Identification of genetic mechanisms underlying lipid metabolism-mediated tumor immunity in head and neck squamous cell carcinoma

Liu, Shaokun; Wang, Shuning; Wang, Zhenlin

doi:10.1186/s12920-023-01543-6

Cited by 3 publications

(1 citation statement)

References 61 publications

(61 reference statements)

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“…The integration of these data with the protein-protein interaction (PPI) network models, as well as the reconstruction of bipartite miRNA-target networks, have proved useful in providing valuable insights into the molecular alterations associated with the disease state. Globally, the identification of more than eight hundred high-confidence differentially expressed genes emphasizes the substantial genomic modulation that occurs in HNSCC as highlighted in other studies [53,54]. Corresponding functional modules highlight the cytoskeletal regulation, immune system, extracellular matrix (ECM), energy metabolism and proteolysis as major players involved in the pathogenesis of HNSCC.…”

Section: Discussionmentioning

confidence: 94%

Differentially Expressed Genes, miRNAs and Network Models: A Strategy to Shed Light on Molecular Interactions Driving HNSCC Tumorigenesis

Arfin,

Kumar,

Lomagno

et al. 2023

Cancers

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Head and neck squamous cell carcinoma (HNSCC) is among the most common cancer worldwide, accounting for hundreds thousands deaths annually. Unfortunately, most patients are diagnosed in an advanced stage and only a percentage respond favorably to therapies. To help fill this gap, we hereby propose a retrospective in silico study to shed light on gene–miRNA interactions driving the development of HNSCC. Moreover, to identify topological biomarkers as a source for designing new drugs. To achieve this, gene and miRNA profiles from patients and controls are holistically reevaluated using protein–protein interaction (PPI) and bipartite miRNA–target networks. Cytoskeletal remodeling, extracellular matrix (ECM), immune system, proteolysis, and energy metabolism have emerged as major functional modules involved in the pathogenesis of HNSCC. Of note, the landscape of our findings depicts a concerted molecular action in activating genes promoting cell cycle and proliferation, and inactivating those suppressive. In this scenario, genes, including VEGFA, EMP1, PPL, KRAS, MET, TP53, MMPs and HOXs, and miRNAs, including mir-6728 and mir-99a, emerge as key players in the molecular interactions driving HNSCC tumorigenesis. Despite the heterogeneity characterizing these HNSCC subtypes, and the limitations of a study pointing to relationships that could be context dependent, the overlap with previously published studies is encouraging. Hence, it supports further investigation for key molecules, both those already and not correlated to HNSCC.

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Section: Discussionmentioning

confidence: 94%