other hand, SLUG hardly affected the expression of E‐cadherin.…”

Section: Discussionsupporting

confidence: 93%

“…The transitioned cells acquire the ability to invade the tissues around the primary lesion, such as fibrous stroma and vessels, leading to metastasis to distant organs. EMT is regulated by some transcription factors such as SNAIL, SLUG, Zinc Finger E‐Box Binding Homeobox 1 (ZEB1), and TWIST 4 . SNAIL and SLUG are members of the Snail family of zinc‐finger transcription factors and the best studied EMT transcription factors, and they are known to be critical inducers of the EMT process 5–8 .…”

Section: Introductionmentioning

confidence: 99%

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SLUG is upregulated and induces epithelial mesenchymal transition in canine oral squamous cell carcinoma

Noguchi

Hirano

Tanimoto

et al. 2021

Vet Comparative Oncology

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SLUG, encoded by the Snai2 gene, is known to play a role in epithelial-mesenchymal transition (EMT), which contributes to cell invasion and metastasis in some types of human carcinomas. However, the mechanisms and roles of EMT in canine squamous cell carcinoma (SCC) have not yet been elucidated. We have previously established canine oral SCC cell lines, including tonsillar SCC, and in this study, we evaluated the effects of SLUG on the phenotypes regarding EMT of canine SCC cells. First, immunohistochemical analysis revealed that SLUG is upregulated in canine oral SCC tissues compared to that in non-tumoural oral mucosa. Furthermore, gain-of-function and loss-of-function of SLUG revealed that SLUG partly contributed to migration and invasion of cells, as well as the upregulation of EMT markers such as vimentin and SNAIL. Thus, the current study suggests that SLUG promotes cell migration and invasion through EMT induction in canine oral SCC, as well as human cancers.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

SLUG is upregulated and induces epithelial mesenchymal transition in canine oral squamous cell carcinoma

Noguchi

Hirano

Tanimoto

et al. 2021

Vet Comparative Oncology

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“…In addition, GIT1 was found to be upregulated in OSCC [ 13 ]. EMT is the initial step of tumor cell invasion and metastasis [ 14 ]. However, the effect of GIT1 on HNSCC tumor's multiplication and EMT progression in vivo is still unknown.…”

Section: Introductionmentioning

confidence: 99%

G-Protein-Coupled Receptor Kinase-Interacting Protein 1 (GIT1) Promotes Head and Neck Squamous Cell Carcinoma Metastases via Activating the PI3K/AKT/mTOR Signal Pathway

Xu²,

Wang³

et al. 2022

Computational and Mathematical Methods in Medicine

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Objective. GIT1 is identified as a novel tumor oncogene in breast cancer. In this article, we aimed to explore the role of GIT1 in the progression of head and neck squamous cell carcinoma (HNSCC). Methods. GIT1 expression in HNSCC was detected by RT-qPCR, immunohistochemistry assay, and Western blot. HNSCC cell proliferation, migration, and invasion were examined by CCK-8 assay, Wound healing assay, and Transwell assay, respectively. Cell apoptosis was detected by flow cytometric analysis. Results. In our study, GIT1 was notably upregulated in HNSCC tissues and cells. Moreover, GIT1 expression level had positive corelation with pathological grade and nodal status of HNSCC. Functional experiments showed that knockdown of GIT1 restrained HNSCC proliferation, invasion, migration, and EMT and facilitated cell apoptosis. Furthermore, GIT1 knockdown was found to restrain HNSCC tumor growth and lung metastasis. Additionally, PI3K/AKT/mTOR signal pathway inhibitors suppressed the effect of GIT1 on HNSCC cell progression. Conclusion. GIT1 was upregulated in HNSCC and facilitated HNSCC cell progression by inducing PI3K/AKT/mTOR signal pathway. Therefore, we suggested that GIT1 might be a potential target for HNSCC treatment.

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“…It is recognized that EMT plays a crucial role in drug resistance [ 39 ]. For example, the suppression of EMT-inducing transcription factors can enhance the chemotherapy sensitivity of head and neck squamous cell carcinoma cells [ 40 ]. Moreover, upregulation of FBXL11 is closely associated with tumorigenesis and lymph node metastasis.…”

Section: Discussionmentioning

confidence: 99%

Nuclear receptor binding SET domain protein 1 promotes epithelial-mesenchymal transition in paclitaxel-resistant breast cancer cells via regulating nuclear factor kappa B and F-box and leucine-rich repeat protein 11

et al. 2021

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Breast cancer (BC) is regarded as the major cause of cancer-associated deaths in women. Paclitaxel exerts a critical impact on the chemotherapy of BC, but the resistance to paclitaxel becomes a great obstacle in treating the disease. It is reported that noncoding RNA nuclear receptor binding SET domain protein 1 (NSD1) plays a significant role in drug resistance; however, the special role of NSD1 in paclitaxel-resistant BC is unclear. Human BC cell line MCF-7 was used to establish paclitaxel-resistant BC cells (MCF-7/PR). Reverse transcription quantitative polymerase chain reaction (RT-qPCR) displayed that NSD1 and F-box and leucine-rich repeat protein 11 (FBXL11) were highly expressed in BC tissues. Western blotting was utilized for protein level assessment. Cell counting kit-8 (CCK-8), Transwell, wound healing assays, and animal experiments were conducted to examine the influence of NSD1 or FBXL11 on the malignant behaviors of BC in vitro and in vivo , respectively. Transfected MCF-7/PR cells were injected subcutaneously into BALB/c nude mice with or without treatment of paclitaxel. The nuclear factor kappa B (NF-kB) activity was evaluated by the luciferase reporter assay. Results showed that NSD1 knockdown inhibited the epithelial-mesenchymal transition (EMT), migration and invasiveness of BC in vitro , which was rescued by FBXL11 overexpression. Furthermore, NSD1 silencing promoted paclitaxel sensitivity of paclitaxel-resistant BC cells and suppressed tumor growth and paclitaxel resistance in vivo . NSD1 knockdown reduced NF-kB activity, while FBXL11 inhibition markedly increased NF-kB activity. Collectively, NSD1 facilitates the EMT, migration and invasion in paclitaxel-resistant BC cells via regulating NF-kB and FBXL11.

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Biological role of epithelial–mesenchymal-transition-inducing transcription factors in head and neck squamous cell carcinoma: A systematic review

Cited by 20 publications

References 47 publications

SLUG is upregulated and induces epithelial mesenchymal transition in canine oral squamous cell carcinoma

SLUG is upregulated and induces epithelial mesenchymal transition in canine oral squamous cell carcinoma

G-Protein-Coupled Receptor Kinase-Interacting Protein 1 (GIT1) Promotes Head and Neck Squamous Cell Carcinoma Metastases via Activating the PI3K/AKT/mTOR Signal Pathway

Nuclear receptor binding SET domain protein 1 promotes epithelial-mesenchymal transition in paclitaxel-resistant breast cancer cells via regulating nuclear factor kappa B and F-box and leucine-rich repeat protein 11

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