Ph.D., Gifu University
Postdoctoral Fellow, University of Minnesota
Senior Research Scientist, Memorial Sloan-Kettering Cancer Center
My lab is currently focusing on using pharmacologic, biochemical and genetic approaches and animal models 1) to understand the biochemical and biologic consequences of mutational activation of growth signaling pathways such as PI3K/AKT/mTOR and RAS/RAF/MEK/ERK pathways in human cancers; 2) to dissect the mechanistic basis of redundancy and crosstalk among oncoprotein-activated signaling pathways; and 3) to use these insights to develop new strategies for cancer therapy. We have recently discovered that the activation of cap-dependent translation plays a critical role in integration of the function of both AKT and ERK pathways in colorectal cancer progression and metastasis and alters the response of colorectal cancer to targeted therapy. We are particularly interested in the identification and characterization of translationally-controlled gene expression and pathways that confer tumor progression and metastasis, as well as their mechanisms involved, with the goal to develop novel target therapy based on the understanding of the mechanistic insights for prevention and treatment of cancer.
1. Nandurkar N, Zhang J, Ye Q, Ponomereva LV, She QB, Thorson JS. The identification of perillyl alcohol glycosides with improved antiproliferative activity. J Med Chem, In press.
2. 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, 2014 Jun 16. [Epub ahead of print].
3. 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. (doi:10.1038/onc.2013.122; published online Apr 29, 2013)
4. Ye Q, She QB. Integration of AKT and ERK signaling pathways in cancer: biological and therapeutic implications. J Pharmacol Clin Toxicol, 1(2), 1009, 2013.
5. Zhang Y, Wang X, Sunkara M, Ye Q, Ponomareva LV, She QB, Morris AJ, Thorson JS. A diastereoselective oxa-Pictet-Spengler-based strategy for (+)-frenolicin B and epi-(+)-frenolicin B synthesis. Organic Letters, 15(21):5566-9, 2013.
6. Liu Y, Liu F, Yu H, Zhao X, Sashida G, Deblasio A, Harr M, She QB, Chen Z, Lin HK, Di Giandomenico S, Elf SE, Yang Y, Miyata Y, Huang G, Menendez S, Mellinghoff IK, Rosen N, Pandolfi PP, Hedvat CV, Nimer SD. Akt phosphorylates the transcriptional repressor bmi1 to block its effects on the tumor-suppressing ink4a-arf locus. Sci Signal. 5: ra77, 2012.
7. Hanrahan AJ, Schultz N, Westfal ML, Sakr RA, Giri DD, Scarperi S, Janikariman M, Olvera N, Stevens EV, She QB, Aghajanian C, King TA, de Stanchina E, Spriggs DR, Heguy A, Taylor BS, Sander C, Rosen N, Levine DA, Solit DB. Genomic complexity and AKT-dependence in serous ovarian cancer. Cancer Discov, 2: 56-67, 2012.
8. Xing F, Persaud Y, Pratilas CA, Taylor BS, Janakiraman M, She QB, Gallardo H, Liu C, Merghoub T, Hefter B, Dolgalev I, Viale A, Heguy A, De Stanchina E, Cobrinik D, Bollag G, Wolchok J, Houghton A, Solit DB. Concurrent loss of the PTEN and RB1 tumor suppressors attenuates RAF dependence in melanomas harboring (V600E)BRAF. Oncogene 31:446-457, 2012.
9. 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.
10. 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.
11. Cherrin C, Haskell KM, Howell B, Jones R, Leander KR, Robinson, R, Watkins A, Bilodeau M, Hoffman J, Sanderson P, Hartman G, Mahan E, Prueksaritanont T, Jiang G, She QB, Rosen N, Sepp-Lorenzino L, DeFeo-Jones D, Huber HE. An allosteric Akt inhibitor effectively blocks Akt signaling and tumor growth with only transient effects on glucose and insulin levels in vivo. Cancer Biol Ther 9:493-503, 2010.
12. 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, 2008.
13. Nelander S, Wang WQ, Nilsson B, She QB, Pratilas C, Rosen N, Gennemark P, Sander C. Models from experiments: combinatorial drug perturbations of cancer cells. Mol Syst Biol 4:216, 2008.
14. Saal LH, Johansson P, Holm K, Gruvberger-Saal SK, She QB, Maurer M, Koujak S, Ferrando AA, Malmstrom P, Memeo L, Isola J, Bendahl PO, Rosen N, Hibshoosh H, Ringner M, Borg A, Parsons R. Poor prognosis in carcinoma is associated with a gene expression signature of aberrant PTEN tumor suppressor pathway activity. Proc Natl Acad Sci USA 104:7564-7569, 2007.
15. O'Reilly KE, Rojo F, She QB, Solit D, Mills GB, Smith D, Lane H, Hofmann F, Hicklin DJ, Ludwig DL, Baselga J, Rosen N. mTOR inhibition induces upstream receptor tyrosine kinase signaling and activates Akt. Cancer Res 66:1500-1508, 2006.
16. Rosen N, She QB. AKT and cancer--is it all mTOR? Cancer Cell 10:254-256, 2006.
17. 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.
18. 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.
19. She QB, Ma WY, Wang M, Kaji A, Ho CT, Dong Z. Inhibition of cell transformation by resveratrol and its derivatives: differential effects and mechanisms involved. Oncogene, 22: 2143-2150, 2003.
20. She QB, Chen N, Bode AM, Flavell RA, Dong Z. Deficiency of c-Jun-NH(2)-terminal kinase-1 in mice enhances skin tumor development by 12-O-tetradecanoylphorbol-13-acetate. Cancer Res, 62: 1343-1348, 2002.
21. She QB, Ma WY, Dong Z. Role of MAP kinases in UVB-induced phosphorylation of p53 at serine 20. Oncogene, 21: 1580-1589, 2002.
22. She QB, Ma WY, Zhong S, Dong Z. Activation of JNK1, RSK2, and MSK1 is involved in serine 112 phosphorylation of Bad by ultraviolet B radiation. J Biol Chem, 277: 24039-24048, 2002.
23. She QB, Huang C, Zhang Y, Dong Z. Involvement of c-jun NH(2)-terminal kinases in resveratrol-induced activation of p53 and apoptosis. Mol Carcinog, 33: 244-250, 2002.
24. Chen N, She QB, Bode AM., Dong Z. Differential gene expression profiles of Jnk1- and Jnk2-deficient murine fibroblast cells. Cancer Res, 62: 1300-1304, 2002.
25. She QB, Bode AM, Ma WY, Chen NY, Dong Z. Resveratrol-induced activation of p53 and apoptosis is mediated by extracellular-signal-regulated protein kinases and p38 kinase. Cancer Res, 61: 1604-1610, 2001.
26. Chen N, Nomura M., She QB, Ma WY, Bode AM., Wang L, Flavell RA, Dong Z. Suppression of skin tumorigenesis in c-Jun NH(2)-terminal kinase-2-deficient mice. Cancer Res, 61: 3908-3912, 2001.
27. Chen N, Ma WY, She QB, Wu E, Liu G, Bode AM., Dong Z. Transactivation of the epidermal growth factor receptor is involved in 12-O-tetradecanoylphorbol-13-acetate-induced signal transduction. J Biol Chem 276: 46722-46728, 2001.
28. Zhong S, Jansen C, She QB, Goto H, Inagaki M, Bode AM, Ma WY, Dong Z. Ultraviolet B-induced phosphorylation of histone H3 at serine 28 is mediated by MSK1. J Biol Chem 276: 33213-33219, 2001.
29. She QB, Chen N, Dong, Z. ERKs and p38 kinase phosphorylate p53 protein at serine 15 in response to UV radiation. J Biol Chem, 275: 20444-20449, 2000.