Search

Your search keyword '"Xie, Qi"' showing total 1,907 results
Start Over Author "Xie, Qi" Publication Type Academic Journals
1,907 results on '"Xie, Qi"'

1. RBBP6 maintains glioblastoma stem cells through CPSF3-dependent alternative polyadenylation.

Author

Lin, Peng, Chen, Wenyan, Long, Zhilin, Yu, Jichuan, Yang, Jiayao, Xia, Zhen, Wu, Qiulian, Min, Xinyu, Tang, Jing, Cui, Ya, Liu, Fuyi, Wang, Chun, Zheng, Jian, Rich, Jeremy, Li, Lei, Xie, Qi, and Li, Wei

Abstract

Glioblastoma is one of the most lethal malignant cancers, displaying striking intratumor heterogeneity, with glioblastoma stem cells (GSCs) contributing to tumorigenesis and therapeutic resistance. Pharmacologic modulators of ubiquitin ligases and deubiquitinases are under development for cancer and other diseases. Here, we performed parallel in vitro and in vivo CRISPR/Cas9 knockout screens targeting human ubiquitin E3 ligases and deubiquitinases, revealing the E3 ligase RBBP6 as an essential factor for GSC maintenance. Targeting RBBP6 inhibited GSC proliferation and tumor initiation. Mechanistically, RBBP6 mediated K63-linked ubiquitination of Cleavage and Polyadenylation Specific Factor 3 (CPSF3), which stabilized CPSF3 to regulate alternative polyadenylation events. RBBP6 depletion induced shortening of the 3UTRs of MYC competing-endogenous RNAs to release miR-590-3p from shortened UTRs, thereby decreasing MYC expression. Targeting CPSF3 with a small molecular inhibitor (JTE-607) reduces GSC viability and inhibits in vivo tumor growth. Collectively, RBBP6 maintains high MYC expression in GSCs through regulation of CPSF3-dependent alternative polyadenylation, providing a potential therapeutic paradigm for glioblastoma.

Published
2024

42. CHMP2A regulates tumor sensitivity to natural killer cell-mediated cytotoxicity

Author

Bernareggi, Davide, Xie, Qi, Prager, Briana C, Yun, Jiyoung, Cruz, Luisjesus S, Pham, Timothy V, Kim, William, Lee, Xiqing, Coffey, Michael, Zalfa, Cristina, Azmoon, Pardis, Zhu, Huang, Tamayo, Pablo, Rich, Jeremy N, and Kaufman, Dan S

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Immunology, Oncology and Carcinogenesis, Dental/Oral and Craniofacial Disease, Rare Diseases, Cancer, Stem Cell Research, Vaccine Related, 2.1 Biological and endogenous factors, Aetiology, Animals, Apoptosis, Cell Line, Tumor, Cytotoxicity, Immunologic, Endosomal Sorting Complexes Required for Transport, Head and Neck Neoplasms, Humans, Immunotherapy, Killer Cells, Natural, Mice, Squamous Cell Carcinoma of Head and Neck
Abstract

Natural killer (NK) cells are known to mediate killing of various cancer types, but tumor cells can develop resistance mechanisms to escape NK cell-mediated killing. Here, we use a "two cell type" whole genome CRISPR-Cas9 screening system to discover key regulators of tumor sensitivity and resistance to NK cell-mediated cytotoxicity in human glioblastoma stem cells (GSC). We identify CHMP2A as a regulator of GSC resistance to NK cell-mediated cytotoxicity and we confirm these findings in a head and neck squamous cells carcinoma (HNSCC) model. We show that deletion of CHMP2A activates NF-κB in tumor cells to mediate increased chemokine secretion that promotes NK cell migration towards tumor cells. In the HNSCC model we demonstrate that CHMP2A mediates tumor resistance to NK cells via secretion of extracellular vesicles (EVs) that express MICA/B and TRAIL. These secreted ligands induce apoptosis of NK cells to inhibit their antitumor activity. To confirm these in vitro studies, we demonstrate that deletion of CHMP2A in CAL27 HNSCC cells leads to increased NK cell-mediated killing in a xenograft immunodeficient mouse model. These findings illustrate a mechanism of tumor immune escape through EVs secretion and identify inhibition of CHMP2A and related targets as opportunities to improve NK cell-mediated immunotherapy.

Published
2022

48. Distinct Evolutionary Profiles and Functions of microRNA156 and microRNA529 in Land Plants.

Author

Xie, Qi, Wang, Xufeng, He, Juan, Lan, Ting, Zheng, Jiayu, Li, Yupeng, Pan, Jinkang, Lin, Ling, Zhao, Junyi, Li, Jing, Yu, Yu, Mo, Beixin, Chen, Xuemei, Gao, Lei, and Liu, Lin

Subjects
SQUAMOSA promoter binding protein-like genes, evolution, land plants, miR156, miR529, Genetics, Biotechnology, Chemical Physics, Other Chemical Sciences, Other Biological Sciences
Abstract

MicroRNA156 (miR156) and miR529 have high sequence similarity and recognize overlapping sites in the same target genes, SQUAMOSA promoter binding protein-like (SPL or SBP box) genes, making it difficult to accurately distinguish their roles in regulatory networks that affect numerous biological functions. Here, we collected data about miR156 and miR529 family members from representative land plants and performed sequence comparisons, phylogenetic analysis, small RNA sequencing, and parallel analysis of RNA ends (PARE) analysis to dissect their evolutionary and functional differences. Although miR156 and miR529 are highly similar, there are differences in their mismatch-sensitive regions, which are essential for target recognition. In land plants, miR156 precursors are conserved mainly within the hairpin region, whereas miR529 precursors are conserved outside the hairpin region, including both the 5' and 3' arms. Phylogenetic analysis showed that MIR156 and MIR529 evolved independently, through divergent evolutionary patterns. The two genes also exhibit different expression patterns, with MIR529 preferentially expressed in reproductive tissues and MIR156 in other tissues. PARE analysis revealed that miR156 and miR529 possess specific targets in addition to common targets in maize, pointing to functional differences between them. Based on our findings, we developed a method for the rapid identification of miR529 and miR156 family members and uncovered the evolutionary divergence of these families, providing insights into their different regulatory roles in plant growth and development.

Published
2021

Catalog

Books, media, physical & digital resources
See catalog results