File Download
There are no files associated with this item.
Supplementary
-
Citations:
- Appears in Collections:
Conference Paper: Characterize the role of cancer associated fibroblast (CAFs) derived IL‐32 in esophageal squamous cell carcinoma (ESCC)
Title | Characterize the role of cancer associated fibroblast (CAFs) derived IL‐32 in esophageal squamous cell carcinoma (ESCC) |
---|---|
Authors | |
Issue Date | 2017 |
Publisher | American Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org |
Citation | The American Association of Immunologists Annual Meeting 2017, Washington, DC, 12-16 May 2017. In Journal of Immunology, 2017, v. 198 n. 1 S, p. 130.8 How to Cite? |
Abstract | Cancer-associated fibroblasts (CAFs) are localized adjacently to cancer cells at all stages of esophageal squamous cell carcinoma (ESCC) progression, and their functional contributions to this process are emerging. Our previous studies have identified FGFR2 as CAFs specific marker in ESCC. In this study, using microarray analysis, we identified IL-32 was the most differentially expressed cytokine in CAFs in patients with ESCC. Flow cytometric analysis and western blot have revealed markedly increased IL-32 in FGFR2+ CAFs from ESCC tumor specimens, compared with non-tumor epithelial tissues. IL-32 treatment could promote prosurvival effect in tumor cell from upon cisplatin or 5-Fu mediated apoptosis in culture and human ESCC tumor-bearing nude mice. In contrast, knockdown of IL-32 expression in CAFs by shRNA reduce tumor cell viability in reconstituted mouse model upon cisplatin or 5-Fu treatment. Mechanistic study shows that IL-32 treatment significantly downregulated caspase 3/9 and upregulated Bcl-2 expression by ESCC tumor upon Cisplatin or 5-Fu stimulation. In contrast, blockage of type II IFN signaling in CAFs resulted in significantly reduced IL-32 secretion and increased apoptotic cell death of ESCC. Together, these findings have suggested a critical role of CAFs derived IL-32 in prosurvival effect ESCC and thereby exacerbating cancer development, which suggested that IL-32 blockade may serve as potential therapeutic target for ESCC. |
Persistent Identifier | http://hdl.handle.net/10722/245627 |
ISSN | 2023 Impact Factor: 3.6 2023 SCImago Journal Rankings: 1.558 |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Chen, M | - |
dc.contributor.author | Guan, X | - |
dc.date.accessioned | 2017-09-18T02:14:02Z | - |
dc.date.available | 2017-09-18T02:14:02Z | - |
dc.date.issued | 2017 | - |
dc.identifier.citation | The American Association of Immunologists Annual Meeting 2017, Washington, DC, 12-16 May 2017. In Journal of Immunology, 2017, v. 198 n. 1 S, p. 130.8 | - |
dc.identifier.issn | 0022-1767 | - |
dc.identifier.uri | http://hdl.handle.net/10722/245627 | - |
dc.description.abstract | Cancer-associated fibroblasts (CAFs) are localized adjacently to cancer cells at all stages of esophageal squamous cell carcinoma (ESCC) progression, and their functional contributions to this process are emerging. Our previous studies have identified FGFR2 as CAFs specific marker in ESCC. In this study, using microarray analysis, we identified IL-32 was the most differentially expressed cytokine in CAFs in patients with ESCC. Flow cytometric analysis and western blot have revealed markedly increased IL-32 in FGFR2+ CAFs from ESCC tumor specimens, compared with non-tumor epithelial tissues. IL-32 treatment could promote prosurvival effect in tumor cell from upon cisplatin or 5-Fu mediated apoptosis in culture and human ESCC tumor-bearing nude mice. In contrast, knockdown of IL-32 expression in CAFs by shRNA reduce tumor cell viability in reconstituted mouse model upon cisplatin or 5-Fu treatment. Mechanistic study shows that IL-32 treatment significantly downregulated caspase 3/9 and upregulated Bcl-2 expression by ESCC tumor upon Cisplatin or 5-Fu stimulation. In contrast, blockage of type II IFN signaling in CAFs resulted in significantly reduced IL-32 secretion and increased apoptotic cell death of ESCC. Together, these findings have suggested a critical role of CAFs derived IL-32 in prosurvival effect ESCC and thereby exacerbating cancer development, which suggested that IL-32 blockade may serve as potential therapeutic target for ESCC. | - |
dc.language | eng | - |
dc.publisher | American Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org | - |
dc.relation.ispartof | Journal of Immunology | - |
dc.title | Characterize the role of cancer associated fibroblast (CAFs) derived IL‐32 in esophageal squamous cell carcinoma (ESCC) | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Guan, X: xyguan@hkucc.hku.hk | - |
dc.identifier.authority | Guan, X=rp00454 | - |
dc.identifier.hkuros | 277039 | - |
dc.identifier.volume | 198 | - |
dc.identifier.issue | 1 S | - |
dc.identifier.spage | 130.8 | - |
dc.identifier.epage | 130.8 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0022-1767 | - |