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Altered apoptotic protein expressions characterize the survival of Bcr-Abl-independent drug-resistant chronic myeloid leukemia cell line

Yıl 2021, Cilt: 5 Sayı: 1, 1 - 5, 26.02.2021
https://doi.org/10.30621/jbachs.848797

Öz

Apoptosis is a programmed cellular process that occurs in pathological and physiological pathways and it is one of the most studied topics in cell biology. To understand the underlying mechanism of apoptosis plays an important role in the molecular pathogenesis of many diseases including cancers. Chronic myeloid leukemia (CML) is a clonal myeloproliferative malignancy arising from the neoplastic transformation of the hematopoietic stem cell. Here, we used a Bcr-Abl-independent, imatinib-resistant K562 subpopulation (K562-IR) generated and characterized earlier in our laboratory. We showed that the proteins Bcl-2, Bim, RIP, p-MAPK(Erk1/Erk2) and NF-кB which play critical roles in cell death pathways are downregulated, Lamin A/C protein expression is upregulated in K562-IR derivative cells compared to K562 ancestral cells. Our data provide new information on the expression of apoptotic molecules in a Bcr-Abl-independent imatinib-resistant CML cell line.

Teşekkür

The authors gratefully acknowledge Dr. Zeynep Yüce for her valuable comments on our work.

Kaynakça

  • 1. Ellis RE, Yuan J, and Horvitz HR. Mechanisms and functions of cell death. Vol. 7, Annual Review of Cell Biology. Annu Rev Cell Biol; 1991; 663–698.
  • 2. Ellis HM and Horvitz HR. Genetic control of programmed cell death in the nematode C. elegans. Cell 1986; 44:817–829.
  • 3. Pistritto G, Trisciuoglio D, Ceci C, Alessia Garufi, and D’Orazi G. Apoptosis as anticancer mechanism: Function and dysfunction of its modulators and targeted therapeutic strategies. Vol. 8, Aging. Impact Journals LLC; 2016; 603–619.
  • 4. Pfeffer CM and Singh ATK. Apoptosis: A target for anticancer therapy. Vol. 19, International Journal of Molecular Sciences. MDPI AG; 2018.
  • 5. Wong RSY. Apoptosis in cancer: From pathogenesis to treatment. Vol. 30, Journal of Experimental and Clinical Cancer Research. BioMed Central; 2011; 87.
  • 6. Quintás-Cardama A and Cortes J. Molecular biology of bcr-abl1-positive chronic myeloid leukemia. Blood 2009; 113:1619–30.
  • 7. Deininger MWN, Goldman JM, Melo J V, Dc W, Deininger MWN, Goldman JM, et al. The molecular biology of chronic myeloid leukemia Review article The molecular biology of chronic myeloid leukemia. 2000; 96:3343–3356.
  • 8. Seke Etet PF, Vecchio L, and Nwabo Kamdje AH. Signaling pathways in chronic myeloid leukemia and leukemic stem cell maintenance: Key role of stromal microenvironment. Cell Signal 2012; 24:1883–1888.
  • 9. Yilmaz M and Jabbour E. Tyrosine Kinase Inhibitors Early in the Disease Course: Lessons From Chronic Myelogenous Leukemia. Semin Oncol 2015; 42:876–886.
  • 10. Hochhaus a, O’Brien SG, Guilhot F, Druker BJ, Branford S, Foroni L, et al. Six-year follow-up of patients receiving imatinib for the first-line treatment of chronic myeloid leukemia. Leukemia 2009; 23:1054–61.
  • 11. Deininger MWN and Druker BJ. Specific Targeted Therapy of Chronic Myelogenous Leukemia with Imatinib. Pharmacol Rev 2003; 55:401–423.
  • 12. Assouline S and Lipton JH. Monitoring response and resistance to treatment in chronic myeloid leukemia. Curr Oncol 2011; 18:e71-83.
  • 13. Bixby D and Talpaz M. Mechanisms of resistance to tyrosine kinase inhibitors in chronic myeloid leukemia and recent therapeutic strategies to overcome resistance. Hematology 2009; 2009:461–476.
  • 14. O’Hare T, Eide CA, and Deininger MWN. Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. Blood 2007; 110:2242–2249.
  • 15. Corbin AS, Agarwal A, Loriaux M, Cortes J, Deininger MW, and Druker BJ. Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity. J Clin Invest 2011; 121:396–409.
  • 16. Mitchell R, Hopcroft LEM, Baquero P, Allan EK, Hewit K, James D, et al. Targeting BCR-ABL-independent TKI resistance in chronic myeloid leukemia by mTOR and autophagy inhibition. J Natl Cancer Inst 2018; 110:467–478.
  • 17. Baykal-Köse S, Acikgoz E, Yavuz AS, Geyik ÖG, Ateş H, Sezerman OU, et al. Adaptive phenotypic modulations lead to therapy resistance in chronic myeloid leukemia cells. PLoS One 2020; 15:1–19.
  • 18. Danial NN and Korsmeyer SJ. Cell Death: Critical Control Points. Vol. 116, Cell. Cell Press; 2004; 205–219. 19. Ewings KE, Wiggins CM, and Cook SJ. Bim and the pro-survival Bcl-2 proteins: Opposites attract, ERK repels. Vol. 6, Cell Cycle. Taylor and Francis Inc.; 2007; 2236–2240.
  • 20. Kaufmann SH. Imatinib spells BAD news for Bcr/abl-positive leukemias. Vol. 103, Proceedings of the National Academy of Sciences of the United States of America. 2006; 14651–14652.
  • 21. Martens S, Hofmans S, Declercq W, Augustyns K, and Vandenabeele P. Inhibitors Targeting RIPK1/RIPK3: Old and New Drugs. Trends Pharmacol Sci 2020; 41:209–224.
  • 22. Zhang X, Dowling JP, and Zhang J. RIPK1 can mediate apoptosis in addition to necroptosis during embryonic development. Cell Death Dis 2019; 10:1–11.
  • 23. Dhuriya YK and Sharma D. Necroptosis: A regulated inflammatory mode of cell death. Vol. 15, Journal of Neuroinflammation. BioMed Central Ltd.; 2018.
  • 24. Galluzzi L, Kepp O, and Kroemer G. RIP kinases initiate programmed necrosis. J Mol Cell Biol 2009; 1:8–10.
  • 25. Aggarwal BB. Tumour necrosis factors receptor associated signalling molecules and their role in activation of apoptosis, JNK and NF-κB. In: Annals of the Rheumatic Diseases. BMJ Publishing Group Ltd; 2000; i6–i16.
  • 26. Kawai T and Akira S. Signaling to NF-κB by Toll-like receptors. Trends Mol Med 2007; 13:460–469.
  • 27. Cusson-Hermance N, Khurana S, Lee TH, Fitzgerald KA, and Kelliher MA. Rip1 mediates the trif-dependent Toll-like receptor 3- and 4-induced NF-κB activation but does not contribute to interferon regulatory factor 3 activation. J Biol Chem 2005; 280:36560–36566.
  • 28. Hsu H, Huang J, Shu HB, Baichwal V, and Goeddel D V. TNF-dependent recruitment of the protein kinase RIP to the TNF receptor-1 signaling complex. Immunity 1996; 4:387–396.
  • 29. Okinaga T, Kasai H, Tsujisawa T, and Nishihara T. Role of caspases in cleavage of lamin A/C and PARP during apoptosis in macrophages infected with a periodontopathic bacterium. J Med Microbiol 2007; 56:1399–1404.
  • 30. Broers JLV and Ramaekers FCS. The role of the nuclear lamina in cancer and apoptosis. Adv Exp Med Biol 2014; 773:27–48.
Yıl 2021, Cilt: 5 Sayı: 1, 1 - 5, 26.02.2021
https://doi.org/10.30621/jbachs.848797

Öz

Kaynakça

  • 1. Ellis RE, Yuan J, and Horvitz HR. Mechanisms and functions of cell death. Vol. 7, Annual Review of Cell Biology. Annu Rev Cell Biol; 1991; 663–698.
  • 2. Ellis HM and Horvitz HR. Genetic control of programmed cell death in the nematode C. elegans. Cell 1986; 44:817–829.
  • 3. Pistritto G, Trisciuoglio D, Ceci C, Alessia Garufi, and D’Orazi G. Apoptosis as anticancer mechanism: Function and dysfunction of its modulators and targeted therapeutic strategies. Vol. 8, Aging. Impact Journals LLC; 2016; 603–619.
  • 4. Pfeffer CM and Singh ATK. Apoptosis: A target for anticancer therapy. Vol. 19, International Journal of Molecular Sciences. MDPI AG; 2018.
  • 5. Wong RSY. Apoptosis in cancer: From pathogenesis to treatment. Vol. 30, Journal of Experimental and Clinical Cancer Research. BioMed Central; 2011; 87.
  • 6. Quintás-Cardama A and Cortes J. Molecular biology of bcr-abl1-positive chronic myeloid leukemia. Blood 2009; 113:1619–30.
  • 7. Deininger MWN, Goldman JM, Melo J V, Dc W, Deininger MWN, Goldman JM, et al. The molecular biology of chronic myeloid leukemia Review article The molecular biology of chronic myeloid leukemia. 2000; 96:3343–3356.
  • 8. Seke Etet PF, Vecchio L, and Nwabo Kamdje AH. Signaling pathways in chronic myeloid leukemia and leukemic stem cell maintenance: Key role of stromal microenvironment. Cell Signal 2012; 24:1883–1888.
  • 9. Yilmaz M and Jabbour E. Tyrosine Kinase Inhibitors Early in the Disease Course: Lessons From Chronic Myelogenous Leukemia. Semin Oncol 2015; 42:876–886.
  • 10. Hochhaus a, O’Brien SG, Guilhot F, Druker BJ, Branford S, Foroni L, et al. Six-year follow-up of patients receiving imatinib for the first-line treatment of chronic myeloid leukemia. Leukemia 2009; 23:1054–61.
  • 11. Deininger MWN and Druker BJ. Specific Targeted Therapy of Chronic Myelogenous Leukemia with Imatinib. Pharmacol Rev 2003; 55:401–423.
  • 12. Assouline S and Lipton JH. Monitoring response and resistance to treatment in chronic myeloid leukemia. Curr Oncol 2011; 18:e71-83.
  • 13. Bixby D and Talpaz M. Mechanisms of resistance to tyrosine kinase inhibitors in chronic myeloid leukemia and recent therapeutic strategies to overcome resistance. Hematology 2009; 2009:461–476.
  • 14. O’Hare T, Eide CA, and Deininger MWN. Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. Blood 2007; 110:2242–2249.
  • 15. Corbin AS, Agarwal A, Loriaux M, Cortes J, Deininger MW, and Druker BJ. Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity. J Clin Invest 2011; 121:396–409.
  • 16. Mitchell R, Hopcroft LEM, Baquero P, Allan EK, Hewit K, James D, et al. Targeting BCR-ABL-independent TKI resistance in chronic myeloid leukemia by mTOR and autophagy inhibition. J Natl Cancer Inst 2018; 110:467–478.
  • 17. Baykal-Köse S, Acikgoz E, Yavuz AS, Geyik ÖG, Ateş H, Sezerman OU, et al. Adaptive phenotypic modulations lead to therapy resistance in chronic myeloid leukemia cells. PLoS One 2020; 15:1–19.
  • 18. Danial NN and Korsmeyer SJ. Cell Death: Critical Control Points. Vol. 116, Cell. Cell Press; 2004; 205–219. 19. Ewings KE, Wiggins CM, and Cook SJ. Bim and the pro-survival Bcl-2 proteins: Opposites attract, ERK repels. Vol. 6, Cell Cycle. Taylor and Francis Inc.; 2007; 2236–2240.
  • 20. Kaufmann SH. Imatinib spells BAD news for Bcr/abl-positive leukemias. Vol. 103, Proceedings of the National Academy of Sciences of the United States of America. 2006; 14651–14652.
  • 21. Martens S, Hofmans S, Declercq W, Augustyns K, and Vandenabeele P. Inhibitors Targeting RIPK1/RIPK3: Old and New Drugs. Trends Pharmacol Sci 2020; 41:209–224.
  • 22. Zhang X, Dowling JP, and Zhang J. RIPK1 can mediate apoptosis in addition to necroptosis during embryonic development. Cell Death Dis 2019; 10:1–11.
  • 23. Dhuriya YK and Sharma D. Necroptosis: A regulated inflammatory mode of cell death. Vol. 15, Journal of Neuroinflammation. BioMed Central Ltd.; 2018.
  • 24. Galluzzi L, Kepp O, and Kroemer G. RIP kinases initiate programmed necrosis. J Mol Cell Biol 2009; 1:8–10.
  • 25. Aggarwal BB. Tumour necrosis factors receptor associated signalling molecules and their role in activation of apoptosis, JNK and NF-κB. In: Annals of the Rheumatic Diseases. BMJ Publishing Group Ltd; 2000; i6–i16.
  • 26. Kawai T and Akira S. Signaling to NF-κB by Toll-like receptors. Trends Mol Med 2007; 13:460–469.
  • 27. Cusson-Hermance N, Khurana S, Lee TH, Fitzgerald KA, and Kelliher MA. Rip1 mediates the trif-dependent Toll-like receptor 3- and 4-induced NF-κB activation but does not contribute to interferon regulatory factor 3 activation. J Biol Chem 2005; 280:36560–36566.
  • 28. Hsu H, Huang J, Shu HB, Baichwal V, and Goeddel D V. TNF-dependent recruitment of the protein kinase RIP to the TNF receptor-1 signaling complex. Immunity 1996; 4:387–396.
  • 29. Okinaga T, Kasai H, Tsujisawa T, and Nishihara T. Role of caspases in cleavage of lamin A/C and PARP during apoptosis in macrophages infected with a periodontopathic bacterium. J Med Microbiol 2007; 56:1399–1404.
  • 30. Broers JLV and Ramaekers FCS. The role of the nuclear lamina in cancer and apoptosis. Adv Exp Med Biol 2014; 773:27–48.
Toplam 29 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Konular Sağlık Kurumları Yönetimi
Bölüm Research Article
Yazarlar

Seda Baykal Köse

Pelin Yalçın

Yayımlanma Tarihi 26 Şubat 2021
Gönderilme Tarihi 28 Aralık 2020
Yayımlandığı Sayı Yıl 2021 Cilt: 5 Sayı: 1

Kaynak Göster

APA Baykal Köse, S., & Yalçın, P. (2021). Altered apoptotic protein expressions characterize the survival of Bcr-Abl-independent drug-resistant chronic myeloid leukemia cell line. Journal of Basic and Clinical Health Sciences, 5(1), 1-5. https://doi.org/10.30621/jbachs.848797
AMA Baykal Köse S, Yalçın P. Altered apoptotic protein expressions characterize the survival of Bcr-Abl-independent drug-resistant chronic myeloid leukemia cell line. JBACHS. Şubat 2021;5(1):1-5. doi:10.30621/jbachs.848797
Chicago Baykal Köse, Seda, ve Pelin Yalçın. “Altered Apoptotic Protein Expressions Characterize the Survival of Bcr-Abl-Independent Drug-Resistant Chronic Myeloid Leukemia Cell Line”. Journal of Basic and Clinical Health Sciences 5, sy. 1 (Şubat 2021): 1-5. https://doi.org/10.30621/jbachs.848797.
EndNote Baykal Köse S, Yalçın P (01 Şubat 2021) Altered apoptotic protein expressions characterize the survival of Bcr-Abl-independent drug-resistant chronic myeloid leukemia cell line. Journal of Basic and Clinical Health Sciences 5 1 1–5.
IEEE S. Baykal Köse ve P. Yalçın, “Altered apoptotic protein expressions characterize the survival of Bcr-Abl-independent drug-resistant chronic myeloid leukemia cell line”, JBACHS, c. 5, sy. 1, ss. 1–5, 2021, doi: 10.30621/jbachs.848797.
ISNAD Baykal Köse, Seda - Yalçın, Pelin. “Altered Apoptotic Protein Expressions Characterize the Survival of Bcr-Abl-Independent Drug-Resistant Chronic Myeloid Leukemia Cell Line”. Journal of Basic and Clinical Health Sciences 5/1 (Şubat 2021), 1-5. https://doi.org/10.30621/jbachs.848797.
JAMA Baykal Köse S, Yalçın P. Altered apoptotic protein expressions characterize the survival of Bcr-Abl-independent drug-resistant chronic myeloid leukemia cell line. JBACHS. 2021;5:1–5.
MLA Baykal Köse, Seda ve Pelin Yalçın. “Altered Apoptotic Protein Expressions Characterize the Survival of Bcr-Abl-Independent Drug-Resistant Chronic Myeloid Leukemia Cell Line”. Journal of Basic and Clinical Health Sciences, c. 5, sy. 1, 2021, ss. 1-5, doi:10.30621/jbachs.848797.
Vancouver Baykal Köse S, Yalçın P. Altered apoptotic protein expressions characterize the survival of Bcr-Abl-independent drug-resistant chronic myeloid leukemia cell line. JBACHS. 2021;5(1):1-5.