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大学・研究所にある論文を検索できる 「Distinct but interchangeable subpopulations of colorectal cancer cells with different growth fates and drug sensitivity」の論文概要。リケラボ論文検索は、全国の大学リポジトリにある学位論文・教授論文を一括検索できる論文検索サービスです。

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Distinct but interchangeable subpopulations of colorectal cancer cells with different growth fates and drug sensitivity

Coppo, Roberto Kondo, Jumpei Iida, Keita Okada, Mariko Onuma, Kunishige Tanaka, Yoshihisa Kamada, Mayumi Ohue, Masayuki Kawada, Kenji Obama, Kazutaka Inoue, Masahiro 京都大学 DOI:10.1016/j.isci.2023.105962

2023.02.17

概要

Dynamic changes in cell properties lead to intratumor heterogeneity; however, the mechanisms of nongenetic cellular plasticity remain elusive. When the fate of each cell from colorectal cancer organoids was tracked through a clonogenic growth assay, the cells showed a wide range of growth ability even within the clonal organoids, consisting of distinct subpopulations; the cells generating large spheroids and the cells generating small spheroids. The cells from the small spheroids generated only small spheroids (S-pattern), while the cells from the large spheroids generated both small and large spheroids (D-pattern), both of which were tumorigenic. Transition from the S-pattern to the D-pattern occurred by various extrinsic triggers, in which Notch signaling and Musashi-1 played a key role. The S-pattern spheroids were resistant to chemotherapy and transited to the D-pattern upon drug treatment through Notch signaling. As the transition is linked to the drug resistance, it can be a therapeutic target.

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参考文献

1. Swanton, C. (2012). Intratumor heterogeneity: evolution through space and time. Cancer Res. 72, 4875–4882. https://doi. org/10.1158/0008-5472.CAN-12-2217.

2. Burrell, R.A., McGranahan, N., Bartek, J., and Swanton, C. (2013). The causes and consequences of genetic heterogeneity in cancer evolution. Nature 501, 338–345. https://doi.org/10.1038/nature12625.

3. McGranahan, N., and Swanton, C. (2017). Clonal heterogeneity and tumor evolution: past, present, and the future. Cell 168, 613–628. https://doi.org/10.1016/j.cell.2017. 01.018.

4. Junttila, M.R., and de Sauvage, F.J. (2013). Influence of tumour micro-environment heterogeneity on therapeutic response. Nature 501, 346–354. https://doi.org/10. 1038/nature12626.

5. Meacham, C.E., and Morrison, S.J. (2013). Tumour heterogeneity and cancer cell plasticity. Nature 501, 328–337. https://doi. org/10.1038/nature12624.

6. Stratton, M.R., Campbell, P.J., and Futreal, P.A. (2009). The cancer genome. Nature 458, 719–724. https://doi.org/10.1038/ nature07943.

7. Brock, A., Chang, H., and Huang, S. (2009). Non-genetic heterogeneity–a mutation- independent driving force for the somatic evolution of tumours. Nat. Rev. Genet. 10, 336–342. https://doi.org/10.1038/nrg2556.

8. Boumahdi, S., and de Sauvage, F.J. (2020). The great escape: tumour cell plasticity in resistance to targeted therapy. Nat. Rev. Drug Discov. 19, 39–56. https://doi.org/10. 1038/s41573-019-0044-1.

9. Marine, J.C., Dawson, S.J., and Dawson, M.A. (2020). Non-genetic mechanisms of therapeutic resistance in cancer. Nat. Rev. Cancer 20, 743–756. https://doi.org/10.1038/ s41568-020-00302-4.

10. Batlle, E., and Clevers, H. (2017). Cancer stem cells revisited. Nat. Med. 23, 1124–1134. https://doi.org/10.1038/nm.4409.

11. Siegel, R.L., Miller, K.D., Fuchs, H.E., and Jemal, A. (2021). Cancer statistics, 2021. CA. Cancer J. Clin. 71, 7–33. https://doi.org/10. 3322/caac.21654.

12. Dieter, S.M., Ball, C.R., Hoffmann, C.M., Nowrouzi, A., Herbst, F., Zavidij, O., Abel, U., Arens, A., Weichert, W., Brand, K., et al. (2011). Distinct types of tumor-initiating cells form human colon cancer tumors and metastases. Cell Stem Cell 9, 357–365. https://doi.org/10.1016/j.stem.2011.08.010.

13. de Sousa e Melo, F., Kurtova, A.V., Harnoss, J.M., Kljavin, N., Hoeck, J.D., Hung, J., Anderson, J.E., Storm, E.E., Modrusan, Z., Koeppen, H., et al. (2017). A distinct role for Lgr5(+) stem cells in primary and metastatic colon cancer. Nature 543, 676–680. https:// doi.org/10.1038/nature21713.

14. Shimokawa, M., Ohta, Y., Nishikori, S., Matano, M., Takano, A., Fujii, M., Date, S., Sugimoto, S., Kanai, T., and Sato, T. (2017). Visualization and targeting of LGR5(+) human colon cancer stem cells. Nature 545, 187–192. https://doi.org/10.1038/nature22081.

15. Hirata, A., Hatano, Y., Niwa, M., Hara, A., and Tomita, H. (2019). Heterogeneity in colorectal cancer stem cells. Cancer Prev. Res. 12, 413–420. https://doi.org/10.1158/1940-6207. CAPR-18-0482.

16. Fumagalli, A., Oost, K.C., Kester, L., Morgner, J., Bornes, L., Bruens, L., Spaargaren, L., Azkanaz, M., Schelfhorst, T., Beerling, E., et al. (2020). Plasticity of Lgr5-negative cancer cells drives metastasis in colorectal cancer. Cell Stem Cell 26, 569–578.e7. https://doi.org/10. 1016/j.stem.2020.02.008.

17. Drost, J., and Clevers, H. (2018). Organoids in cancer research. Nat. Rev. Cancer 18, 407–418. https://doi.org/10.1038/s41568-018-0007-6.

18. Kondo, J., Endo, H., Okuyama, H., Ishikawa, O., Iishi, H., Tsujii, M., Ohue, M., and Inoue, M. (2011). Retaining cell-cell contact enables preparation and culture of spheroids composed of pure primary cancer cells from colorectal cancer. Proc. Natl. Acad. Sci. USA 108, 6235–6240. https://doi.org/10.1073/ pnas.1015938108.

19. Kondo, J., Ekawa, T., Endo, H., Yamazaki, K., Tanaka, N., Kukita, Y., Okuyama, H., Okami, J., Imamura, F., Ohue, M., et al. (2019). High- throughput screening in colorectal cancer tissue-originated spheroids. Cancer Sci. 110, 345–355. https://doi.org/10.1111/cas.13843.

20. Endo, H., Kondo, J., Onuma, K., Ohue, M., and Inoue, M. (2020). Small subset of Wnt- activated cells is an initiator of regrowth in colorectal cancer organoids after irradiation. Cancer Sci. 111, 4429–4441. https://doi.org/ 10.1111/cas.14683.

21. Roesch, A., Fukunaga-Kalabis, M., Schmidt, E.C., Zabierowski, S.E., Brafford, P.A., Vultur, A., Basu, D., Gimotty, P., Vogt, T., and Herlyn, M. (2010). A temporarily distinct subpopulation of slow-cycling melanoma cells is required for continuous tumor growth. Cell 141, 583–594. https://doi.org/10.1016/j. cell.2010.04.020.

22. Kurtova, A.V., Xiao, J., Mo, Q., Pazhanisamy, S., Krasnow, R., Lerner, S.P., Chen, F., Roh, T.T., Lay, E., Ho, P.L., and Chan, K.S. (2015). Blocking PGE2-induced tumour repopulation abrogates bladder cancer chemoresistance. Nature 517, 209–213. https://doi.org/10. 1038/nature14034.

23. Rehman, S.K., Haynes, J., Collignon, E., Brown, K.R., Wang, Y., Nixon, A.M.L., Bruce, J.P., Wintersinger, J.A., Singh Mer, A. , Lo, E.B.L., et al. (2021). Colorectal cancer cells enter a diapause-like DTP state to survive chemotherapy. Cell 184, 226– 242.e21. https://doi.org/10.1016/j.cell.2020. 11.018.

24. Shiokawa, D., Sakai, H., Ohata, H., Miyazaki, T., Kanda, Y., Sekine, S., Narushima, D., Hosokawa, M., Kato, M., Suzuki, Y., et al. (2020). Slow-Cycling cancer stem cells regulate progression and chemoresistance in colon cancer. Cancer Res. 80, 4451–4464. https://doi.org/10.1158/0008-5472.CAN-20-0378.

25. Richichi, C., Brescia, P., Alberizzi, V., Fornasari, L., and Pelicci, G. (2013). Marker- independent method for isolating slow- dividing cancer stem cells in human glioblastoma. Neoplasia 15, 840–847. https:// doi.org/10.1593/neo.13662.

26. Dalerba, P., Kalisky, T., Sahoo, D., Rajendran, P.S., Rothenberg, M.E., Leyrat, A.A., Sim, S., Okamoto, J., Johnston, D.M., Qian, D., et al. (2011). Single-cell dissection of transcriptional heterogeneity in human colon tumors. Nat. Biotechnol. 29, 1120–1127. https://doi.org/10.1038/nbt.2038.

27. Zeller, K.I., Jegga, A.G., Aronow, B.J., O’Donnell, K.A., and Dang, C.V. (2003). An integrated database of genes responsive to the Myc oncogenic transcription factor: identification of direct genomic targets. Genome Biol. 4, R69. https://doi.org/10. 1186/gb-2003-4-10-r69.

28. Dang, C.V. (2012). MYC on the path to cancer. Cell 149, 22–35. https://doi.org/10.1016/j. cell.2012.03.003.

29. Schaefer, C.F., Anthony, K., Krupa, S., Buchoff, J., Day, M., Hannay, T., and Buetow, K.H. (2009). PID: the pathway interaction database. Nucleic Acids Res. 37, D674–D679. https://doi.org/10.1093/nar/gkn653.

30. Bu, P., Chen, K.Y., Chen, J.H., Wang, L., Walters, J., Shin, Y.J., Goerger, J.P., Sun, J., Witherspoon, M., Rakhilin, N., et al. (2013). A microRNA miR-34a-regulated bimodal switch targets Notch in colon cancer stem cells. Cell Stem Cell 12, 602–615. https://doi.org/10.1016/j.stem.2013.03.002.

31. Srinivasan, T., Than, E.B., Bu, P., Tung, K.L., Chen, K.Y., Augenlicht, L., Lipkin, S.M., and Shen, X. (2016). Notch signalling regulates asymmetric division and inter-conversion between lgr5 and bmi1 expressing intestinal stem cells. Sci. Rep. 6, 26069. https://doi.org/ 10.1038/srep26069.

32. Barrett, S.D., Bridges, A.J., Dudley, D.T., Saltiel, A.R., Fergus, J.H., Flamme, C.M., Delaney, A.M., Kaufman, M., LePage, S., Leopold, W.R., et al. (2008). The discovery of the benzhydroxamate MEK inhibitors CI-1040 and PD 0325901. Bioorg. Med. Chem. Lett. 18, 6501–6504. https://doi.org/10.1016/j. bmcl.2008.10.054.

33. Potten, C.S., Booth, C., Tudor, G.L., Booth, D., Brady, G., Hurley, P., Ashton, G., Clarke, R., Sakakibara, S.i., and Okano, H. (2003). Identification of a putative intestinal stem cell and early lineage marker; musashi-1. Differentiation 71, 28–41. https://doi.org/10. 1046/j.1432-0436.2003.700603.x.

34. Schulenburg, A., Cech, P., Herbacek, I., Marian, B., Wrba, F., Valent, P., and Ulrich- Pur, H. (2007). CD44-positive colorectal adenoma cells express the potential stem cell markers musashi antigen (msi1) and ephrin B2 receptor (EphB2). J. Pathol. 213, 152–160. https://doi.org/10.1002/path.2220.

35. Yousefi, M., Li, N., Nakauka-Ddamba, A., Wang, S., Davidow, K., Schoenberger, J., Yu, Z., Jensen, S.T., Kharas, M.G., and Lengner, C.J. (2016). Msi RNA-binding proteins control reserve intestinal stem cell quiescence. J. Cell Biol. 215, 401–413. https://doi.org/10.1083/ jcb.201604119.

36. Sureban, S.M., May, R., George, R.J., Dieckgraefe, B.K., McLeod, H.L., Ramalingam, S., Bishnupuri, K.S., Natarajan, G., Anant, S., and Houchen, C.W. (2008). Knockdown of RNA binding protein musashi-1 leads to tumor regression in vivo. Gastroenterology 134, 1448–1458. https://doi.org/10.1053/j.gastro.2008.02.057.

37. Li, N., Yousefi, M., Nakauka-Ddamba, A., Li, F., Vandivier, L., Parada, K., Woo, D.H., Wang, S., Naqvi, A.S., Rao, S., et al. (2015). The Msi family of RNA-binding proteins function redundantly as intestinal oncoproteins. Cell Rep. 13, 2440–2455. https://doi.org/10.1016/ j.celrep.2015.11.022.

38. Glazer, R.I., Vo, D.T., and Penalva, L.O.F. (2012). Musashi1: an RBP with versatile functions in normal and cancer stem cells. Front. Biosci. 17, 54–64. https://doi.org/10. 2741/3915.

39. Huang, S. (2009). Non-genetic heterogeneity of cells in development: more than just noise. Development 136, 3853–3862. https://doi. org/10.1242/dev.035139.

40. Pisco, A.O., and Huang, S. (2015). Non- genetic cancer cell plasticity and therapy- induced stemness in tumour relapse: ‘What does not kill me strengthens me’. Br. J. Cancer 112, 1725–1732. https://doi.org/10. 1038/bjc.2015.146.

41. Todaro, M., Alea, M.P., Di Stefano, A.B., Cammareri, P., Vermeulen, L., Iovino, F., Tripodo, C., Russo, A., Gulotta, G., Medema, J.P., and Stassi, G. (2007). Colon cancer stem cells dictate tumor growth and resist cell death by production of interleukin-4. Cell Stem Cell 1, 389–402. https://doi.org/10. 1016/j.stem.2007.08.001.

42. Vermeulen, L., De Sousa E Melo, F., van der Heijden, M., Cameron, K., de Jong, J.H., Borovski, T., Tuynman, J.B., Todaro, M., Merz, C., Rodermond, H., et al. (2010). Wnt activity defines colon cancer stem cells and is regulated by the microenvironment. Nat. Cell Biol. 12, 468–476. https://doi.org/10.1038/ ncb2048.

43. Kudinov, A.E., Karanicolas, J., Golemis, E.A., and Boumber, Y. (2017). Musashi RNA- binding proteins as cancer drivers and novel therapeutic targets. Clin. Cancer Res. 23, 2143–2153. https://doi.org/10.1158/1078-0432.CCR-16-2728.

44. Gao, C., Han, C., Yu, Q., Guan, Y., Li, N., Zhou, J., Tian, Y., and Zhang, Y. (2015). Downregulation of Msi1 suppresses the growth of human colon cancer by targeting p21cip1. Int. J. Oncol. 46, 732–740. https:// doi.org/10.3892/ijo.2014.2749.

45. O’Brien, C.A., Kreso, A., Ryan, P., Hermans, K.G., Gibson, L., Wang, Y., Tsatsanis, A., Gallinger, S., and Dick, J.E. (2012). ID1 and ID3 regulate the self-renewal capacity of human colon cancer-initiating cells through p21. Cancer Cell 21, 777–792. https://doi.org/ 10.1016/j.ccr.2012.04.036.

46. Srinivasan, T., Walters, J., Bu, P., Than, E.B., Tung, K.L., Chen, K.Y., Panarelli, N., Milsom, J., Augenlicht, L., Lipkin, S.M., and Shen, X. (2016). NOTCH signaling regulates asymmetric cell fate of fast- and slow-cycling colon cancer-initiating cells. Cancer Res. 76, 3411–3421. https://doi.org/10.1158/0008-5472.CAN-15-3198.

47. Nakamura, M., Okano, H., Blendy, J.A., and Montell, C. (1994). Musashi, a neural RNA- binding protein required for Drosophila adult external sensory organ development. Neuron 13, 67–81. https://doi.org/10.1016/0896-6273(94)90460-x.

48. Cojoc, M., Ma¨ bert, K., Muders, M.H., and Dubrovska, A. (2015). A role for cancer stem cells in therapy resistance: cellular and molecular mechanisms. Semin. Cancer Biol. 31, 16–27. https://doi.org/10.1016/j. semcancer.2014.06.004.

49. Sharma, S.V., Lee, D.Y., Li, B., Quinlan, M.P., Takahashi, F., Maheswaran, S., McDermott, U., Azizian, N., Zou, L., Fischbach, M.A., et al. (2010). A chromatin-mediated reversible drug-tolerant state in cancer cell subpopulations. Cell 141, 69–80. https://doi. org/10.1016/j.cell.2010.02.027.

50. Liau, B.B., Sievers, C., Donohue, L.K., Gillespie, S.M., Flavahan, W.A., Miller, T.E., Venteicher, A.S., Hebert, C.H., Carey, C.D., Rodig, S.J., et al. (2017). Adaptive chromatin remodeling drives glioblastoma stem cell plasticity and drug tolerance. Cell Stem Cell 20, 233–246.e7. https://doi.org/10.1016/j. stem.2016.11.003.

51. Oren, Y., Tsabar, M., Cuoco, M.S., Amir- Zilberstein, L., Cabanos, H.F., Hu¨ tter, J.C., Hu, B., Thakore, P.I., Tabaka, M., Fulco, C.P., et al. (2021). Cycling cancer persister cells arise from lineages with distinct programs. Nature 596, 576–582. https://doi.org/10. 1038/s41586-021-03796-6.

52. Piulats, J.M., Kondo, J., Endo, H., Ono, H., Hagihara, T., Okuyama, H., Nishizawa, Y., Tomita, Y., Ohue, M., Okita, K., et al. (2018). Promotion of malignant phenotype after disruption of the three-dimensional structure of cultured spheroids from colorectal cancer. Oncotarget 9, 15968–15983. https://doi.org/ 10.18632/oncotarget.24641.

53. Onuma, K., Sato, Y., Okuyama, H., Uematsu, H., Homma, K., Ohue, M., Kondo, J., and Inoue, M. (2021). Aberrant activation of Rho/ ROCK signaling in impaired polarity switching of colorectal micropapillary carcinoma. J. Pathol. 255, 84–94. https://doi. org/10.1002/path.5748.

54. Heckl, D., Kowalczyk, M.S., Yudovich, D., Belizaire, R., Puram, R.V., McConkey, M.E., Thielke, A., Aster, J.C., Regev, A., and Ebert, B. L. (2014). Generation of mouse models of myeloid malignancy with combinatorial genetic lesions using CRISPR-Cas9 genome editing. Nat. Biotechnol. 32, 941–946. https:// doi.org/10.1038/nbt.2951.

55. Endo, H., Okami, J., Okuyama, H., Nishizawa, Y., Imamura, F., and Inoue, M. (2017). The induction of MIG6 under hypoxic conditions is critical for dormancy in primary cultured lung cancer cells with activating EGFR mutations. Oncogene 36, 2824–2834. https:// doi.org/10.1038/onc.2016.431.

56. Kusuhashi, N., and Okamoto, T. (2015). A nonparametric multimodality test— Silverman’s test—and its introduction into paleontology. Fossils 97, 23–37. https://doi. org/10.14825/kaseki.97.0_23.

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