KIF22 promotes the proliferation and glycolysis of melanoma by activating EGFR/STAT3 signaling.
EGFR/STAT3 signaling
Glycolysis
KIF22
Melanoma
Proliferation
Journal
Clinics (Sao Paulo, Brazil)
ISSN: 1980-5322
Titre abrégé: Clinics (Sao Paulo)
Pays: United States
ID NLM: 101244734
Informations de publication
Date de publication:
2023
2023
Historique:
received:
01
08
2023
revised:
23
10
2023
accepted:
25
10
2023
medline:
24
11
2023
pubmed:
9
11
2023
entrez:
9
11
2023
Statut:
epublish
Résumé
Melanoma is one of the leading causes of cancer death. Kinesin Family member 22 (KIF22) is essential for the invasion of melanoma cells, but the role and mechanism of KIF22 in the proliferation and glycolysis in melanoma remains unknown. KIF22 expression in melanoma tissues and the relationship between KIF22 high expression and overall survival rate in patients with melanoma were analyzed using the Tnmplot database. KIF22 expression in melanoma cells was examined by western blot. Then, KIF22 was silenced and CCK-8 assay, EDU staining and flow cytometry analysis were adopted for assessing cell proliferation and apoptosis. In addition, the glycolysis metabolism of melanoma cells was reflected by detecting Extracellular Acidification Rates (ECAR) and Oxygen Consumption Rates (OCR). The expression of proteins related to apoptosis, glycolysis and EGFR/STAT3 signaling was tested by western blot. Subsequently, melanoma cells were treated with EGF or Colivelin to further elucidate the regulatory effect of KIF22 on EGFR/STAT3 signaling. KIF22 expression was notably upregulated in melanoma tissues and cells, and KIF22 high expression was associated with a poor prognosis. Moreover, KIF22 insufficiency suppressed proliferation and accelerated apoptosis of melanoma cells. Additionally, glycolysis was reduced by KIF22 depletion, evidenced by the decreased ECAR and increased OCR, accompanied by the downregulated expression of HK2, PKM2 and LDHA. Importantly, the impacts of KIF22 depletion on the progression of melanoma were partially attenuated after EGF or Colivelin treatment. Collectively, KIF22 knockdown suppressed the proliferation and glycolysis and facilitated the apoptosis of melanoma cells by inactivating EGFR/STAT3 signaling.
Identifiants
pubmed: 37944197
pii: S1807-5932(23)00143-6
doi: 10.1016/j.clinsp.2023.100307
pmc: PMC10661841
pii:
doi:
Substances chimiques
Epidermal Growth Factor
62229-50-9
ErbB Receptors
EC 2.7.10.1
KIF22 protein, human
0
DNA-Binding Proteins
0
Kinesins
EC 3.6.4.4
STAT3 protein, human
0
STAT3 Transcription Factor
0
EGFR protein, human
EC 2.7.10.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
100307Informations de copyright
Copyright © 2023 HCFMUSP. Published by Elsevier España, S.L.U. All rights reserved.
Déclaration de conflit d'intérêts
Conflicts of interest The authors declare no conflicts of interest.
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