EBV-Associated Hub Genes as Potential Biomarkers for Predicting the Prognosis of Nasopharyngeal Carcinoma

Ding, Tengteng; Zhang, Yuanbin; Ren, Zhixuan; Cong, Ying; Long, Jingyi; Peng, Manli; Faleti, Oluwasijibomi Damola; Yang, Yinggui; Li, Xin; Lyu, Xiaoming

doi:10.3390/v15091915

Cited by 1 publication

(1 citation statement)

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“…Although its function is unknown, overall C16orf54 appears as a potential marker of the poor prognosis of various tumours, suggesting that C16orf54 may participate in the progression of tumours ( Du et al, 2022 ). C16orf54 expression is significantly associated with various immune-related pathways, such as PI3K/Akt/mTOR and Wnt/Beta catenin signalling pathways, inflammatory response, and interferon-gamma response ( Ding et al, 2023 ). However, its specific biological function is still obscure and its role in 16p11.2 CNVs has not been investigated yet.…”

Section: Role Of the 16p112 Genesmentioning

confidence: 99%

Understanding copy number variations through their genes: a molecular view on 16p11.2 deletion and duplication syndromes

Leone,

Zuglian,

Brambilla

et al. 2024

Front. Pharmacol.

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Neurodevelopmental disorders (NDDs) include a broad spectrum of pathological conditions that affect >4% of children worldwide, share common features and present a variegated genetic origin. They include clinically defined diseases, such as autism spectrum disorders (ASD), attention-deficit/hyperactivity disorder (ADHD), motor disorders such as Tics and Tourette’s syndromes, but also much more heterogeneous conditions like intellectual disability (ID) and epilepsy. Schizophrenia (SCZ) has also recently been proposed to belong to NDDs. Relatively common causes of NDDs are copy number variations (CNVs), characterised by the gain or the loss of a portion of a chromosome. In this review, we focus on deletions and duplications at the 16p11.2 chromosomal region, associated with NDDs, ID, ASD but also epilepsy and SCZ. Some of the core phenotypes presented by human carriers could be recapitulated in animal and cellular models, which also highlighted prominent neurophysiological and signalling alterations underpinning 16p11.2 CNVs-associated phenotypes. In this review, we also provide an overview of the genes within the 16p11.2 locus, including those with partially known or unknown function as well as non-coding RNAs. A particularly interesting interplay was observed between MVP and MAPK3 in modulating some of the pathological phenotypes associated with the 16p11.2 deletion. Elucidating their role in intracellular signalling and their functional links will be a key step to devise novel therapeutic strategies for 16p11.2 CNVs-related syndromes.

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Section: Role Of the 16p112 Genesmentioning

confidence: 99%