Interleukin-6 Promotes Epithelial-Mesenchymal Transition and Cell Invasion through Integrin ß6 Upregulation in Colorectal Cancer.
Oxid Med Cell Longev
; 2020: 8032187, 2020.
Article
in En
| MEDLINE
| ID: mdl-32855767
ABSTRACT
The metastatic potential of colorectal cancer (CRC) is intensively promoted by the tumor microenvironment (TME) in a paracrine manner. As a pleiotropic inflammatory cytokine, Interleukin-6 (IL-6) is produced and involved in CRC, the same scenario where integrin αvß6 also becomes upregulated. However, the relationship between IL-6 and integrin αvß6 as well as their involvement in the crosstalk between CRC and TME remains largely unclear. In the present study, we demonstrated a positive correlation between the expression of IL-6 and integrin ß6 in CRC samples. The mutually promotive interaction between CRC and TME was further determined by an indirect coculture system. CRC cells could augment the secretion of IL-6 from fibroblasts, which in return induced invasion and integrin ß6 expression of CRC cells. Through the classic IL-6 receptor/STAT-3 signaling pathway, IL-6 mediated the upregulation of integrin ß6, which was involved in the invasion and epithelial-mesenchymal transition of CRC cells induced by IL-6. Taken together, our results reveal a paracrine crosstalk between IL-6 signals originating from the TME and increased the integrin ß6 level of CRC. IL-6 induces CRC invasion via upregulation of integrin ß6 through the IL-6 receptor/STAT-3 signaling pathway. Combined inhibition of IL-6 along with integrin ß6-targeted strategy may indicate new directions for antitumor strategies for CRC.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Colorectal Neoplasms
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Gene Expression Regulation, Neoplastic
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Up-Regulation
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Interleukin-6
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Integrin beta Chains
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Epithelial-Mesenchymal Transition
Limits:
Female
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Humans
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Male
/
Middle aged
Language:
En
Journal:
Oxid Med Cell Longev
Journal subject:
METABOLISMO
Year:
2020
Document type:
Article
Affiliation country: