DOI QR코드

DOI QR Code

Treatment of Vemurafenib-Resistant SKMEL-28 Melanoma Cells with Paclitaxel

  • Nguyen, Dinh Thang (Department of Biochemistry and Plant Physiology, Key Laboratory of Enzyme and Protein Technology, VNU University of Science, Vietnam National University) ;
  • Phan, Tuan Nghia (Department of Biochemistry and Plant Physiology, Key Laboratory of Enzyme and Protein Technology, VNU University of Science, Vietnam National University) ;
  • Kumasaka, Mayuko Y. (Department of Occupational and Environmental Health, Nagoya University Graduate School of Medicine) ;
  • Yajima, Ichiro (Department of Occupational and Environmental Health, Nagoya University Graduate School of Medicine) ;
  • Kato, Masashi (Department of Occupational and Environmental Health, Nagoya University Graduate School of Medicine)
  • 발행 : 2015.02.25

초록

Vemurafenib has recently been used as drug for treatment of melanomas with $BRAF^{V600E}$ mutation. Unfortunately, treatment with only vemurafenib has not been sufficiently effective, with recurrence after a short period. In this study, three vemurafenib-resistant $BRAF^{V600E}$ melanoma cell lines, $A375P^R$, $A375M^R$ and SKMEL-$28^R$, were established from the original A375P, A375M and SKMEL-28 cell lines. Examination of the molecular mechanisms showed that the phosphorylation levels of MEK and ERK, which play key roles in the RAS/RAF/MEK/ERK signaling pathway, were reduced in these three cell lines, with increased phosphorylation levels of pAKTs limited to SKMEL-$28^R$ cells. Treatment of SKMEL-$28^R$ cells with 100 nM paclitaxel resulted in increased apoptosis and decreased cellular proliferation, invasion and colony formation via reduction of expression levels of EGFR and pAKTs. Moreover, vemurafenib-induced pAKTs in SKMEL-$28^R$ were decreased by treatment with an AKT inhibitor, MK-2206. Taken together, our results revealed that resistance mechanisms of $BRAF^{V600E}$-mutation melanoma cells to vemurafenib depended on the cell type. Our results suggested that paclitaxel should be considered as a drug in combination with vemurafenib to treat melanoma cells.

키워드

참고문헌

  1. Atefi M, von Euw E, Attar N, et al (2011). Reversing melanoma cross-resistance to BRAF and MEK inhibitors by cotargeting the AKT/mTOR pathway. PLoS One, 6, 28973. https://doi.org/10.1371/journal.pone.0028973
  2. Bhattacharya S, Darjatmoko SR, Polans AS (2011). Resveratrol modulates the malignant properties of cutaneous melanoma through changes in the activation and attenuation of the antiapoptotic protooncogenic protein Akt/PKB. Melanoma Res, 21, 180-7. https://doi.org/10.1097/CMR.0b013e3283456dfc
  3. Bollag G, Hirth P, Tsai J, et al (2010). Clinical efficacy of a RAF inhibitor needs broad target blockade in BRAF-mutant melanoma. Nature, 467, 596-9. https://doi.org/10.1038/nature09454
  4. Bollag G, Tsai J, Zhang J, et al (2012). Vemurafenib: the first drug approved for BRAF-mutant cancer. Nat Rev Drug Discov, 11, 873-86. https://doi.org/10.1038/nrd3847
  5. Chen B, Tardell C, Higgins B, et al (2012). BRAFV600E negatively regulates the AKT pathway in melanoma cell lines. PLoS One, 7, 42598. https://doi.org/10.1371/journal.pone.0042598
  6. Cohen C, Zavala-Pompa A, Sequeira JH, et al (2002). Mitogenactived protein kinase activation is an early event in melanoma progression. Clin Cancer Res, 8, 3728-33.
  7. Corcoran RB, Rothenberg SM, Hata AN, et al (2013). TORC1 suppression predicts responsiveness to RAF and MEK inhibition in BRAF-mutant melanoma. Sci Transl Med, 5, 196-8.
  8. Dankort D, Curley DP, Cartlidge RA, et al (2009). Braf (V600E) cooperates with Pten loss to induce metastatic melanoma. Nat Genet, 415, 544-52.
  9. Davies H, Bignell GR, Cox C, et al (2002). Mutations of the BRAF gene in human cancer. Nature, 417, 949-54. https://doi.org/10.1038/nature00766
  10. Dhawan P, Singh AB, Ellis DL, et al (2002). Constitutive activation of Akt/protein kinase B in melanoma leads to up-egulation of nuclear factor-kappaB and tumor progression. Cancer Res, 62, 7335-42.
  11. Flaherty KT, Puzanov I, Kim KB, et al (2010). Inhibition of mutated, activated BRAF in metastatic melanoma. N Engl J Med, 363, 809-19. https://doi.org/10.1056/NEJMoa1002011
  12. Fontanini G, Vignati S, Bigini D, et al (1995). Epidermal growth factor receptor (EGFr) expression in non-small cell lung carcinomas correlates with metastatic involvement of hilar and mediastinal lymph nodes in the squamous subtype. Eur J Cancer, 31, 78-183.
  13. Girotti MR, Marais R (2013). Deja vu: EGF receptors drive resistance to BRAF inhibitors. Cancer Discov, 3, 487-90. https://doi.org/10.1158/2159-8290.CD-13-0131
  14. Gray-Schopfer V, Wellbrock C, Marais R (2007). Melanoma biology and new targeted therapy. Nature, 445, 851-57. https://doi.org/10.1038/nature05661
  15. Gross A, Niemetz-Rahn A, Nonnenmacher A, et al (2014). Expression and activity of EGFR in human cutaneous melanoma cell lines and influence of vemurafenib on the EGFR pathway. Target Oncol, [Epub ahead of print].
  16. Guan H, Singh NP, Singh UP, et al (2012). Resveratrol prevents endothelial cells injury in high-dose interleukin-2 therapy against melanoma. PLoS One, 7, 35650. https://doi.org/10.1371/journal.pone.0035650
  17. Halaban R, Zhang W, Bacchiocchi A, et al (2010). PLX4032, a selective BRAF (V600E) kinase inhibitor, activates the ERK pathway and enhances cell migration and proliferation of BRAF melanoma cells. Pigment Cell Melanoma Res, 23, 190-200. https://doi.org/10.1111/j.1755-148X.2010.00685.x
  18. Johannessen CM, Boehm JS, Kim SY, et al (2010). COT drives resistance to RAF inhibition through MAP kinase pathway reactivation. Nature, 468, 68-972.
  19. Joseph EW, Pratilas CA, Poulikakos PI, et al (2010). The RAF inhibitor PLX4032 inhibits ERK signalingand tumor cell proliferation in a V600E BRAF selective manner. Proc Natl Acad Sci U S A, 107, 14903-8. https://doi.org/10.1073/pnas.1008990107
  20. Kato M, Takeda K, Hossain K, et al (2010). A redox-linked novel pathway for arsenic-mediated RET tyrosine kinase activation. J Cell Biochem, 110, 399-407.
  21. Kawada K, Sonoshita M, Sakashita H, et al (2004). Pivotal role of CXCR3 in melanoma cell metastasis to lymph nodes. Cancer Res, 64, 4010-7. https://doi.org/10.1158/0008-5472.CAN-03-1757
  22. Lassen A, Atefi M, Robert L, et al (2014). Comin-Anduix B, Ribas A. Effects of AKT inhibitor therapy in response and resistance to BRAF inhibition in melanoma. Mol Cancer, 13, 83. https://doi.org/10.1186/1476-4598-13-83
  23. Lucchetti C, Rizzolio F, Castronovo M, et al (2011). Research highlights. Overcoming BRAF resistance to PLX4032 by AKT inhibition in PTEN-deficient melanoma cells. Pharmacogenomics, 12, 1381.
  24. McCubrey JA, Steelman LS, Chappell WH, et al (2007). Roles of the Raf/MEK/ERK pathway in cell growth, malignant transformation and drug resistance. Biochim Biophys Acta, 1773, 1263-84. https://doi.org/10.1016/j.bbamcr.2006.10.001
  25. Meier F, Schittek B, Busch S, et al (2005). The RAS/RAF/MEK/ERK and PI3K/AKT signaling pathways present molecular targets for the effective treatment of advanced melanoma. Front Biosci, 10, 2986-3001. https://doi.org/10.2741/1755
  26. Nazarian R, Shi H, Wang Q, et al (2010). Melanomas acquire resistance to B-RAF (V600E) inhibition by RTK or N-RAS upregulation. Nature, 468, 973-7. https://doi.org/10.1038/nature09626
  27. Osmond GW, Masko EM, Tyler DS, et al (2013). In vitro and in vivo evaluation of resveratrol and 3, 5-dihydroxy-4'-acetoxy-trans-stilbene in the treatment of human prostate carcinoma and melanoma. J Surg Res, 179, 141-8. https://doi.org/10.1016/j.jss.2012.02.057
  28. Paraiso KH, Haarberg HE, Wood E, et al (2012). The HSP90 inhibitor XL888 overcomes BRAF inhibitor resistance mediated through diverse mechanisms. Clin Cancer Res, 18, 2502-14. https://doi.org/10.1158/1078-0432.CCR-11-2612
  29. Patel PS, Varney ML, Dave BJ, et al (2002). Regulation of constitutive and induced NF-kappaB activation in malignant melanoma cells by capsaicin modulates interleukin-8 production and cell proliferation. J Interferon Cytokine Res, 22, 427-35. https://doi.org/10.1089/10799900252952217
  30. Peinado H, Aleckovic M, Lavotshkin S, et al (2012). Melanoma exosomes educate bone marrow progenitor cells toward a pro-metastatic phenotype through MET. Nat Med, 18, 883-91. https://doi.org/10.1038/nm.2753
  31. Prahallad A, Sun C, Huang S, et al (2012). Unresponsiveness of colon cancer to BRAF (V600E) inhibition through feedback activation of EGFR. Nature, 483, 100-3. https://doi.org/10.1038/nature10868
  32. Rebecca VW, Massaro RR, Fedorenko IV, et al (2014). Inhibition of autophagy enhances the effects of the AKT inhibitor MK-2206 when combined with paclitaxel and carboplatin in BRAF wild-type melanoma. Pigment Cell Melanoma Res, 27, 465-78. https://doi.org/10.1111/pcmr.12227
  33. Rigel DS (2010). Epidemiology of melanoma. Semin Cutan Med Surg, 29, 204-9. https://doi.org/10.1016/j.sder.2010.10.005
  34. Schutte B, Nuydens R, Geerts H, et al (1998). Annexin V binding assay as a tool to measure apoptosis in differentiated neuronal cells. J Neurosci Methods, 86, :63-9. https://doi.org/10.1016/S0165-0270(98)00147-2
  35. Shao Y, Aplin AE (2010). Akt3-mediated resistance to apoptosis in B-RAF-targeted melanoma cells. Cancer Res, 70, 6670-81. https://doi.org/10.1158/0008-5472.CAN-09-4471
  36. Shin DH, Kim OH, Jun HS, et al (2008). Inhibitory effect of capsaicin on B16-F10 melanoma cell migration via the phosphatidylinositol 3-kinase/Akt/Rac1 signal pathway. Exp Mol Med, 40, 486-94. https://doi.org/10.3858/emm.2008.40.5.486
  37. Shin H, Hong A, Kong X, et al (2013). A novel AKT1 mutant amplifies an adaptive melanoma response to BRAF inhibition. Cancer Discov, 4, 69-79.
  38. Smalley KS (2010). PLX-4032, a small-molecule B-Raf inhibitor for the potential treatment of malignant melanoma. Curr Opin Investig Drugs, 11, 699-706.
  39. Su F, Bradley WD, Wang Q, et al (2012). Resistance to selective BRAF inhibition can be mediated by modest upstream pathway activation. Cancer Res, 72, 969-78. https://doi.org/10.1158/0008-5472.CAN-11-1875
  40. Sviderskaya E, Kallenberg DM, Bennett D (2010). The wellcome Trust functional genomics cell bank: holdings. Pigment Cell Melanoma Res, 23, 147-50. https://doi.org/10.1111/j.1755-148X.2009.00641.x
  41. Thang ND, Yajima I, Kumasaka MY, et al (2011). Barium promotes Anchorage-independent growth and invasion of human HaCaT Keratinocytes via activation of c-SRC Kinase. PloS ONE, 6, 25636. https://doi.org/10.1371/journal.pone.0025636
  42. Vergara D, Simeone P, Toraldo D, et al (2012). Resveratrol downregulates Akt/GSK and ERK signaling pathways in OVCAR-3 ovarian cancer cells. Mol Biosyst, 8, 1078-87. https://doi.org/10.1039/c2mb05486h
  43. Wang J, Chen J, Miller DD, et al (2014). Synergistic combination of novel tubulin inhibitor ABI-274 and vemurafenib overcome vemurafenib acquired resistance in BRAFV600E melanoma. Mol Cancer Ther, 13, 16-26.
  44. Yajima I, Uemura N, Nizam S, et al (2012). Barium inhibits arsenic-mediated cell death in human squamous carcinoma cells. Arch Toxicol, 86, 961-73. https://doi.org/10.1007/s00204-012-0848-9

피인용 문헌

  1. Translocation of BBAP from the cytoplasm to the nucleus reduces the metastatic ability of vemurafenib-resistant SKMEL28 cells vol.15, pp.1, 2017, https://doi.org/10.3892/mmr.2016.5976
  2. Toxicological and melanin synthesis effects of Polygonum multiflorum root extracts on zebrafish embryos and human melanocytes vol.3, pp.9, 2016, https://doi.org/10.7603/s40730-016-0042-4
  3. A Computational Approach for Identifying Synergistic Drug Combinations vol.13, pp.1, 2017, https://doi.org/10.1371/journal.pcbi.1005308
  4. Growth Hormone Receptor Knockdown Sensitizes Human Melanoma Cells to Chemotherapy by Attenuating Expression of ABC Drug Efflux Pumps vol.8, pp.3, 2017, https://doi.org/10.1007/s12672-017-0292-7