In:
PLOS ONE, Public Library of Science (PLoS), Vol. 17, No. 12 ( 2022-12-8), p. e0278774-
Abstract:
Increasing evidence from epidemiological studies indicate that Alzheimer’s disease (AD) has a negative relationship with the incidence of cancers. Whether the Alzheimer’s genetic risk factor, named as fermitin family homolog-2 (FERMT2), plays a pivotal part in the progressive process of colorectal carcinoma (CRC) yet remains unclear. This study revealed that FERMT2 was upregulated in CRC tissues which predicted an unfavorable outcome of CRC using the PrognoScan web tool. FERMT2 was co-expressed with a variety of genes have been linked with CRC occurrence and implicated in the infiltration of immune cell in CRC tissues. Overexpressing FERMT2 promoted CRC progression with upregulation of Wnt/β-catenin signaling. Knockdown of FERMT2 suppressed the cell multiplication, colony formation rate, migration and invasion, along with the epithelial to mesenchymal transition (EMT) with downregulation Wnt/β-catenin proteins in cells of CRC, while overexpressing β-catenin reversed the inhibitory effects of silencing FERMT2 on the migration or invasion of CRC cells. Furthermore, Aβ 1–42 treated HT22 cells induced downregulation of FERMT2 and inhibited the migration, invasion and EMT in co-cultured CT26 cells through Wnt/β-catenin signaling. Our results revealed that the downregulated FERMT2 gene during AD is prominently activated in CRC, which promotes its progression via Wnt/β-catenin pathway.
Type of Medium:
Online Resource
ISSN:
1932-6203
DOI:
10.1371/journal.pone.0278774
DOI:
10.1371/journal.pone.0278774.g001
DOI:
10.1371/journal.pone.0278774.g002
DOI:
10.1371/journal.pone.0278774.g003
DOI:
10.1371/journal.pone.0278774.g004
DOI:
10.1371/journal.pone.0278774.g005
DOI:
10.1371/journal.pone.0278774.g006
DOI:
10.1371/journal.pone.0278774.g007
DOI:
10.1371/journal.pone.0278774.g008
DOI:
10.1371/journal.pone.0278774.g009
DOI:
10.1371/journal.pone.0278774.g010
DOI:
10.1371/journal.pone.0278774.t001
DOI:
10.1371/journal.pone.0278774.t002
DOI:
10.1371/journal.pone.0278774.t003
DOI:
10.1371/journal.pone.0278774.s001
DOI:
10.1371/journal.pone.0278774.s002
DOI:
10.1371/journal.pone.0278774.s003
DOI:
10.1371/journal.pone.0278774.s004
DOI:
10.1371/journal.pone.0278774.s005
DOI:
10.1371/journal.pone.0278774.s006
DOI:
10.1371/journal.pone.0278774.s007
DOI:
10.1371/journal.pone.0278774.r001
DOI:
10.1371/journal.pone.0278774.r002
DOI:
10.1371/journal.pone.0278774.r003
DOI:
10.1371/journal.pone.0278774.r004
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2022
detail.hit.zdb_id:
2267670-3
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