FILIP1L Loss Is a Driver of Aggressive Mucinous Colorectal Adenocarcinoma and Mediates Cytokinesis Defects through PFDN1.
Adenocarcinoma, Mucinous
/ genetics
Animals
Apoptosis
Biomarkers, Tumor
/ genetics
Cell Proliferation
Colorectal Neoplasms
/ genetics
Cytokinesis
Female
Gene Expression Regulation, Neoplastic
Humans
Intracellular Signaling Peptides and Proteins
/ genetics
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, Nude
Molecular Chaperones
/ genetics
Prognosis
Tumor Cells, Cultured
Xenograft Model Antitumor Assays
Journal
Cancer research
ISSN: 1538-7445
Titre abrégé: Cancer Res
Pays: United States
ID NLM: 2984705R
Informations de publication
Date de publication:
01 11 2021
01 11 2021
Historique:
received:
19
03
2021
revised:
25
06
2021
accepted:
17
08
2021
pubmed:
22
8
2021
medline:
12
1
2022
entrez:
21
8
2021
Statut:
ppublish
Résumé
Aneuploid mucinous colorectal adenocarcinoma (MAC) is an aggressive subtype of colorectal cancer with poor prognosis. The tumorigenic mechanisms in aneuploid MAC are currently unknown. Here we show that downregulation of Filamin A-interacting protein 1-like (FILIP1L) is a driver of MAC. Loss of FILIP1L increased xenograft growth, and, in colon-specific knockout mice, induced colonic epithelial hyperplasia and mucin secretion. The molecular chaperone prefoldin 1 (PFDN1) was identified as a novel binding partner of FILIP1L at the centrosomes throughout mitosis. FILIP1L was required for proper centrosomal localization of PFDN1 and regulated proteasome-dependent degradation of PFDN1. Importantly, increased PFDN1, caused by downregulation of FILIP1L, drove multinucleation and cytokinesis defects
Identifiants
pubmed: 34417201
pii: 0008-5472.CAN-21-0897
doi: 10.1158/0008-5472.CAN-21-0897
pmc: PMC8563430
mid: NIHMS1735936
doi:
Substances chimiques
Biomarkers, Tumor
0
FILIP1L protein, human
0
Intracellular Signaling Peptides and Proteins
0
Molecular Chaperones
0
prefoldin
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
5523-5539Subventions
Organisme : NCI NIH HHS
ID : P30 CA072720
Pays : United States
Informations de copyright
©2021 The Authors; Published by the American Association for Cancer Research.
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