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- W2897749150 abstract "Abstract Chemotherapy and radiation not only trigger cancer cell apoptosis but also damage stromal cells in the tumour microenvironment (TME), inducing a senescence-associated secretory phenotype (SASP) characterized by chronic secretion of diverse soluble factors. Here we report serine protease inhibitor Kazal type I (SPINK1), a SASP factor produced in human stromal cells after genotoxic treatment. DNA damage causes SPINK1 expression by engaging NF-κB and C/EBP, while paracrine SPINK1 promotes cancer cell aggressiveness particularly chemoresistance. Strikingly, SPINK1 reprograms the expression profile of cancer cells, causing prominent epithelial-endothelial transition (EET), a phenotypic switch mediated by EGFR signaling but hitherto rarely reported for a SASP factor. In vivo, SPINK1 is expressed in the stroma of solid tumours and is routinely detectable in peripheral blood of cancer patients after chemotherapy. Our study substantiates SPINK1 as both a targetable SASP factor and a novel noninvasive biomarker of therapeutically damaged TME for disease control and clinical surveillance." @default.
- W2897749150 created "2018-10-26" @default.
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- W2897749150 date "2018-10-17" @default.
- W2897749150 modified "2023-10-09" @default.
- W2897749150 title "Targeting SPINK1 in the damaged tumour microenvironment alleviates therapeutic resistance" @default.
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- W2897749150 doi "https://doi.org/10.1038/s41467-018-06860-4" @default.
- W2897749150 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6193001" @default.
- W2897749150 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30333494" @default.
- W2897749150 hasPublicationYear "2018" @default.
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