Schwann Cells Induce Phenotypic Changes in Oral Cancer Cells.
Schwann cells
invasion
metabolism
metastasis
oral squamous cell carcinoma
perineural invasion
proliferation
Journal
Advanced biology
ISSN: 2701-0198
Titre abrégé: Adv Biol (Weinh)
Pays: Germany
ID NLM: 101775319
Informations de publication
Date de publication:
09 2022
09 2022
Historique:
revised:
18
07
2022
received:
04
07
2022
pubmed:
5
8
2022
medline:
14
9
2022
entrez:
4
8
2022
Statut:
ppublish
Résumé
Head and neck cancer (HNC) is the seventh most common cancer worldwide, the majority being oral squamous cell carcinoma. Despite advances in cancer diagnosis and treatment, the survival rate of patients with HNC remains stagnant. The cancer-nerve interaction has been recognized as an important driver of cancer progression. Schwann cells, a type of peripheral glia, have been implicated in promoting cancer cell growth, migration, dispersion, and invasion into the nerve in many cancers. Here, it is demonstrated that the presence of Schwann cells makes oral cancer cells more aggressive by promoting their proliferation, extracellular matrix breakdown, and altering cell metabolism. Furthermore, oral cancer cells became larger, more circular, with more projections and nuclei following co-culturing with Schwann cells. RNA-sequencing analysis in oral cancer cells following exposure to Schwann cells shows corresponding changes in genes involved in the hallmarks of cancer and cell metabolism; the enriched KEGG pathways are spliceosome, RNA transport, cell cycle, axon guidance, signaling pathways regulating pluripotency of stem cells, cAMP signaling, WNT signaling, proteoglycans in cancer and PI3K-Akt signaling. Taken together, these results suggest a significant role for Schwann cells in facilitating oral cancer progression, highlighting their potential as a target to treat oral cancer progression.
Identifiants
pubmed: 35925609
doi: 10.1002/adbi.202200187
pmc: PMC9474679
mid: NIHMS1828822
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2200187Subventions
Organisme : NIDCR NIH HHS
ID : K23 DE030250
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE029493
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE031395
Pays : United States
Organisme : NIDCR NIH HHS
ID : R03 DE027777
Pays : United States
Informations de copyright
© 2022 Wiley-VCH GmbH.
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