Membrane metallo-endopeptidase mediates cellular senescence induced by oncogenic PIK3CA
Animals
Breast Neoplasms
/ enzymology
Cell Line, Tumor
Cell Proliferation
Cellular Senescence
/ physiology
Chemokine CCL2
/ metabolism
Class I Phosphatidylinositol 3-Kinases
/ antagonists & inhibitors
Epithelial Cells
/ cytology
Glycosylation
Humans
Interleukin-6
/ metabolism
Mammary Glands, Human
/ cytology
Metalloendopeptidases
/ metabolism
Mice
Mice, Inbred BALB C
Proto-Oncogene Proteins c-akt
/ antagonists & inhibitors
TOR Serine-Threonine Kinases
/ antagonists & inhibitors
Tumor Suppressor Protein p53
/ metabolism
PI3Kα
breast cancer
macrophage
membrane metallo-endopeptidase
senescence
Journal
International journal of cancer
ISSN: 1097-0215
Titre abrégé: Int J Cancer
Pays: United States
ID NLM: 0042124
Informations de publication
Date de publication:
01 08 2019
01 08 2019
Historique:
received:
20
07
2018
revised:
05
12
2018
accepted:
08
01
2019
pubmed:
24
1
2019
medline:
18
12
2019
entrez:
24
1
2019
Statut:
ppublish
Résumé
The hotspot mutation H1047R in the oncogenic PIK3CA gene is frequently detected in breast cancer and enhances the enzymatic activity of PI3K to activate AKT/mTOR signaling cascade. Aberrant elevated PI3K activation has been reported to promote the tumorigenesis of breast cancer, but the mechanisms underlying are still needed to be elucidated. Here, we found that continuously activating PIK3CA
Substances chimiques
CCL2 protein, human
0
Chemokine CCL2
0
IL6 protein, human
0
Interleukin-6
0
TP53 protein, human
0
Tumor Suppressor Protein p53
0
MTOR protein, human
EC 2.7.1.1
Class I Phosphatidylinositol 3-Kinases
EC 2.7.1.137
PIK3CA protein, human
EC 2.7.1.137
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
TOR Serine-Threonine Kinases
EC 2.7.11.1
Metalloendopeptidases
EC 3.4.24.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
817-829Informations de copyright
© 2019 UICC.