Crosstalk of Sp1 and Stat3 signaling in pancreatic cancer pathogenesis
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Updated: May 24, 2026

Growing Desmoplastic Three-Dimensional Pancreatic Cancer Spheroids from Co-Culture
Published on: September 27, 2024
1Shanghai Key Laboratory of Pancreatic Diseases Research, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai, People's Republic of China.
Abstract:
Pancreatic cancer progression is attributed to genetic and epigenetic alterations and a chaotic tumor microenvironment. Those diverse "upstream signal" factors appear to converge on specific sets of central nuclear regulators, namely, transcription factors. Specificity Protein 1 (Sp1) and signal transducer and activator of transcription 3 (Stat3) are central transcription factors that regulate a number of pathways important to tumorigenesis, including tumor cell-cycle progression, apoptosis, angiogenesis, metastasis, and evasion of the immune system. Recently, researchers demonstrated many types of crosstalk of Sp1 and Stat3 in tumor signal transduction and that these factors function cooperatively to activate targeted genes and promote tumorigenesis in pancreatic cancer. Therefore, targeting both Sp1 and Stat3 is a potential preventive and therapeutic strategy for pancreatic cancer.
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