Functional and Mechanistic Insights into the Pathogenesis of P63-Associated Disorders

Mollo, Maria Rosaria; Cirillo, Luisa; Russo, Claudia; Antonini, Dario; Missero, Caterina

doi:10.1016/j.jisp.2018.10.004

Cited by 3 publications

(2 citation statements)

References 20 publications

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“…p63, a homolog of the well‐known tumor suppressor p53, contains several variant isoforms including the contain transactivation domain (TAp63) and the lack transactivation domain (ΔNp63) 72 . TAp63 acts as a tumor suppressor, but ΔNp63 is an oncoprotein 73 .…”

Section: Emt‐inducing Transcription Factorsmentioning

confidence: 99%

“…29,71 4.4 | ΔNp63 p63, a homolog of the well-known tumor suppressor p53, contains several variant isoforms including the contain transactivation domain (TAp63) and the lack transactivation domain (ΔNp63). 72 TAp63 acts as a tumor suppressor, but ΔNp63 is an oncoprotein. 73 Recent studies indicated that ΔNp63 is involved in tumor progression, because its upregulation is associated with the tumor grade and advanced stage in various types of squamous cell carcinoma include OSCC.…”

Section: Zeb Familymentioning

confidence: 99%

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Epithelial‐to‐mesenchymal transition in oral squamous cell carcinoma: Challenges and opportunities

Ling

Cheng

Tao

2020

Intl Journal of Cancer

134

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Oral squamous cell carcinoma (OSCC) is the most common malignancy representing 90% of all forms of oral cancer worldwide. Although great efforts have been made in the past decades, the 5‐year survival rate of OSCC patients is no more than 60% due to tumor metastasis and subsequent recurrence. The metastasis from the primary site is due to a complex process known as epithelial‐to‐mesenchymal transition (EMT). During the EMT, epithelial cells gradually acquire the structural and functional characteristics of mesenchymal cells, leading to the upregulation of cell migration and the promotion of tumor cell dissemination. Therefore, EMT attracted broad attention due to its close relationship with cancer invasion and metastasis. Therefore, in the present review, an extensive description of the current research on OSCC and the role of EMT in this cancer type is provided, including diverse EMT markers, regulatory networks and crucial EMT‐inducing transcription factors in OSCC. Moreover, a brief summary was made regarding the current application of EMT‐correlated indexes in the prognostic analysis of OSCC patients, and the potential therapeutic approaches against OSCC and difficulties in the development of an effective anti‐EMT treatment are discussed. Our aim is to provide novel insights to develop new strategies to combat OSCC by targeting EMT.

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Section: Emt‐inducing Transcription Factorsmentioning

confidence: 99%

Section: Zeb Familymentioning

confidence: 99%

Epithelial‐to‐mesenchymal transition in oral squamous cell carcinoma: Challenges and opportunities

Ling

Cheng

Tao

2020

Intl Journal of Cancer

134

View full text Add to dashboard Cite

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Unravelling the role of EMT in OSCC: A quick peek into HPV-mediated pathogenesis

Saraf

Suresh

Das

2023

Oral Oncology Reports

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Molecular Crosstalk between the Immunological Mechanism of the Tumor Microenvironment and Epithelial–Mesenchymal Transition in Oral Cancer

et al. 2022

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Oral cancer is a significant non-communicable disease affecting both emergent nations and developed countries. Squamous cell carcinoma of the head and neck represent the eight major familiar cancer types worldwide, accounting for more than 350,000 established cases every year. Oral cancer is one of the most exigent tumors to control and treat. The survival rate of oral cancer is poor due to local invasion along with recurrent lymph node metastasis. The tumor microenvironment contains a different population of cells, such as fibroblasts associated with cancer, immune-infiltrating cells, and other extracellular matrix non-components. Metastasis in a primary site is mainly due to multifaceted progression known as epithelial-to-mesenchymal transition (EMT). For the period of EMT, epithelial cells acquire mesenchymal cell functional and structural characteristics, which lead to cell migration enhancement and promotion of the dissemination of tumor cells. The present review links the tumor microenvironment and the role of EMT in inflammation, transcriptional factors, receptor involvement, microRNA, and other signaling events. It would, in turn, help to better understand the mechanism behind the tumor microenvironment and EMT during oral cancer.

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Functional and Mechanistic Insights into the Pathogenesis of P63-Associated Disorders

Cited by 3 publications

References 20 publications

Epithelial‐to‐mesenchymal transition in oral squamous cell carcinoma: Challenges and opportunities

Epithelial‐to‐mesenchymal transition in oral squamous cell carcinoma: Challenges and opportunities

Unravelling the role of EMT in OSCC: A quick peek into HPV-mediated pathogenesis

Molecular Crosstalk between the Immunological Mechanism of the Tumor Microenvironment and Epithelial–Mesenchymal Transition in Oral Cancer

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