Radiotherapy for oral cavity cancers

Lapeyre, M.; Racadot, S.; Renard, S.; Biau, J.; Moreira, J.; Biston, M.C.; Pointreau, Y.; Thariat, Juliette; Graff-Cailleaud, Pierre

doi:10.1016/j.canrad.2021.11.012

Cited by 8 publications

(4 citation statements)

References 60 publications

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“…OSCC is a malignant tumor with a poor prognosis, accounting for more than 90% of all oral cancers. Radiotherapy is a common treatment for patients with OSCC; the treatment effectively inhibits tumor growth, increases the probability of patient survival, and improves patients’ quality of life [ 19 ]. However, the response of patients with OSCC varies widely, with increasing incidence of resistance to RT [ 20 ], greatly limiting the RT efficacy.…”

Section: Discussionmentioning

confidence: 99%

SALL4 promotes cancer stem-like cell phenotype and radioresistance in oral squamous cell carcinomas via methyltransferase-like 3-mediated m6A modification

Huang,

Li,

Yang

et al. 2024

Cell Death Dis

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Radioresistance imposes a great challenge in reducing tumor recurrence and improving the clinical prognosis of individuals having oral squamous cell carcinoma (OSCC). OSCC harbors a subpopulation of CD44(+) cells that exhibit cancer stem-like cell (CSC) characteristics are involved in malignant tumor phenotype and radioresistance. Nevertheless, the underlying molecular mechanisms in CD44( + )-OSCC remain unclear. The current investigation demonstrated that methyltransferase-like 3 (METTL3) is highly expressed in CD44(+) cells and promotes CSCs phenotype. Using RNA-sequencing analysis, we further showed that Spalt-like transcription factor 4 (SALL4) is involved in the maintenance of CSCs properties. Furthermore, the overexpression of SALL4 in CD44( + )-OSCC cells caused radioresistance in vitro and in vivo. In contrast, silencing SALL4 sensitized OSCC cells to radiation therapy (RT). Mechanistically, we illustrated that SALL4 is a direct downstream transcriptional regulation target of METTL3, the transcription activation of SALL4 promotes the nuclear transport of β-catenin and the expression of downstream target genes after radiation therapy, there by activates the Wnt/β-catenin pathway, effectively enhancing the CSCs phenotype and causing radioresistance. Herein, this study indicates that the METTL3/SALL4 axis promotes the CSCs phenotype and resistance to radiation in OSCC via the Wnt/β-catenin signaling pathway, and provides a potential therapeutic target to eliminate radioresistant OSCC.

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Section: Discussionmentioning

confidence: 99%

SALL4 promotes cancer stem-like cell phenotype and radioresistance in oral squamous cell carcinomas via methyltransferase-like 3-mediated m6A modification

Huang,

Li,

Yang

et al. 2024

Cell Death Dis

View full text Add to dashboard Cite

show abstract

“…OSCC is a malignant tumor with a poor prognosis, accounting for more than 90% of all oral cancers. Radiotherapy is a common treatment for patients with OSCC; the treatment effectively inhibits tumor growth, increases the probability of patient survival, and improves patients' quality of life [19]. However, the response of patients with OSCC varies widely, with increasing incidence of resistance to RT [20], greatly limiting the RT e cacy.…”

Section: Discussionmentioning

confidence: 99%

SALL4 promotes cancer stem-like cell phenotype and radioresistance in oral squamous cell carcinomas via methyltransferase-like 3-mediated m6A modification

Wei,

Huang,

et al. 2023

Preprint

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Radioresistance imposes a great challenge in reducing tumor recurrence and improving the clinical prognosis of individuals having oral squamous cell carcinoma (OSCC). OSCC harbors a subpopulation of CD44(+) cells that exhibit cancer stem-like cell (CSC) characteristics are involved in malignant tumor phenotype and radioresistance. Nevertheless, the underlying molecular mechanisms in CD44(+)-OSCC remain unclear. The current investigation demonstrated that methyltransferase-like 3 (METTL3) is highly expressed in CD44(+) cells and promotes CSCs phenotype. Using RNA-sequencing analysis, we further showed that Spalt-like transcription factor 4 (SALL4) is involved in the maintenance of CSCs properties. Furthermore, the overexpression of SALL4 in CD44(+)-OSCC cells caused radioresistance in vitro and in vivo. In contrast, silencing SALL4 sensitized OSCC cells to radiation therapy (RT). Mechanistically, we illustrated that SALL4 is a direct downstream transcriptional regulation target of METTL3, the transcription activation of SALL4 promotes the nuclear transport of β-catenin and the expression of downstream target genes after radiation therapy; thereby activates the Wnt/β-catenin pathway, effectively enhancing the CSCs phenotype and causing radioresistance. Herein, this study indicates that the METTL3/SALL4 axis promotes the CSCs phenotype and resistance to radiation in OSCC via the Wnt/β-catenin signaling pathway, and provides a potential therapeutic target to eliminate radioresistant OSCC.

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“…Surgery has become the gold standard for neck management in OSCC patients. Currently, only those patients who are unsuitable for, or unwilling to undergo, surgery will consider radical radiotherapy as a neck treatment 78 . Since 2009, intensity‐modulated radiation therapy (IMRT) has progressively replaced traditional radiation therapy for neck LNM.…”

Section: Neck Management For Osccmentioning

confidence: 99%

“…Currently, only those patients who are unsuitable for, or unwilling to undergo, surgery will consider radical radiotherapy as a neck treatment. 78 Since 2009, intensity-modulated radiation therapy (IMRT) has progressively replaced traditional radiation therapy for neck LNM. As the most precise radiation therapy technique, IMRT delivers smallest possible dose and radiation field to achieve optimal clinical outcomes.…”

Section: Association Between Radiotherapy and Clnsmentioning

confidence: 99%

Lymph node metastasis in oral squamous cell carcinoma: Where we are and where we are going

Cao

Zhong

et al. 2023

Clinical and Translational Dis

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BackgroundOral cancer is a common malignant tumour in the head and neck region, with over 90% of cases being oral squamous cell carcinoma (OSCC). Lymph node metastasis (LNM) is a significant adverse prognostic factor in OSCC; however, the mechanism of LNM in OSCC remains unclear, while the strategies for managing cervical lymph nodes (CLNs) in OSCC continue to evolve. At present, neck dissection is necessary for the vast majority of OSCC patients, but complications of surgery can significantly impair patients’ postoperative quality of life. A recent clinical trial discovery indicates that immunotherapy can activate anti‐tumour T cells in nearby lymph nodes, leading to vibrant discussions among clinicians about the importance of preserving lymph nodes during surgical treatment.AimThis review aims to provide an overview of where we are: the current knowledge of OSCC LNM patterns and management strategies, and where we are going: prospects for clinical and basic research on the issue of OSCC LNM in the era of cancer immunotherapy.ResultWe summarize the general patterns and management strategies of OSCC LNM. The process of LNM in OSCC encompasses four stages: Preparation, Unleash, Migration, and Planting (‘PUMP’ principle). We propose adopting the ‘PRECISE’ model, an overall workflow that includes seven elements—prevention, radiology, preoperative evaluation, chemotherapy, immunotherapy, surgery, and postoperative evaluation—for neck management in OSCC, promoting personalized precision medicine augmented by neoadjuvant therapy. We further discussed recent advances in clinical and basic research on OSCC LNM and provided an outlook on future research directions.ConclusionOver the past two centuries, our understanding and management strategies of LNM in OSCC have evolved, seeking more precise and personalized approaches to reduce patient burden and enhance survival and quality of life. Further research should explore lymph nodes’ role in cancer immunotherapy and OSCC interactions, leading to better, less invasive treatments and improved outcomes.

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Radiotherapy for oral cavity cancers

Cited by 8 publications

References 60 publications

SALL4 promotes cancer stem-like cell phenotype and radioresistance in oral squamous cell carcinomas via methyltransferase-like 3-mediated m6A modification

SALL4 promotes cancer stem-like cell phenotype and radioresistance in oral squamous cell carcinomas via methyltransferase-like 3-mediated m6A modification

SALL4 promotes cancer stem-like cell phenotype and radioresistance in oral squamous cell carcinomas via methyltransferase-like 3-mediated m6A modification

Lymph node metastasis in oral squamous cell carcinoma: Where we are and where we are going

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