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Cited by 69

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Rapamycin inhibits FBXW7 loss-induced epithelial–mesenchymal transition and cancer stem cell-like characteristics in colorectal cancer cells

Wang, Yuli, Liu, Yueyong, Lu, Jing, Zhang, Pengju, Wang, Yunshan, Xu, Yangyang, Wang, Zeran, Mao, Jian-Hua, Wei, Guangwei·2013·Biochemical and Biophysical Research Communications
DOI 10.1016/j.bbrc.2013.03.077PMC PMC3646979
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Citations

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Research works printed but not linked: 20

  1. Thiery, 2002, Epithelial–mesenchymal transitions in tumour progression, Nat. Rev. Cancer, 2, 442, 10.1038/nrc822 · DOI
  2. Thiery, 2009, Epithelial–mesenchymal transitions in development and disease, Cell, 139, 871, 10.1016/j.cell.2009.11.007 · DOI · Paper page
  3. Reya, 2001, Stem cells, cancer, and cancer stem cells, Nature, 414, 105, 10.1038/35102167 · DOI · Paper page
  4. Abdullah, 2013, Mechanisms of chemoresistance in cancer stem cells, Clin. Transl. Med., 2, 3, 10.1186/2001-1326-2-3 · DOI
  5. Mani, 2008, The epithelial–mesenchymal transition generates cells with properties of stem cells, Cell, 133, 704, 10.1016/j.cell.2008.03.027 · DOI
  6. Cheng, 2012, Role of the ubiquitin ligase Fbw7 in cancer progression, Cancer Metastasis Rev., 31, 75, 10.1007/s10555-011-9330-z · DOI
  7. Tetzlaff, 2004, Defective cardiovascular development and elevated cyclin E and Notch proteins in mice lacking the Fbw7 F-box protein, Proc. Natl. Acad. Sci. USA, 101, 3338, 10.1073/pnas.0307875101 · DOI
  8. Tsunematsu, 2004, Mouse Fbw7/Sel-10/Cdc4 is required for notch degradation during vascular development, J. Biol. Chem., 279, 9417, 10.1074/jbc.M312337200 · DOI
  9. Rajagopalan, 2004, Inactivation of hCDC4 can cause chromosomal instability, Nature, 428, 77, 10.1038/nature02313 · DOI
  10. Rice, 2012, Metastasis: the rude awakening, Nature, 485, S55, 10.1038/485S55a · DOI
  11. Gulhati, 2011, MTORC1 and mTORC2 regulate EMT, motility, and metastasis of colorectal cancer via RhoA and Rac1 signaling pathways, Cancer Res., 71, 3246, 10.1158/0008-5472.CAN-10-4058 · DOI
  12. Mao, 2008, FBXW7 targets mTOR for degradation and cooperates with PTEN in tumor suppression, Science, 321, 1499, 10.1126/science.1162981 · DOI
  13. Liu, 2013, Temporal mTOR inhibition protects Fbxw7-deficient mice from radiation-induced tumor development, Aging (Albany, NY), 5, 111, 10.18632/aging.100535 · DOI
  14. Arabi, 2012, Proteomic screen reveals Fbw7 as a modulator of the NF-kappaB pathway, Nat. Commun., 3, 976, 10.1038/ncomms1975 · DOI · Paper page
  15. A.B. D’Assoro, T. Liu, C. Quatraro, A. Amato, M. Opyrchal, A. Leontovich, Y. Ikeda, S. Ohmine, W. Lingle, V. Suman, J. Ecsedy, I. Iankov, A. Di Leonardo, J. Ayers-Inglers, A. Degnim, D. Billadeau, J. McCubrey, J. Ingle, J.L. Salisbury, E. Galanis, The mitotic kinase Aurora-A promotes distant metastases by inducing epithelial-to-mesenchymal transition in ERalpha(+) breast cancer cells. Oncogene (2013). [Epub ahead of print] · DOI
  16. Chou, 2013, Chromosome Instability Modulated by BMI1-AURKA Signaling Drives Progression in Head and Neck Cancer, Cancer Res., 73, 953, 10.1158/0008-5472.CAN-12-2397 · DOI
  17. Wang, 2012, Overexpression of Aurora-A enhances invasion and matrix metalloproteinase-2 expression in esophageal squamous cell carcinoma cells, Mol. Cancer Res., 10, 588, 10.1158/1541-7786.MCR-11-0416 · DOI
  18. Kwon, 2012, Pten regulates Aurora-A and cooperates with Fbxw7 in modulating radiation-induced tumor development, Mol. Cancer Res., 10, 834, 10.1158/1541-7786.MCR-12-0025 · DOI
  19. Lu, 2012, MiR-25 regulates Wwp2 and Fbxw7 and promotes reprogramming of mouse fibroblast cells to iPSCs, PLoS One, 7, e40938, 10.1371/journal.pone.0040938 · DOI
  20. Okita, 2012, Increased efficiency in the generation of induced pluripotent stem cells by Fbxw7 ablation, Genes Cells, 17, 768, 10.1111/j.1365-2443.2012.01626.x · DOI

Cited by

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Metadata

Authors
Wang, Y., Liu, Y., Lu, J., Zhang, P., Wang, Y., Xu, Y., Wang, Z., Mao, J.-H., & Wei, G.
Venue
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Published
2013-05
Volume
434
Issue
2
Pages
352-356
ISSN
0006-291X
DOI
10.1016/j.bbrc.2013.03.077
PMC
PMC3646979
Cited by
69
References
3
Language
en
Licence
Funders
  • National Natural Science Foundation of China (31271461, 81172528)
  • National Institutes of Health
  • Ministry of Education of the People's Republic of China (20110131110035)
  • U.S. Department of Energy (DE-AC02-05CH11231)
  • Natural Science Foundation of Shandong Province (ZR2011HM034)
  • National Cancer Institute (R01 CA116481)
  • Laboratory Directed Research and Development
  • Biological and Environmental Research

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