Ph.D., Gifu UniversityPostdoctoral Fellow, University of MinnesotaSenior Research Scientist, Memorial Sloan-Kettering Cancer Center




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Research in my lab focuses on identification & characterization of oncogenic factors và pathways that drive disease progression và therapeutic resistance in colorectal cancer (CRC). We particularly study the mechanistic basis of redundancy & crosstalk among oncoprotein-activated signaling pathways and how the functional crosstalk among these pathways promotes cancer progression & alters the therapeutic response to CRC. We employ a combination of molecular, cellular, biochemical, genetic, pharmacologic, imaging, bioinformatic, animal và clinical association approaches to lớn decipher the transcriptional & post-transcriptional mechanisms controlling ren expression and pathways important for the malignant transformation & metastatic progression of CRC, with the ultimate goal of developing novel biomarkers và therapies for improving the diagnosis & treatment of this disease. Through molecular analysis of mRNA translation states, our work establishes dysregulation of cap-dependent translation downstream of mTOR at the màn chơi of 4E-BP1/eIF4E, as a key khổng lồ tumor formation, metastasis và resistance to lớn upstream kinase-targeted therapies. Specifically, we identify 4E-BP1 as a critical node that integrates the oncogenic effects of the PI3K/AKT and RAS/RAF/MEK/ERK pathways in CRC progression. In addition, we discover several natural product-based small molecular inhibitors with a novel mechanism of kích hoạt in targeting translational control of CRC và potentially other major cancers. Moreover, our recent work uncovers 1) two novel neuropilin-1 (NRP1) splice variants that can promote CRC metastasis by activating endosomal signals, and 2) a novel function of spemine synthase (SMS), a polyamine biosynthetic enzyme, in cooperation with MYC oncogene to maintain CRC tumorigenesis. The key insights of the NRP1 variants and SMS function in metabolic reprograming in CRC as well as their modulations of therapeutic outcomes are further characterizing in the lab.


ActiveNIH R01CA175105NIH R01CA203257NIH R21ES031712

Completed1. ACS IRG85-001-222. UK CCTS KL2TR000116


1.Guo Y, Ye Q, Deng P, Cao Y, He D, Zhou Z, Wang C, Zaytseva YY, Schwartz CE, Lee EY, Evers BM, Morris AJ, Liu S, She QB. Spermine synthase and MYC cooperate to lớn maintain colorectal cancer cell survival by convergent repression of Bim expression. Nat Commun, 11:3243, 2020. PMCID: PMC73201372.Huang X, Ye Q, Chen M, Li A, ngươi W, Fang Y, Zaytseva YY, O’Connor KL, Vander Kooi CW, Liu S, She QB. N-glycosylation-defective splice variants of neuropilin-1 promote metastasis by activating endosomal signals. Nat Commun, 10:3708, 2019. PMCID: PMC6697747 (selected by Faculty 1000 rated exceptional)3.Zhang Y, Ye Q, Ponomareva LV, Liu Y, Cao Y, Cui Z, Van Lanen, SG, Voss SR, She QB*, Thorson JS*. Total synthesis of griseusins and elucidation of the griseusin mechanism of action. Chem Sci, 10:7641-7648, 2019. PMCID: PMC6755659 (Edge Article; *Co-corresponding author)4.Ye Q, Zhang Y, Cao Y, Wang X, Guo Y, Chen J, Horn J, Ponomareva LV, Chaiswing L, Shaaban KA, Wei Q, Anderson BD, St Clair KD, Zhu H, Leggas M, Thorson JS, She QB. Frenolicin B targets peroxiredoxin 1 và glutaredoxin 3 khổng lồ trigger ROS/4E-BP1-aryannations88.comiated antitumor effects. Cell Chem Biol 26:366-377, 2019. PMCID: PMC6557261. (Featured Article)5.Wang J, Ye Q, Cao Y, Guo Y, Huang X, mi W, Liu S, Wang C, Yang HS, Zhou BP, Evers BM, She QB. Snail determines the therapeutic response khổng lồ mTOR kinase inhibitors by transcriptional repression of 4E-BP1. Nat Commun 8:2207, 2017. PMCID: PMC57383506.Mi W, Ye Q, Liu S, She QB. AKT inhibition overcomes rapamycin resistance by enhancing the repressive function of PRAS40 on mTORC1/4E-BP1 axis. Oncotarget 6:13962-13977, 2015. PMCID: PMC4546444. (Priority Research Paper)7.Cai W, Ye Q, She QB. Loss of 4E-BP1 function induces EMT & promotes cancer cell migration và invasion via translational activation of snail. Oncotarget 5:6015-6027, 2014. PMCID: PMC41716098.Ye Q, Cai W, Zhen Y, Evers BM, She QB. ERK and AKT signaling cooperate to translationally regulate survivin expression for metastatic progression of colorectal cancer. Oncogene 33:1828-1839, 2014. PMCID: PMC39669799.She QB, Halilovic E, Ye Q, Zhen W, Shirasawa S, Sasazuki T, Solit, DB, Rosen N. 4E-BP1 is a key effector of the oncogenic activation of the AKT & ERK signaling pathways that integrates their function in tumors. Cancer Cell 18:39-51, 2010. PMCID: PMC328665010.Halilovic E, She QB, Ye Q, Pagliarini R, Sellers WR, Solit DB, Rosen N. PIK3CA mutation uncouples tumor growth & cyclin D1 regulation from MEK/ERK & mutant KRAS signaling. Cancer Res 70:6804-6814, 2010.11.She QB, Chandarlapaty S, Ye Q, Lobo J, Haskell KM, Leander KR, DeFeo-Jones D, Huber HE, Rosen N. Breast tumor cells with PI3K mutation or HER2 amplification are selectively addicted khổng lồ Akt signaling. PLoS ONE 3:e3065, 2010.12.Rosen N, She QB. AKT & cancer--is it all mTOR? Cancer Cell 10:254-256, 2006.13.She, QB, Solit DB, Ye Q, O'Reilly KE, Lobo J, Rosen N. The BAD protein integrates survival signaling by EGFR/MAPK and PI3K/Akt kinase pathways in PTEN-deficient tumor cells. Cancer Cell 8:287-297, 2005.14.She QB, Solit D, Basso A, Moasser MM.

Xem thêm: Định Nghĩa, Tính Chất Hình Thang Cân Là Gì? Định Nghĩa, Tính Chất Về Hình Thang Cân Chi Tiết

Resistance to lớn gefitinib in PTEN-null HER-overexpressing tumor cells can be overcome through restoration of PTEN function or pharmacologic modulation of constitutive phosphatidylinositol 3'-kinase/Akt pathway signaling. Clin Cancer Res 9:4340-4346, 2003.

https://www.ncbi.nlm.nih.gov/myncbi/qing-bai.she.1/bibliography/public/https://scholar.google.com/citations?user=_Wyw_d8AAAAJ&hl=en&oi=ao