@article {69643,
	title = {IRE1α silences dsRNA to prevent taxane-induced pyroptosis in triple-negative breast cancer.},
	journal = {Cell},
	year = {2024},
	month = {2024 Oct 14},
	abstract = {<p>Chemotherapy is often combined with immune checkpoint inhibitor (ICIs) to enhance immunotherapy responses. Despite the approval of chemo-immunotherapy in multiple human cancers, many immunologically cold tumors remain unresponsive. The mechanisms determining the immunogenicity of chemotherapy are elusive. Here, we identify the ER stress sensor IRE1α as a critical checkpoint that restricts the immunostimulatory effects of taxane chemotherapy and prevents the innate immune recognition of immunologically cold triple-negative breast cancer (TNBC). IRE1α RNase silences taxane-induced double-stranded RNA (dsRNA) through regulated IRE1-dependent decay (RIDD) to prevent NLRP3 inflammasome-dependent pyroptosis. Inhibition of IRE1α in Trp53 TNBC allows taxane to induce extensive dsRNAs that are sensed by ZBP1, which in turn activates NLRP3-GSDMD-mediated pyroptosis. Consequently, IRE1α RNase inhibitor plus taxane converts PD-L1-negative, ICI-unresponsive TNBC tumors into PD-L1 immunogenic tumors that are hyper-sensitive to ICI. We reveal IRE1α as a cancer cell defense mechanism that prevents taxane-induced danger signal accumulation and pyroptotic cell death.</p>
},
	issn = {1097-4172},
	doi = {10.1016/j.cell.2024.09.032},
	url = {https://doi.org/10.1016/j.cell.2024.09.032},
	author = {Xu, Longyong and Peng, Fanglue and Luo, Qin and Ding, Yao and Yuan, Fei and Zheng, Liting and He, Wei and Zhang, Sophie S and Fu, Xin and Liu, Jin and Mutlu, Ayse Sena and Wang, Shuyue and Nehring, Ralf Bernd and Li, Xingyu and Tang, Qianzi and Li, Catherine and Lv, Xiangdong and Dobrolecki, Lacey E and Zhang, Weijie and Han, Dong and Zhao, Na and Jaehnig, Eric and Wang, Jingyi and Wu, Weiche and Graham, Davis A and Li, Yumei and Chen, Rui and Peng, Weiyi and Chen, Yiwen and Catic, Andre and Zhang, Zhibin and Zhang, Bing and Mustoe, Anthony M and Koong, Albert C and Miles, George and Lewis, Michael T and Wang, Meng C and Rosenberg, Susan M and O{\textquoteright}Malley, Bert W and Westbrook, Thomas F and Xu, Han and Zhang, Xiang H-F and Osborne, C Kent and Li, Jin Billy and Ellis, Matthew J and Rimawi, Mothaffar F and Rosen, Jeffrey M and Chen, Xi}
}
@article {65659,
	title = {Cell types promoting goosebumps form a niche to regulate hair follicle stem cells.},
	journal = {Cell},
	volume = {182},
	year = {2020},
	month = {2020 Aug 6},
	pages = {578},
	abstract = {<p>Piloerection (goosebumps) requires concerted actions of the hair follicle, the arrector pili muscle (APM), and the sympathetic nerve, providing a model to study interactions across epithelium, mesenchyme, and nerves. Here, we show that APMs and sympathetic nerves form a dual-component niche to modulate hair follicle stem cell (HFSC) activity. Sympathetic nerves form synapse-like structures with HFSCs and regulate HFSCs through norepinephrine, whereas APMs maintain sympathetic innervation to HFSCs. Without norepinephrine signaling, HFSCs enter deep quiescence by down-regulating the cell cycle and metabolism while up-regulating quiescence regulators Foxp1 and Fgf18. During development, HFSC progeny secretes Sonic Hedgehog (SHH) to direct the formation of this APM-sympathetic nerve niche, which in turn controls hair follicle regeneration in adults. Our results reveal a reciprocal interdependence between a regenerative tissue and its niche at different stages and demonstrate sympathetic nerves can modulate stem cells through synapse-like connections and neurotransmitters to couple tissue production with demands.</p>
},
	issn = {1097-4172},
	doi = {10.1016/j.cell.2020.06.031},
	author = {Shwartz, Yulia and Gonzalez-Celeiro, Meryem and Chen, Chih-Lung and Pasolli, H Amalia and Sheu, Shu-Hsien and Fan, Sabrina Mai-Yi and Shamsi, Farnaz and Assaad, Steven and Lin, Edrick Tai-Yu and Zhang, Bing and Tsai, Pai-Chi and He, Megan and Tseng, Yu-Hua and Lin, Sung-Jan and Hsu, Ya-Chieh}
}
