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4. Table S4 from Cotargeting CDK4/6 and BRD4 Promotes Senescence and Ferroptosis Sensitivity in Cancer

Author

Zhu, Xianbing, primary, Fu, Zheng, primary, Dutchak, Kendall, primary, Arabzadeh, Azadeh, primary, Milette, Simon, primary, Steinberger, Jutta, primary, Morin, Geneviève, primary, Monast, Anie, primary, Pilon, Virginie, primary, Kong, Tim, primary, Adams, Bianca N., primary, Prando Munhoz, Erika, primary, Hosein, Hannah J.B., primary, Fang, Tianxu, primary, Su, Jing, primary, Xue, Yibo, primary, Rayes, Roni, primary, Sangwan, Veena, primary, Walsh, Logan A., primary, Chen, Guojun, primary, Quail, Daniela F., primary, Spicer, Jonathan D., primary, Park, Morag, primary, Dankort, David, primary, and Huang, Sidong, primary

Published
2024
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5. Supplementary Data from Cotargeting CDK4/6 and BRD4 Promotes Senescence and Ferroptosis Sensitivity in Cancer

Author

Zhu, Xianbing, primary, Fu, Zheng, primary, Dutchak, Kendall, primary, Arabzadeh, Azadeh, primary, Milette, Simon, primary, Steinberger, Jutta, primary, Morin, Geneviève, primary, Monast, Anie, primary, Pilon, Virginie, primary, Kong, Tim, primary, Adams, Bianca N., primary, Prando Munhoz, Erika, primary, Hosein, Hannah J.B., primary, Fang, Tianxu, primary, Su, Jing, primary, Xue, Yibo, primary, Rayes, Roni, primary, Sangwan, Veena, primary, Walsh, Logan A., primary, Chen, Guojun, primary, Quail, Daniela F., primary, Spicer, Jonathan D., primary, Park, Morag, primary, Dankort, David, primary, and Huang, Sidong, primary

Published
2024
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6. Data from Cotargeting CDK4/6 and BRD4 Promotes Senescence and Ferroptosis Sensitivity in Cancer

Author

Zhu, Xianbing, primary, Fu, Zheng, primary, Dutchak, Kendall, primary, Arabzadeh, Azadeh, primary, Milette, Simon, primary, Steinberger, Jutta, primary, Morin, Geneviève, primary, Monast, Anie, primary, Pilon, Virginie, primary, Kong, Tim, primary, Adams, Bianca N., primary, Prando Munhoz, Erika, primary, Hosein, Hannah J.B., primary, Fang, Tianxu, primary, Su, Jing, primary, Xue, Yibo, primary, Rayes, Roni, primary, Sangwan, Veena, primary, Walsh, Logan A., primary, Chen, Guojun, primary, Quail, Daniela F., primary, Spicer, Jonathan D., primary, Park, Morag, primary, Dankort, David, primary, and Huang, Sidong, primary

Published
2024
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15. Bioinspired microneedle patches: Biomimetic designs, fabrication, and biomedical applications

Author

Makvandi, Pooyan, Maleki, Aziz, Shabani, Majid, Hutton, Aaron RJ, Jamaledin, Rezvan, Fang, Tianxu, He, Jiahuan, Lee, Jesse, Mazzolai, Barbara, Donnelly, Ryan F, Tay, Franklin R, Chen, Guojun, and Mattoli, Virgilio

Abstract

This is the unformatted version of the accepted review paper manuscript "Bioinspired microneedle patches: Biomimetic designs, fabrication, and biomedical applications" published on Matter, 5(2): 390 (2022), by P. Makvandi*†, A. Maleki†, M. Shabani†, A.R.J. Hutton, M. Kirkby, R. Jamaledin, T. Fang, J. He, J. Lee, B. Mazzolai, R.F. Donnelly, F.R. Tay, G. Chen*, V. Mattoli*. &nbsp

Published
2022
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17. Bioinspired microneedle patches: Biomimetic designs, fabrication, and biomedical applications

Author

Makvandi, Pooyan, primary, Maleki, Aziz, additional, Shabani, Majid, additional, Hutton, Aaron R.J., additional, Kirkby, Melissa, additional, Jamaledin, Rezvan, additional, Fang, Tianxu, additional, He, Jiahuan, additional, Lee, Jesse, additional, Mazzolai, Barbara, additional, Donnelly, Ryan F., additional, Tay, Franklin R., additional, Chen, Guojun, additional, and Mattoli, Virgilio, additional

Published
2022
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24. Bioresponsive and immunotherapeutic nanomaterials to remodel tumor microenvironment for enhanced immune checkpoint blockade

Author

Fang, Tianxu, Cao, Xiaona, Wang, Li, Chen, Mo, Deng, Yueyang, and Chen, Guojun

Abstract

Immune checkpoint blockade (ICB) therapy is a revolutionary approach to treat cancers, but still have limited clinical applications. Accumulating evidence pinpoints the immunosuppressive characteristics of the tumor microenvironment (TME) as one major obstacle. The TME, characterized by acidity, hypoxia and elevated ROS levels, exerts its detrimental effects on infiltrating anti-tumor immune cells. Here, we developed a TME-responsive and immunotherapeutic catalase-loaded calcium carbonate nanoparticles (termed as CAT@CaCO3NPs) as the simple yet versatile multi-modulator for TME remodeling. CaCO3NPs can consume protons in the acidic TME to normalize the TME pH. CAT catalyzed the decomposition of ROS and thus generated O2. The released Ca2+led to Ca2+overload in the tumor cells which then release DAMP signals to initiate anti-tumor immune responses, including tumor antigen presentation by dendritic cells. Meanwhile, CAT@CaCO3NPs-induced immunosupportive TME also promoted the polarization of the M2 tumor-associated macrophages to the M1 phenotype, further enhancing antigen presentation. Consequently, T cell-mediated anti-tumor responses were then activated, the efficacy of which was further boosted by aPD-1 immune checkpoint blockade. Our study demonstrated that local treatment of CAT@CaCO3NPs and aPD-1 combination can effectively evoke local and systemic anti-tumor immune responses, inhibiting the growth of treated tumors and distant diseases.

Published
2023
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25. Cotargeting CDK4/6 and BRD4 Promotes Senescence and Ferroptosis Sensitivity in Cancer.

Author

Zhu X, Fu Z, Dutchak K, Arabzadeh A, Milette S, Steinberger J, Morin G, Monast A, Pilon V, Kong T, Adams BN, Prando Munhoz E, Hosein HJB, Fang T, Su J, Xue Y, Rayes R, Sangwan V, Walsh LA, Chen G, Quail DF, Spicer JD, Park M, Dankort D, and Huang S

Subjects
Animals, Mice, Cyclin-Dependent Kinase 4, Nuclear Proteins metabolism, Proto-Oncogene Proteins p21(ras) metabolism, Reactive Oxygen Species metabolism, Cell Line, Tumor, Transcription Factors metabolism, Cyclin-Dependent Kinase 6, Protein Kinase Inhibitors pharmacology, Carcinoma, Non-Small-Cell Lung drug therapy, Carcinoma, Non-Small-Cell Lung genetics, Cytostatic Agents therapeutic use, Ferroptosis, Lung Neoplasms genetics
Abstract

Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors are approved for breast cancer treatment and show activity against other malignancies, including KRAS-mutant non-small cell lung cancer (NSCLC). However, the clinical efficacy of CDK4/6 inhibitors is limited due to frequent drug resistance and their largely cytostatic effects. Through a genome-wide cDNA screen, we identified that bromodomain-containing protein 4 (BRD4) overexpression conferred resistance to the CDK4/6 inhibitor palbociclib in KRAS-mutant NSCLC cells. Inhibition of BRD4, either by RNA interference or small-molecule inhibitors, synergized with palbociclib to induce senescence in NSCLC cells and tumors, and the combination prolonged survival in a KRAS-mutant NSCLC mouse model. Mechanistically, BRD4-inhibition enhanced cell-cycle arrest and reactive oxygen species (ROS) accumulation, both of which are necessary for senescence induction; this in turn elevated GPX4, a peroxidase that suppresses ROS-triggered ferroptosis. Consequently, GPX4 inhibitor treatment selectively induced ferroptotic cell death in the senescent cancer cells, resulting in tumor regression. Cotargeting CDK4/6 and BRD4 also promoted senescence and ferroptosis vulnerability in pancreatic and breast cancer cells. Together, these findings reveal therapeutic vulnerabilities and effective combinations to enhance the clinical utility of CDK4/6 inhibitors., Significance: The combination of cytostatic CDK4/6 and BRD4 inhibitors induces senescent cancer cells that are primed for activation of ferroptotic cell death by targeting GPX4, providing an effective strategy for treating cancer., (©2024 American Association for Cancer Research.)

Published
2024
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