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STAT3 Plays a Critical Role in KRAS -Induced Pancreatic Tumorigenesis
Open accessPublished version of a preprint
Abstract
The STAT3 transcription factor is an important regulator of stem cell self-renewal, cancer cell survival, and inflammation. In the pancreas, STAT3 is dispensable for normal development, whereas the majority of pancreatic ductal adenocarcinomas (PDAC) show constitutive activation of STAT3, suggesting its potential as a therapeutic target in this cancer. Here, we sought to define the mechanisms of STAT3 activation and its functional importance in PDAC pathogenesis. Large-scale screening of cancer cell lines with a JAK2 inhibitor that blocks STAT3 function revealed a more than 30-fold range in sensitivity in PDAC, and showed a close correlation of sensitivity with levels of tyrosine-phosphorylated STAT3 and of the gp130 receptor, an upstream signaling component. Correspondingly, upregulation of the IL6/LIF-gp130 pathway accounted for the strong STAT3 activation in PDAC subsets. To define functions of STAT3 in vivo, we developed mouse models that test the impact of conditional inactivation of STAT3 in KRAS-driven PDAC. We showed that STAT3 is required for the development of the earliest premalignant pancreatic lesions, acinar-to-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia (PanIN). Moreover, acute STAT3 inactivation blocked PDAC initiation in a second in vivo model. Our results show that STAT3 has critical roles throughout the course of PDAC pathogenesis, supporting the development of therapeutic approaches targeting this pathway. Moreover, our work suggests that gp130 and phospho-STAT3 expression may be effective biomarkers for predicting response to JAK2 inhibitors. Cancer Res; 71(14); 5020–9. ©2011 AACR.
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“KRAS mutations activate Yes-associated protein-tafazzin (YAP-TAZ) and Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathways, leading to release of immunosuppressive cytokines such as CSF-1, IL-4, IL-6.”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [66]
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Citations
Cites
Darnell, J. E., Kerr, L. M., & Stark, G. R. (1994) · Science · doi:10.1126/science.8197455 · Cited by 6,080
Hingorani, S. R., Wang, L., Multani, A. S., Combs, C., Deramaudt, T. B., Hruban, R. H., Rustgi, A. K., Chang, S., & Tuveson, D. A. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.04.023 · Cited by 2,609
Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse
Hingorani, S. R., Petricoin, E. F., Maitra, A., Rajapakse, V., King, C., Jacobetz, M. A., Ross, S., Conrads, T. P., Veenstra, T. D., Hitt, B. A., et al. (2003) · Cancer Cell · doi:10.1016/s1535-6108(03)00309-x · Cited by 2,471
Zhong, Z., Wen, Z., & Darnell, J. E. (1994) · Science · doi:10.1126/science.8140422 · Cited by 2,070 · cited 1×
“Classically, STAT tyrosine phosphorylation is mediated by the Janus-activated kinase (JAK) family of tyrosine kinases, which themselves are activated by cytokine and growth factor receptors (10, 11).”
Genetics and biology of pancreatic ductal adenocarcinomaPreprint
Hezel, A. F., Kimmelman, A. C., Stanger, B. Z., Bardeesy, N. M., & DePinho, R. A. (2006) · Genes & Development · doi:10.1101/gad.1415606 · Cited by 1,611
Self-citationGu, G., Dubauskaite, J., & Melton, D. A. (2002) · Development · doi:10.1242/dev.129.10.2447 · Cited by 1,518
Iliopoulos, D., Hirsch, H. A., & Struhl, K. (2009) · Cell · doi:10.1016/j.cell.2009.10.014 · Cited by 1,374
Interleukin-6 family of cytokines and gp130.
Kishimoto, T., Akira, S., Narazaki, M., & Taga, T. (1995) · Blood · doi:10.1182/blood.v86.4.1243.bloodjournal8641243 · Cited by 1,362 · cited 2×
“STAT3 is activated by numerous growth factor and cytokine signaling pathways as well as by oncogenic RAS (7, 34, 43).”
The transcriptional network for mesenchymal transformation of brain tumours
Carro, M. S., Lim, W. K., Alvarez, M. J., Bollo, R. J., Zhao, X., Snyder, E. Y., Sulman, E. P., Anne, S. L., Doetsch, F. K., Colman, H., et al. (2009) · Nature · doi:10.1038/nature08712 · Cited by 1,268
The role of STATs in transcriptional control and their impact on cellular function
Bromberg, J., & Darnell, J. E. (2000) · Oncogene · doi:10.1038/sj.onc.1203476 · Cited by 1,201 · cited 1×
“Subsequent studies identified key functions for STAT proteins in the maintenance of self-renewal of embryonic stem cells and in the activation of proliferative, antiapoptotic, and inflammatory pathways to initiate and maintain growth of a number of tumor types (7, 13, 14).”
Warshaw, A. L., & Castillo, C. F. F.-D. (1992) · New England Journal of Medicine · doi:10.1056/nejm199202133260706 · Cited by 1,200
Aguirre, A. J., Bardeesy, N., Sinha, M., Lopez, L., Tuveson, D. A., Horner, J., Redston, M. S., & DePinho, R. A. (2003) · Genes & Development · doi:10.1101/gad.1158703 · Cited by 1,033
Self-citationFunction of Mitochondrial Stat3 in Cellular Respiration
Wegrzyn, J., Potla, R., Chwae, Y.-J., Sepuri, N. B. V., Zhang, Q., Koeck, T., Derecka, M., Szczepanek, K., Szelag, M., Gornicka, A., et al. (2009) · Science · doi:10.1126/science.1164551 · Cited by 1,014
Hereditary Pancreatitis and the Risk of Pancreatic Cancer
Lowenfels, A. B., Maisonneuve, P., DiMagno, E. P., Elitsur, Y., Gates, L. K., Perrault, J., Whitcomb, D. C., & International Hereditary Pancreatitis Study Group (1997) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/89.6.442 · Cited by 988
Progression model for pancreatic cancer.
Hruban, R. H., Goggins, M., Parsons, J., & Kern, S. E. (2000) · PubMed · Cited by 872
Shuai, K., Horvath, C. M., Huang, L. H. T., Qureshi, S. A., Cowburn, D., & Darnell, J. E. (1994) · Cell · doi:10.1016/0092-8674(94)90357-3 · Cited by 807
A Single Phosphotyrosine Residue of Stat91 Required for Gene Activation by Interferon-γ
Shuai, K., Stark, G. R., Kerr, L. M., & Darnell, J. E. (1993) · Science · doi:10.1126/science.7690989 · Cited by 802 · cited 2×
“The STAT proteins were originally identified as factors required for downstream signaling in response to interferon and other inflammatory cytokines (8).”
Kitamura, T., Tange, T., Terasawa, T., Chiba, S., Kuwaki, T., Miyagawa, K., Piao, Y., Miyazono, K., Urabe, A., & Takaku, F. (1989) · Journal of Cellular Physiology · doi:10.1002/jcp.1041400219 · Cited by 784 · cited 1×
“neutralizing antibody to gp130, known to block signaling by multiple IL6 cytokine family members (35).”
Mitochondrial STAT3 Supports Ras-Dependent Oncogenic Transformation
Gough, D. J., Corlett, A., Schlessinger, K., Wegrzyn, J., Larner, A. C., & Levy, D. E. (2009) · Science · doi:10.1126/science.1171721 · Cited by 716 · cited 1×
“STAT3 is activated by numerous growth factor and cytokine signaling pathways as well as by oncogenic RAS (7, 34, 43).”
Self-citationTumor-suppressive pathways in pancreatic carcinoma.
Rozenblum, E., Schutte, M. E. M., Goggins, M., Hahn, S. A., Panzer, S., ZAHURAK, M. L., Goodman, S. N., Sohn, T. A., Hruban, R. H., Yeo, C. J., et al. (1997) · PubMed · Cited by 693
Hruban, R. H., van Mansfeld, A. D. M., Offerhaus, G. J. A., van Weering, D. H. J., Allison, D. C., Goodman, S. N., Kensler, T. W., Bose, K., Cameron, J. L., & Bos, J. L. (1993) · PubMed Central · Cited by 650
Bardeesy, N. M., Aguirre, A. J., Chu, G. C., Cheng, K., Lopez, L. V., Hezel, A. F., Feng, B., Brennan, C., Weissleder, R., Mahmood, U., et al. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0601273103 · Cited by 584
Self-citationRequirement of Serine Phosphorylation for Formation of STAT-Promoter Complexes
Zhang, X., Blenis, J., Li, H., Schindler, C., & Chen‐Kiang, S. (1995) · Science · doi:10.1126/science.7701321 · Cited by 573 · cited 1×
“1D), a modification known to be JAK2 independent (31, 32).”
Probing tumor phenotypes using stable and regulated synthetic microRNA precursors
Dickins, R., Hemann, M., Zilfou, J. T., Simpson, D. R., Ibarra, I., Hannon, G., & Lowe, S. (2005) · Nature Genetics · doi:10.1038/ng1651 · Cited by 561
Wei, D., Le, X., Zheng, L., Wang, L., Frey, J. A., Gao, A. C., Peng, Z., Huang, S., Xiong, H. Q., Abbruzzese, J. L., et al. (2003) · Oncogene · doi:10.1038/sj.onc.1206122 · Cited by 561 · cited 2×
“In addition to this potential role in early PDACs, STAT3 has been suggested as a therapeutic target in established PDAC since examination of a limited number of cell lines for the impact of chemical STAT3 pathway inhibitors and dominant-negative STAT3 constructs has shown that the pathway may contribute to the prolife…”
The JAK2 Inhibitor AZD1480 Potently Blocks Stat3 Signaling and Oncogenesis in Solid Tumors
Hedvat, M., Huszar, D., Herrmann, A., Gozgit, J. M., Schroeder, A., Sheehy, A. M., Buettner, R., Proia, D. A., Kowolik, C. M., Xin, H., et al. (2009) · Cancer Cell · doi:10.1016/j.ccr.2009.10.015 · Cited by 529 · cited 1×
“Importantly, several JAK2 inhibitors are in advanced clinical development (41), and our studies suggest the potential of using levels of P-STAT3 and gp130 as biomarkers for patient selection in future clinical trials for PDAC using these compounds.”
STAT3 Is Required for Proliferation and Maintenance of Multipotency in Glioblastoma Stem Cells
Sherry, M. M., Reeves, A., Wu, J. K., & Cochran, B. H. (2009) · Stem Cells · doi:10.1002/stem.185 · Cited by 478 · cited 1×
“The early role of STAT3 in ADM driven either by oncogenic KRAS or by the aberrant expression of Pdx1, may reflect a requirement for STAT3 in developmental reprogramming as is observed in glioma (45, 46), whereas, alternate processes may be operative in more advanced lesions that harbor additional gene mutations.”
p16 and K-ras gene mutations in the intraductal precursors of human pancreatic adenocarcinoma.
Moskaluk, C. A., Hruban, R. H., & Kern, S. E. (1997) · PubMed · Cited by 429
Epigenetic reversion of post-implantation epiblast to pluripotent embryonic stem cells
Bao, S., Tang, F., Li, X., Hayashi, K., Gillich, A., Lao, K., & Surani, M. A. (2009) · Nature · doi:10.1038/nature08534 · Cited by 384
STAT3 as a central mediator of neoplastic cellular transformation
Frank, D. A. (2006) · Cancer Letters · doi:10.1016/j.canlet.2006.10.017 · Cited by 368 · cited 3×
“STAT3 is activated by numerous growth factor and cytokine signaling pathways as well as by oncogenic RAS (7, 34, 43).”
Activation and Association of Stat3 with Src in v-Src-Transformed Cell Lines
Cao, X., Tay, A., Guy, G. R., & Tan, Y. H. (1996) · Molecular and Cellular Biology · doi:10.1128/mcb.16.4.1595 · Cited by 359 · cited 1×
“Other tyrosine kinases, such as src, have also been reported to mediate tyrosine phosphorylation of STAT proteins (12).”
Chan, K. S., Sano, S., Kiguchi, K., Anders, J., Komazawa, N., Takeda, J., & DiGiovanni, J. (2004) · Journal of Clinical Investigation · doi:10.1172/jci21032 · Cited by 355 · cited 1×
“STAT3 has been identified as a key oncogenic factor in a number of epithelial malignancies and is required for oncogenesis inmousemodels of skin and gastric cancers (15, 16).”
McDermott, U., Sharma, S. V., Dowell, L., Greninger, P., Montagut, C. O., Lamb, J. A., Archibald, H., Raudales, R., Tam, A., Lee, D. W., et al. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0707498104 · Cited by 352 · cited 2×
“To more broadly define the role of this pathway in PDAC tumor maintenance, we evaluated the drug sensitivity profile for the JAK2-selective inhibitor AZ960 across a large-scale cell line repository containing over 500 solid tumor cell lines, including 46 PDAC cell lines (23, 30).”
Self-citationWen, Z. (1997) · Nucleic Acids Research · doi:10.1093/nar/25.11.2062 · Cited by 330 · cited 1×
“1D), a modification known to be JAK2 independent (31, 32).”
Jenkins, B. J., Grail, D., Nheu, T., Najdovska, M., Wang, B., Waring, P., Inglese, M., McLoughlin, R. M., Jones, S. A., Topley, N., et al. (2005) · Nature Medicine · doi:10.1038/nm1282 · Cited by 308 · cited 1×
“STAT3 has been identified as a key oncogenic factor in a number of epithelial malignancies and is required for oncogenesis inmousemodels of skin and gastric cancers (15, 16).”
Scholz, A., Heinze, S., Detjen, K. M., Peters, M., Welzel, M., Hauff, P., Schirner, M., Wiedenmann, B., & Rosewicz, S. (2003) · Gastroenterology · doi:10.1016/s0016-5085(03)01064-3 · Cited by 255 · cited 3×
“In addition to this potential role in early PDACs, STAT3 has been suggested as a therapeutic target in established PDAC since examination of a limited number of cell lines for the impact of chemical STAT3 pathway inhibitors and dominant-negative STAT3 constructs has shown that the pathway may contribute to the prolife…”
Lee, C.-K., Raz, R., Gimeno, R., Gertner, R., Wistinghausen, B., Takeshita, K., DePinho, R. A., & Levy, D. E. (2002) · Immunity · doi:10.1016/s1074-7613(02)00336-9 · Cited by 242
Self-citationAcinar Cells Contribute to the Molecular Heterogeneity of Pancreatic Intraepithelial Neoplasia
Zhu, L., Shi, G., Schmidt, C. M., Hruban, R. H., & Konieczny, S. F. (2007) · American Journal Of Pathology · doi:10.2353/ajpath.2007.061176 · Cited by 213
Taga, T., Narazaki, M., Yasukawa, K., Saito, T., Miki, D., Hamaguchi, M., Davis, S. H., SHOYAB, M., Yancopoulos, G. D., & Kishimoto, T. (1992) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.89.22.10998 · Cited by 198 · cited 1×
“family members (including the IL6, leukemia inhibitory factor (LIF), oncostatin M, and ciliary neurotrophic factor receptors), thereby serving as an important activator of JAK–STAT signaling (33, 34).”
K-ras mutations in pancreatic ductal proliferative lesions.
Klimstra, D. S., & Longnecker, D. S. (1994) · PubMed · Cited by 197
Miyatsuka, T., Kaneto, H., Shiraiwa, T., Matsuoka, T., Yamamoto, K., Kato, K., Nakamura, Y., Akira, S., Takeda, K., Kajimoto, Y., et al. (2006) · Genes & Development · doi:10.1101/gad.1412806 · Cited by 177
McDermott, U., & Settleman, J. (2009) · Journal of Clinical Oncology · doi:10.1200/jco.2009.22.9054 · Cited by 131 · cited 1×
“Recent clinical successes with targeted therapies directed at subsets of solid tumors harboring specific genetic or protein biomarkers, such as mutations in EGFR, ALK, or BRAF or amplification/overexpression of HER2 have created a paradigm for personalized approaches to cancer therapy (49).”
Self-citationToyonaga, T., Nakano, K., Nagano, M., Zhao, G., Yamaguchi, K., Kuroki, S., Eguchi, T., Chijiiwa, K., Tsuneyoshi, M., & Tanaka, M. (2003) · Cancer Letters · doi:10.1016/s0304-3835(03)00482-8 · Cited by 122 · cited 3×
“In addition to this potential role in early PDACs, STAT3 has been suggested as a therapeutic target in established PDAC since examination of a limited number of cell lines for the impact of chemical STAT3 pathway inhibitors and dominant-negative STAT3 constructs has shown that the pathway may contribute to the prolife…”
Shi, C., Hong, S., Lim, P., Kamiyama, H., Khan, M. A., Anders, R. A., Goggins, M., Hruban, R. H., & Eshleman, J. R. (2009) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-08-0206 · Cited by 109 · cited 1×
“Loss of STAT3 reduces ADM and PanIN formation induced by oncogenic KRAS ADM is the earliest change observed in models of KRASinduced pancreatic oncogenesis and is a potential precursor to PanIN (39, 40).”
Gozgit, J. M., Bebernitz, G. A., Patil, P. B., Ye, M., Parmentier, J. M., Wu, J., Su, N., Wang, T., Ioannidis, S., Davies, A. M., et al. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m803813200 · Cited by 103 · cited 2×
“To more broadly define the role of this pathway in PDAC tumor maintenance, we evaluated the drug sensitivity profile for the JAK2-selective inhibitor AZ960 across a large-scale cell line repository containing over 500 solid tumor cell lines, including 46 PDAC cell lines (23, 30).”
Mohammad, R. M., Al-Katib, A. M., Pettit, G. R., Vaitkevicius, V. K., Joshi, U. S., Adsay, V. N., Majumdar, A. P. N., & Sarkar, F. H. (1998) · PubMed · Cited by 46
Agbunag, C., Lee, K. E., Buontempo, S., & Bar‐Sagi, D. (2006) · Methods in enzymology on CD-ROM/Methods in enzymology · doi:10.1016/s0076-6879(05)07055-2 · Cited by 44
The transcription factor Stat3 is dispensable for pancreatic β-cell development and function
Lee, J., & Hennighausen, L. G. (2005) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2005.06.162 · Cited by 40
Jaganathan, S., Yue, P., & Turkson, J. (2010) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.109.162669 · Cited by 38 · cited 1×
“In addition to this potential role in early PDACs, STAT3 has been suggested as a therapeutic target in established PDAC since examination of a limited number of cell lines for the impact of chemical STAT3 pathway inhibitors and dominant-negative STAT3 constructs has shown that the pathway may contribute to the prolife…”
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Background
Metadata
- Authors
- Corcoran, R. B., Contino, G., Deshpande, V., Tzatsos, A., Conrad, C., Benes, C. H., Levy, D. E., Settleman, J., Engelman, J. A., & Bardeesy, N.
- Affiliations
- Harvard University (US)
- Corresponding author
- Bardeesy, Nabeel
- ORCID
- Venue
- Cancer Research
- Published
- 2011-07-14
- Volume
- 71
- Issue
- 14
- Pages
- 5020-5029
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- PMC
- PMC3693754
- OpenAlex
- W2133591242
- Cited by
- 413
- References
- 51
- Citations by year
- 2026: 14 · 2025: 16 · 2024: 18 · 2023: 32 · 2022: 28 · 2021: 39 · 2020: 30 · 2019: 32 · 2018: 24 · 2017: 35 · 2016: 35 · 2015: 30 · 2014: 32 · 2013: 28 · 2012: 18
- FWCI
- 12.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Fondazione Umberto Veronesi
- National Institutes of Health
- National Cancer Institute (P50CA127003, R01CA133557, P01CA117969, T32CA071345)
- National Institute of Allergy and Infectious Diseases (R0AI28900)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- STAT3, pancreatic ductal adenocarcinoma, JAK2 inhibitors, acinar-to-ductal metaplasia, pancreatic intraepithelial neoplasia, premalignant pancreatic lesions, predictive biomarkers
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Humans, Mice, Transgenic, Pancreatic Neoplasms, Phosphorylation, Precancerous Conditions, Genes, ras, Transcriptional Activation, Mice, SCID, Genetic Predisposition to Disease, Carcinoma, Pancreatic Ductal, Cell Line, Tumor, STAT3 Transcription Factor, Mice
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