Are cancer stem cells the sole source of tumor?
Tóm tắt
Tumors are believed to consist of a heterogeneous population of tumor cells originating from rare cancer stem cells (CSCs). However, emerging evidence suggests that tumor may also originate from non-CSCs. To support this viewpoint, we are here to present definitive evidence indicating that the number of tumorigenic tumor cells is greater than that of CSCs in tumor, and tumor can also derive from non-CSCs. To achieve this, an idealized mathematical model was employed in the present study and theoretical calculation revealed that non-CSCs could initiate the occurrence of tumor if their proliferation potential was adequate. Further, experimental studies demonstrated that 17.7%, 38.6% and 5.2% of tumor cells in murine B16 solid melanoma, H22 hepatoma and Lewis lung carcinoma, respectively, were potentially tumorigenic. Thus, based on the aforementioned findings, we propose that the scarce CSCs, if exist, are not the sole source of a tumor.
Tài liệu tham khảo
Pardal R, Clarke MF, Morrison SJ. Applying the principles of stem-cell biology to cancer. Nat Rev Cancer 2003,3(12):895–902
Bjerkvig R, Tysnes BB, Aboody KS, et al. Opinion: the origin of the cancer stem cell: current controversies and new insights. Nat Rev Cancer, 2005,5(11):899–904
Rosen JM, Jordan CT. The increasing complexity of the cancer stem cell paradigm. Science, 2009,324(5935): 1670–1673
Smith A. A glossary for stem-cell biology. Nature, 2006, 441(7097):1060–1060
O’Brien CA, Pollett A, Gallinger S, et al. A human colon cancer cell capable of initiating tumour growth in immunodeficient mice. Nature, 2007,445(7123):106–110
Maccalli C, Volontè A, Cimminiello C, et al. Immunology of cancer stem cells in solid tumours. A review. Eur J Cancer, 2014,50(6):649–55
Sourisseau T, Hassan KA, Wistuba I, et al. Lung cancer stem cell: fancy conceptual model of tumor biology or cornerstone of a forthcoming therapeutic breakthrough? J Thorac Oncol, 2014,9(1):7–17
Yamashita T, Wang XW. Cancer stem cells in the development of liver cancer. J Clin Invest, 2013, 123(5):1911–1918
Nishikawa S, Dewi DL, Ishii H, et al. Transcriptomic study of dormant gastrointestinal cancer stem cells. Int J Oncol, 2012,41(3): 979–984
Kelly PN, Dakic A, Adams JM, et al. Tumor growth need not be driven by rare cae]s. Science, 2007,317e](5836): 337
Quintana E, Shackleton M, Sabel MS, et al. Efficient tumour formation by single human melanoma cells. Nature, 2008,456(7222):593–598
He YF, Liu YK, Lu HJ, et al. Comparative proteomic analysis of primary mouse liver c-Kit-(CD45/TER119)-stem/progenitor cells. J Cell Biochem, 2007,102(4): 936–946
He YF, Zhang GM, Wang XH, et al. Blocking programmed death-1 ligand-PD-1 interactions by local gene therapy results in enhancement of antitumor effect of secondary lymphoid tissue chemokine. J Immunol, 2004,173(9):4919–4928
Collani E, Dräger K. Binomial distribution handbook for scientists and engineers. Birkhauser Boston Press, 2001, Boston.
Enderling H, Hlatky L, Hahnfeldt P. Migration rules: tumours are conglomerates of self-metastases. Br J Cancer, 2009,100(12):1917–1925
Roose T, Netti PA, Munn LL, et al. Solid stress generated by spheroid growth estimated using a linear poroelasticity model small star, filled. Microvasc Res, 2003,66(3): 204–212
Al-Hajj M1, Wicha MS, Benito-Hernandez A, et al. Prospective identification of tumorigenic breast cancer cells. Proc Natl Acad Sci U S A, 2003,100(7):3983–3988
Adams JM, Kelly PN, Dakic A, et al. Response to comment on “tumor growth need not be driven by rare cancer stem cells”. Science, 2007,318(5857):1722