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Qing-Bai She


HKRB 417


  • Professor, Department of Pharmacology & Nutritional Sciences
  • Markey Cancer Center

College Unit(s)

Other Affiliation(s)
  • Markey Cancer Center
  • Pharmacology and Nutritional Sciences Center Affiliated Faculty

Biography and Education


Ph.D., Gifu University
Postdoctoral Fellow, University of Minnesota
Senior Research Scientist, Memorial Sloan-Kettering Cancer Center


Research in our lab focuses on the identification and characterization of oncogenic factors and pathways that drive disease progression and therapeutic resistance in colorectal cancer (CRC). We particularly investigate the mechanistic basis of redundancy and crosstalk among oncoprotein-activated signaling pathways and understand how this functional interplay promotes tumor progression and alters the response to CRC therapies. We employ a combination of molecular cell biology, biochemistry, chemical biology, pharmacology, multiomics, and mouse modeling approaches to elucidate the underlying mechanisms that control CRC progression and metastasis as well as therapeutic resistance, with the ultimate goal of developing novel biomarkers and therapies that can enhance the diagnosis and treatment of CRC. Through molecular analysis of mRNA translation states, our work establishes dysregulation of cap-dependent translation downstream of mTOR at the level of 4E-BP1/eIF4E, as a key to tumor formation, metastasis and resistance to 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 during CRC progression. Furthermore, we have discovered and developed two new classes of natural product-based small molecular inhibitors with distinct mechanisms of action in targeting translational control of CRC and another major cancer. Recently, our group has uncovered two novel splice variants of neuropilin-1 (NRP1) that promote CRC metastasis by activating endosomal signals. Additionally, we have identified a previously unknown function of spermine synthase (SMS), a polyamine biosynthetic enzyme, that cooperates with MYC oncogene to facilitate CRC tumorigenesis. The key insights into the role of NRP1 variants in CRC metastasis and the function of SMS in CRC metabolic reprograming as well as their modulation of therapeutic outcomes are further characterizing in our lab.

Selected Publications

  1. Cao Y, Ye Q, Ma M, She QB. Enhanced bypass of PD-L1 translation reduces the therapeutic response to mTOR kinase inhibitors. Cell Reports, 42:112764, 2023. PMCID: PMC10491412
  2. Hong, Liu T, Wan L, Fa P, Kumar P, Cao Y, Prasad C, Qiu Z, Liu J, Wang H, Li Z, Wang QE, Guo P, Guo D, Yilmaz AS, Lu L, Papandreou I, Jacob NK, Yan C, Zhang X, She QB, Ma Z, Zhang J. Targeting squalene epoxidase interrupts homologous recombination via the ER stress response and promotes radiotherapy efficacy. Cancer Res, 82:1298-1312, 2022. PMCID: PMC8983553
  3. 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 maintain colorectal cancer cell survival by convergent repression of Bim expression. Nat Commun, 11:3243, 2020. PMCID: PMC7320137
  4. Huang X, Ye Q, Chen M, Li A, Mi 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)
  5. 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)
  6. 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 and glutaredoxin 3 to trigger ROS/4E-BP1-mediated antitumor effects. Cell Chem Biol 26:366-377, 2019. PMCID: PMC6557261. (Featured Article
  7. 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 to mTOR kinase inhibitors by transcriptional repression of 4E-BP1. Nat Commun 8:2207, 2017. PMCID: PMC5738350
  8. 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)
  9. Cai W, Ye Q, She QB. Loss of 4E-BP1 function induces EMT and promotes cancer cell migration and invasion via translational activation of snail. Oncotarget 5:6015-6027, 2014. PMCID: PMC4171609
  10. 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: PMC3966979
  11. 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 and ERK signaling pathways that integrates their function in tumors. Cancer Cell 18:39-51, 2010. PMCID: PMC3286650
  12. Halilovic E, She QB, Ye Q, Pagliarini R, Sellers WR, Solit DB, Rosen N.  PIK3CA mutation uncouples tumor growth and cyclin D1 regulation from MEK/ERK and mutant KRAS signaling. Cancer Res 70:6804-6814, 2010.
  13. 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 to Akt signaling.  PLoS ONE 3:e3065, 2010.
  14. Rosen N, She QB.  AKT and cancer--is it all mTOR?  Cancer Cell 10:254-256, 2006.
  15. 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.
  16. She QB, Solit D, Basso A, Moasser MM.  Resistance to 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.