Nouveautés dans la prise en charge des carcinomes nasopharyngés

Blanchard, Pierre; Nguyen, F.; Moya‐Plana, Antoine; Pignon, Jean-Pierre; Even, Caroline; Bidault, François; Temam, Stéphane; Ruffier, A.; Tao, Yungan

doi:10.1016/j.canrad.2018.06.003

Cited by 11 publications

(10 citation statements)

References 23 publications

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“…NPC is still a serious health problem with remarkable ethnic and geographic distribution in southern China and Southeast Asia [ 1 ]. Recently, epigenetic abnormalities are reported to play important roles in tumor development [ 37 ], and TET protein family, which demethylates DNA via catalyzing 5-mC to 5-hmC, are found to be participated in several tumor pathogenesis [ 8 – 14 ].…”

Section: Discussionmentioning

confidence: 99%

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TET2 suppresses nasopharyngeal carcinoma progression by inhibiting glycolysis metabolism

et al. 2020

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Background Nasopharyngeal carcinoma (NPC) is a common malignant tumor. Ten-eleven translocation (TET) protein 2 (TET2), an evolutionarily conserved dioxygenases, is reported to be involved in various malignant tumor developments. Here, we aim to investigate the effect of TET2 on NPC progress in vitro and in vivo, and its detailed underlying mechanism. Methods Real-time PCR and western blotting were used to determine the expression levels of TET1/2/3 in NPC cell lines. The effects of TET2 on NPC progression were evaluated using CCK8 and invasion assays in vitro. Proteins interacted with TET2 in NPC cells were detected by immunoprecipitation and mass spectrometry. The effects of TET2 or pyruvate kinase, muscle (PKM) on glycolysis in NPC cells were examined by detecting glucose uptake and lactate production. The effects of TET2 on NPC progression were evaluated using xenograft tumor model in vivo. Results TET2 expression was decreased in NPC cells, and TET2 overexpression inhibited proliferation and invasion of NPC cells, which is independent on TET2’s catalytic activity. In mechanism, TET2 N-terminal domain interacts with PKM in cytoplasm to prevent PKM dimers from translocating into nucleus, suppressing glycolysis in NPC cells, thereby inhibiting proliferation and invasion of NPC cells. Moreover, using xenograft tumor model, we found that TET2 knockout promoted NPC progression and decreased survival rate. However, administration with the inhibitor of PKM, shikonin, decreased the tumor volume of TET2-cas9 group, and increased the survival rate. Conclusion TET2 suppresses NPC development through interacting with PKM to inhibit glycolysis.

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Section: Discussionmentioning

confidence: 99%

“…Nasopharyngeal carcinoma (NPC) is characterized by distinct geographical distribution and has a high incidence in southeast Asia and north Africa [ 1 ]. Multiple factors, such as Epstein-Barr virus infection, host genetics, and environmental factors contribute to NPC development [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

TET2 suppresses nasopharyngeal carcinoma progression by inhibiting glycolysis metabolism

et al. 2020

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“…Great technological progress has been achieved in radiation therapy over the past decades, which greatly improve the outcome of NPC patient, with an 8-year overall survival (OS) of 68.5% and progression-free survival (PFS) of 62.6% in total patients as reported by Au et al 22 However, the N stage still regarded as a single adverse prognostic factor for NPC regional control, and distant metastasis is the most common form of treatment failure. 23,24 Therefore, a better and clearer understanding of the molecular mechanism of NPC invasion and metastasis is needed.…”

Section: Discussionmentioning

confidence: 99%

<p>MiR-154-5p Suppresses Cell Invasion and Migration Through Inhibiting KIF14 in Nasopharyngeal Carcinoma</p>

Chen¹,

Ma²,

Zhang³

et al. 2020

OTT

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Background: Mounting evidence has reported that microRNA-154-5p (miR-154-5p) is involved in the development of multiple cancers, but its function in nasopharyngeal carcinoma (NPC) remains not well investigated. Methods: Real-time quantitative PCR (qRT-PCR) was used to detect miR-154-5p expression in NPC tissues and cells. CCK8, colony formation, wound healing and transwell assays were performed to assess cell proliferation, migration and invasion. Dual-luciferase reporter assays and Western blots were performed to confirm the target gene of miR-154-5p. Rescue experiments were conducted to explore the influence of target gene KIF14 on the functions of miR-154-5p. Xenograft tumor model was conducted to detect the effect of miR-154-5p in vivo. Results: qRT-PCR results revealed that the expression of miR-154-5p was down-regulated in NPC tissues and cell lines compared to normal nasopharyngeal tissues and cell line. Overexpression of miR-154-5p inhibited cell migration and invasion. However, miR-154-5p had no influence on the proliferation of NPC cells. MiR-154-5p overexpression suppressed xenograft tumor metastasis in vivo. Dual-luciferase reporter analysis identified KIF14 as a target gene of miR-154-5p. Rescue experiments showed that knockdown of KIF14 reversed the effect of inhibiting miR-154-5p expression on NPC cell migration and invasion. Conclusion: Taken together, miR-154-5p suppresses tumor migration and invasion by targeting KIF14 in NPC. The newly identified miR-154-5p/KIF14 interaction offers further insights into the progression of NPC, which may represent a novel target for NPC diagnosis and treatment.

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“…It is effective for all cases except distant metastases [54]. NPCs are also highly chemosensitive; hence, in advanced regional disease, chemoradiotherapy is the mainstay of treatment, while chemotherapy is the management of choice when distant metastases are involved [55]. The nasopharynx is a small and deep region, rendering surgical access difficult.…”

Section: Nasopharyngeal Carcinomamentioning

confidence: 99%

From Basic Mechanisms to Clinical Research: Photodynamic Therapy Applications in Head and Neck Malignancies and Vascular Anomalies

Ramsay

Stevenson

Jerjes

2021

JCM

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Head and neck cancers are largely squamous cell carcinomas derived from the epithelial lining of the structures in the region, and are often classified anatomically into oral, oropharyngeal, nasopharyngeal and laryngeal carcinomas. The region’s component structures serve complex and intricate functions, such as speaking, swallowing and breathing, which are often compromised by these neoplasms. Such lesions may also cause disfigurement, leading to distressing social and psychological issues. Conventional treatments of these neoplasms usually involve surgical intervention with or without chemoradiotherapy. These have shown to be efficacious; however, they can also cause damage to healthy as well as diseased tissue, exacerbating the aforementioned problems. Access to a given region to deliver the treatments is also often a problem, due to the complex anatomical structures involved. The use of photodynamic therapy in the head and neck region has been established for about two decades. In this review, we looked at the basic mechanisms of this intervention, examined its use in common head and neck malignancies and vascular anomalies, and reported on the most recent clinical studies. We further included a clinical guide which can help replicate the use of this technology by any unit. Based on this review, photodynamic therapy has been shown to be efficacious in the treatment of head and neck malignancies and vascular tumours. This therapy can be targeted to the diseased tissue and causes no damage to underlying structures. Recent studies have shown this therapy to be as effective as conventional therapies, without causing major adverse effects.

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Nouveautés dans la prise en charge des carcinomes nasopharyngés

Cited by 11 publications

References 23 publications

TET2 suppresses nasopharyngeal carcinoma progression by inhibiting glycolysis metabolism

TET2 suppresses nasopharyngeal carcinoma progression by inhibiting glycolysis metabolism

<p>MiR-154-5p Suppresses Cell Invasion and Migration Through Inhibiting KIF14 in Nasopharyngeal Carcinoma</p>

From Basic Mechanisms to Clinical Research: Photodynamic Therapy Applications in Head and Neck Malignancies and Vascular Anomalies

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