HRAS-driven cancer cells are vulnerable to TRPML1 inhibition.
Animals
Calcium
/ metabolism
Calcium Signaling
Cell Membrane
/ metabolism
Cell Proliferation
Drosophila
Endosomes
/ metabolism
Extracellular Signal-Regulated MAP Kinases
/ metabolism
Gene Expression
Gene Regulatory Networks
Humans
Lysosomes
/ metabolism
Models, Biological
Mutation
Neoplasms
/ genetics
Phosphorylation
Prognosis
Proto-Oncogene Proteins p21(ras)
/ genetics
Signal Transduction
Transcriptome
Transient Receptor Potential Channels
/ antagonists & inhibitors
HRAS
TRPML1
cancer
cholesterol
endolysosomes
Journal
EMBO reports
ISSN: 1469-3178
Titre abrégé: EMBO Rep
Pays: England
ID NLM: 100963049
Informations de publication
Date de publication:
04 2019
04 2019
Historique:
received:
03
07
2018
revised:
28
01
2019
accepted:
01
02
2019
pubmed:
23
2
2019
medline:
1
5
2020
entrez:
22
2
2019
Statut:
ppublish
Résumé
By serving as intermediaries between cellular metabolism and the bioenergetic demands of proliferation, endolysosomes allow cancer cells to thrive under normally detrimental conditions. Here, we show that an endolysosomal TRP channel, TRPML1, is necessary for the proliferation of cancer cells that bear activating mutations in
Identifiants
pubmed: 30787043
pii: embr.201846685
doi: 10.15252/embr.201846685
pmc: PMC6446245
pii:
doi:
Substances chimiques
MCOLN1 protein, human
0
Transient Receptor Potential Channels
0
Extracellular Signal-Regulated MAP Kinases
EC 2.7.11.24
HRAS protein, human
EC 3.6.5.2
Proto-Oncogene Proteins p21(ras)
EC 3.6.5.2
Calcium
SY7Q814VUP
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NCI NIH HHS
ID : P30 CA125123
Pays : United States
Organisme : NCI NIH HHS
ID : R00 CA188593
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS081301
Pays : United States
Organisme : NINDS NIH HHS
ID : R21 NS094860
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2019 The Authors.
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