The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Pancreatic Cancer-Associated Stellate Cells Promote Differentiation of Myeloid-Derived Suppressor Cells in a STAT3-Dependent Manner
Open accessAbstract
Pancreatic stellate cells (PSC) are a subset of pancreatic cancer-associated fibroblasts. These cells provide prosurvival signals to tumors; however, little is known regarding their interactions with immune cells within the tumor microenvironment. We hypothesized that factors produced by human PSC could enhance myeloid-derived suppressor cell (MDSC) differentiation and function, which promotes an immunosuppressive microenvironment. Primary PSC cell lines (n = 7) were generated from human specimens and phenotypically confirmed via expression of vimentin, α-smooth muscle actin (α-SMA), and glial fibrillary acidic protein (GFAP). Luminex analysis indicated that PSC but not human fetal primary pancreatic fibroblast cells (HPF; negative controls) produced MDSC-promoting cytokines [interleukin (IL-6), VEGF, macrophage colony-stimulating factor (M-CSF) ] and chemokines (SDF-1, MCP-1). Culture of peripheral blood mononuclear cells [peripheral blood mononuclear cell (PBMC), n = 3 donors] with PSC supernatants or IL-6/granulocyte macrophage colony-stimulating factor (GM-CSF; positive control) for 7 days promoted PBMC differentiation into an MDSC (CD11b+CD33+) phenotype and a subpopulation of polymorphonuclear CD11b+CD33+CD15+ cells. The resulting CD11b+CD33+ cells functionally suppressed autologous T-lymphocyte proliferation. In contrast, supernatants from HPF did not induce an MDSC phenotype in PBMCs. Culture of normal PBMCs with PSC supernatants led to STAT3 but not STAT1 or STAT5 phosphorylation. IL-6 was an important mediator as its neutralization inhibited PSC supernatant-mediated STAT3 phosphorylation and MDSC differentiation. Finally, the FLLL32 STAT3 inhibitor abrogated PSC supernatant-mediated MDSC differentiation, PSC viability, and reduced autocrine IL-6 production indicating these processes are STAT3 dependent. These results identify a novel role for PSC in driving immune escape in pancreatic cancer and extend the evidence that STAT3 acts as a driver of stromal immunosuppression to enhance its interest as a therapeutic target. Cancer Res; 73(10); 3007–18. ©2013 AACR.
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Cites
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STATs in cancer inflammation and immunity: a leading role for STAT3
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Coordinated regulation of myeloid cells by tumours
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“This mixture of factors is likely to synergize with other cancer derived factors such as GM-CSF that promote MDSC accumulation in the tumor microenvironment (34, 35) or HMGB1 which regulates a positive feedback loop between autophagy, IL-6 and pSTAT3 (36).”
BackgroundYang, L., Huang, J., Ren, X., Gorska, A. E., Chytil, A., Aakre, M., Carbone, D. P., Matrisian, L. M., Richmond, A., Lin, P. C., et al. (2008) · Cancer Cell · doi:10.1016/j.ccr.2007.12.004 · Cited by 918
Oncogenic Kras-induced GM-CSF production promotes the development of pancreatic neoplasia
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“cumulation in the tumor microenvironment (34, 35) or HMGB1, which regulates a positive feedback loop between autophagy, IL-6, and pSTAT3 (36).”
BackgroundDesmoplastic Reaction in Pancreatic Cancer: Role of Pancreatic Stellate Cells
Apte, M. V., Park, S., Phillips, P. A., Santucci, N., Goldstein, D., Kumar, R. K., Ramm, G. A., Buchler, M., Friess, H., McCarroll, J. A., et al. (2004) · Pancreas · doi:10.1097/00006676-200410000-00002 · Cited by 591
STAT3 Plays a Critical Role in KRAS -Induced Pancreatic Tumorigenesis
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“immunosuppressive cells, and now in PSC within the stroma (49, 50).”
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The evolving tumor microenvironment: From cancer initiation to metastatic outgrowth
de Visser, K. E., & Joyce, J. A. (2023) · Cancer Cell · doi:10.1016/j.ccell.2023.02.016 · Cited by 4,059
Macrophages as regulators of tumour immunity and immunotherapy
DeNardo, D. G., & Ruffell, B. (2019) · Nature Reviews Immunology · doi:10.1038/s41577-019-0127-6 · Cited by 2,528
Mao, X., Xu, J., Wang, W., Liang, C., Hua, J., Liu, J., Zhang, B., Meng, Q., Yu, X., & Shi, S. (2021) · Molecular Cancer · doi:10.1186/s12943-021-01428-1 · Cited by 2,290
Fibroblast heterogeneity in the cancer wound
Öhlund, D., Elyada, E., & Tuveson, D. (2014) · Journal of Experimental Medicine · doi:10.1084/jem.20140692 · Cited by 926
Cancer-associated fibroblasts: an emerging target of anti-cancer immunotherapy
Liu, T., Han, C., Wang, S., Fang, P., Ma, Z., Xu, L., & Yin, R. (2019) · Journal of Hematology & Oncology · doi:10.1186/s13045-019-0770-1 · Cited by 860
“(GFAP), CAFs secret macrophage colony-stimulating factor 1 (M-CSF), IL-6, and CC-chemokine ligand 2 (CCL2) to promote monocyte recruitment encourage macrophage differentiation and M2 polarization [55].”
Background
Metadata
- Authors
- Mace, T. A., Ameen, Z., Collins, A., Wojcik, S., Mair, M., Young, G. S., Fuchs, J. R., Eubank, T. D., Frankel, W. L., Bekaii-Saab, T., Bloomston, M., & Lesinski, G. B.
- Venue
- Cancer Research
- Published
- 2013-05-12
- Volume
- 73
- Issue
- 10
- Pages
- 3007-3018
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W1993381640
- Cited by
- 410
- References
- 12
- FWCI
- 14.00
- Type
- journal article
- Language
- en
- Open access
- green
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- Mace, T. A., Ameen, Z., Collins, A., Wojcik, S., Mair, M., Young, G. S., Fuchs, J. R., Eubank, T. D., Frankel, W. L., Bekaii-Saab, T., Bloomston, M., & Lesinski, G. B. (2013). Pancreatic Cancer-Associated Stellate Cells Promote Differentiation of Myeloid-Derived Suppressor Cells in a STAT3-Dependent Manner. Cancer Research. https://doi.org/10.1158/0008-5472.can-12-4601
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