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Updated: Apr 13, 2026
![Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA](/_next/image?url=https%3A%2F%2Fcloudfront.jove.com%2FCDNSource%2Fteasers%2F60445.jpg&w=3840&q=50)
Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA
Published on: December 19, 2019
An unexpected alliance between stress responses to drive oncogenesis
Melissa M Keenan1,2, Chien-Kuang Cornelia Ding3,4, Jen-Tsan Chi5,6
1Department of Molecular Genetics and Microbiology, Duke University Medical Center, 268 CARL Building, Research Drive, Box 3054 DUMC, Durham, NC, 27710, USA. melissa.keenan@duke.edu.
Abstract:
XBP1 is a well-characterized regulator of the unfolding protein response that is activated in response to unfolded or misfolded proteins or nutrient deprivation. The conventional wisdom is that XBP1 is activated to coordinate the unfolded protein response and promote cellular survival under stresses. A recent study provides intriguing evidence that, in triple-negative breast cancer, XBP1 plays a major role in promoting oncogenesis and cancer stem cell properties. Unexpectedly, XBP1 accomplishes this by recruiting hypoxia-inducible factor 1α and activating oncogenic transcriptional programs. This study reveals a surprising hierarchy and alliance between two stress regulators with distinct transcriptional outputs to promote an aggressive oncogenic state.
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