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2018 ; 8
(1
): 11285
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Annexin A2 overexpression associates with colorectal cancer invasiveness and
TGF-ß induced epithelial mesenchymal transition via Src/ANXA2/STAT3
#MMPMID30050103
Rocha MR
; Barcellos-de-Souza P
; Sousa-Squiavinato ACM
; Fernandes PV
; de Oliveira IM
; Boroni M
; Morgado-Diaz JA
Sci Rep
2018[Jul]; 8
(1
): 11285
PMID30050103
show ga
Annexin A2 (ANXA2) is upregulated in several malignancies, including colorectal
cancer (CRC). However, there is little knowledge on the molecular mechanisms
involved to its upregulation. The aim of this study was to identify the mechanism
through which ANXA2 overexpression leads to CRC progression and evaluate its
potential prognostic value. We used human CRC samples to analyse the correlation
between ANXA2 levels and tumour staging. ANXA2 expression was increased in CRC
tissues compared to normal colon tissues. In addition, we observe increased ANXA2
levels in stage IV tumours and metastasis, when compared to stage I-III. Whereas
E-cadherin, an epithelial marker, decreased in stage II-IV and increased in
metastasis. We've also shown that TGF-?, a classic EMT inductor, caused
upregulation of ANXA2, and internalization of both E-cadherin and ANXA2 in CRC
cells. ANXA2 silencing hindered TGF-?-induced invasiveness, and inhibitors of the
Src/ANXA2/STAT3 pathway reversed the EMT. In silico analysis confirmed
overexpression of ANXA2 and association to the consensus moleculars subtypes
(CMS) with the worst prognosis. Therefore, ANXA2 overexpression play a pivotal
role in CRC invasiveness through Src/ANXA2/STAT3 pathway activation. The
association of ANXA2 to distinct CMSs suggests the possible use of ANXA2 as a
prognostic marker or directed target therapy.
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