Prevention of mammary carcinogenesis in MMTV-neu mice by targeting RLIP.
ATP-Binding Cassette Transporters
/ metabolism
Animals
Anticarcinogenic Agents
/ pharmacology
Breast Neoplasms
/ metabolism
Cell Line, Tumor
Female
Flavanones
/ pharmacology
GTPase-Activating Proteins
/ genetics
Humans
Lymphocytes, Tumor-Infiltrating
/ drug effects
Mammary Glands, Animal
/ drug effects
Mammary Neoplasms, Experimental
/ genetics
Mice, Transgenic
Molecular Targeted Therapy
Proto-Oncogene Proteins c-akt
/ metabolism
Proto-Oncogene Proteins c-bcl-2
/ metabolism
Receptor, ErbB-2
/ metabolism
MMTV-neu mice
RLIP
RalBP1
breast cancer
prevention
Journal
Molecular carcinogenesis
ISSN: 1098-2744
Titre abrégé: Mol Carcinog
Pays: United States
ID NLM: 8811105
Informations de publication
Date de publication:
03 2021
03 2021
Historique:
received:
12
12
2020
revised:
19
01
2021
accepted:
20
01
2021
pubmed:
6
2
2021
medline:
10
4
2021
entrez:
5
2
2021
Statut:
ppublish
Résumé
The overexpression and amplification of the protooncogene neu (ERBB2) play an important role in the development of aggressive breast cancer (BC) in humans. Ral-interacting protein (RLIP), a modular stress-response protein with pleiotropic functions, is overexpressed in several types of cancer, including BC. Here, we show that blocking RLIP attenuates the deleterious effects caused by the loss of the tumor suppressor p53 and inhibits the growth of human BC both in vitro and in vivo in MMTV-neu mice. In addition, we show that treatment with the diet-derived, RLIP-targeting chemotherapeutic 2'-hydroxyflavanone (2HF), alone or in combination with RLIP-specific antisense RNA or antibodies, significantly reduced the cumulative incidence and/or burden of mammary hyperplasia and carcinoma in MMTV-neu mice. 2HF treatment correlated with reduced tumor cell proliferation and increased apoptosis, and the average number of Ki67-positive (proliferating) cells was significantly lower in the tumors of 2HF-treated mice than in the tumors of control mice. Furthermore, targeting RLIP also resulted in the overexpression of E-cadherin and the infiltration of CD3
Identifiants
pubmed: 33544936
doi: 10.1002/mc.23285
pmc: PMC7952002
mid: NIHMS1671997
doi:
Substances chimiques
2'-hydroxyflavanone
0
ATP-Binding Cassette Transporters
0
Anticarcinogenic Agents
0
Flavanones
0
GTPase-Activating Proteins
0
Proto-Oncogene Proteins c-bcl-2
0
RALBP1 protein, human
0
Ralbp1 protein, mouse
0
Erbb2 protein, mouse
EC 2.7.10.1
Receptor, ErbB-2
EC 2.7.10.1
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
213-223Subventions
Organisme : NCI NIH HHS
ID : P30 CA033572
Pays : United States
Informations de copyright
© 2021 Wiley Periodicals LLC.
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