Quinacrine overcomes resistance to erlotinib by inhibiting FACT, NF-κB, and cell-cycle progression in non-small cell lung cancer

Molecular Cancer Therapeutics

Volumn 13, Issue 9, 2014, Pages 2203-2214

  Dermawan, Josephine Kam Tai ^a   Gurova, Katerina ^b   Pink, John ^c   Dowlati, Afshin ^c   De, Sarmishtha ^a   Narla, Goutham ^d   Sharma, Neelesh ^c   Stark, George R ^a  

^a LERNER RESEARCH INSTITUTE   (United States)

^b ROSWELL PARK CANCER INSTITUTE   (United States)

^c CASE WESTERN RESERVE UNIVERSITY   (United States)

^d CASE WESTERN RESERVE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANTINEOPLASTIC AGENT; DNA; DNA BINDING PROTEIN; ERLOTINIB; HIGH MOBILITY GROUP PROTEIN; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; LUCIFERASE; MEPACRINE; NFKB1 PROTEIN, HUMAN; QUINAZOLINE DERIVATIVE; SMALL INTERFERING RNA; SSRP1 PROTEIN, HUMAN; TRANSCRIPTION ELONGATION FACTOR;

ANIMAL; APOPTOSIS; CARCINOMA, NON-SMALL-CELL LUNG; CELL CYCLE; CELL PROLIFERATION; CHEMISTRY; DRUG EFFECTS; DRUG RESISTANCE; DRUG SCREENING; GENE EXPRESSION REGULATION; HUMAN; LUNG NEOPLASMS; METABOLISM; MOUSE; NUDE MOUSE; TUMOR CELL LINE;

ANIMALS; ANTINEOPLASTIC AGENTS; APOPTOSIS; CARCINOMA, NON-SMALL-CELL LUNG; CELL CYCLE; CELL LINE, TUMOR; CELL PROLIFERATION; DNA; DNA-BINDING PROTEINS; DRUG RESISTANCE, NEOPLASM; ERLOTINIB HYDROCHLORIDE; GENE EXPRESSION REGULATION, NEOPLASTIC; HIGH MOBILITY GROUP PROTEINS; HUMANS; LUCIFERASES; LUNG NEOPLASMS; MICE; MICE, NUDE; NF-KAPPA B P50 SUBUNIT; QUINACRINE; QUINAZOLINES; RNA, SMALL INTERFERING; TRANSCRIPTIONAL ELONGATION FACTORS; XENOGRAFT MODEL ANTITUMOR ASSAYS;

EID: 84907210240     PISSN: 15357163     EISSN: 15388514     Source Type: Journal    
DOI: 10.1158/1535-7163.MCT-14-0013     Document Type: Article

References (32)

1. Lynch TJ, Bell DW, Sordella R, Gurubhagavatula S., Okimoto RA, Brannigan BW, et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small cell lung cancer to gefitinib. N Engl J Med 2004; 350:2129-39.
2. Garassino MC, Martelli O, Broggini M., Farina G, Veronese S, Rulli E., et al. Erlotinib versus docetaxel as second-line treatment of patients with advanced non-small cell lung cancer and wild-type EGFR tumors (TAILOR): a randomized controlled trial. Lancet Oncol 2013; 14:981-8.
3. Shepherd FA, Rodrigues PJ, Ciuleanu T, Tan E.H., Hirsh V., Thongpra-sert S, et al. Erlotinib in previously treated non-small cell lung cancer. N Engl J Med 2005; 353:123-32.
4. Kobayashi S, Boggon TJ, Dayaram T, Janne P.A., Kocher O., Meyerson M, et al. EGFR mutation and resistance of non-small cell lung cancer to gefitinib. N Engl J Med 2005; 352:786-92.
5. Bean J, Brennan C, Shih J.Y., Riely G., Viale A, Wang L, et al. MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib. Proc Natl Acad Sci U S A 2007; 104:20932-7.
6. Sequist LV, Waltman BA, Dias-Santagata D, Digumarthy S., Turke AB, Fidias P, et al. Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors. Sci Transl Med 2011; 3: 75ra26.
7. Ehsanian R, Van Waes C, Feller SM. Beyond DNA binding - a review of the potential mechanisms mediating quinacrine's therapeutic activities in parasitic infections, inflammation, and cancers. Cell Commun Signal 2011; 9:13.
8. Gurova K. New hopes from old drugs: revisiting DNA-binding small molecules as anticancer agents. Future Oncol 2009; 5:1685-704.
9. Gurova KV, Hill JE, Guo C, Prokvolit A., Burdelya LG, Samoylova E, et al. Small molecules that reactivate p53 in renal cell carcinoma reveal a NF-kB-dependent mechanism of p53 suppression in tumors. Proc Natl Acad Sci U S A 2005; 102:17448-53.
10. Gasparian AV, Burkhart CA, Purmal A.A., Brodsky L., Pal M, Saranadasa M, et al. Curaxins: anticancer compounds that simultaneously suppress NF-kB and activate p53 by targeting FACT. Sci Transl Med 2011; 3:1-12.
11. Lu T, Sathe SS, Swiatkowski S.M., Hampole CV, Stark GR. Secretion of cytokines and growth factors as a general cause of constitutive NFkB activation in cancer. Oncogene 2004; 23; 2138-45.
12. Nakanishi C, Toi M. Nuclear factor-kappaB inhibitors as sensitizers to anticancer drugs. Nat Rev Cancer 2005; 5:297-309.
13. Tanaka K, Babic I, Nathanson D., Akhavan D, Guo D, Gini B., et al. OncogenicEGFRsignaling activates an mTORC2-NF-kB pathway that promotes chemotherapy resistance. Cancer Discov 2011; 1:524-38.
14. Bivona TG, Hieronymus H, Parker J., Chang K, Taron M, Rosell R., et al. FAS and NF-kB signaling modulate dependence of lung cancers on mutant EGFR. Nature 2011; 471:523-6.
15. Brown M, Cohen J, Arun P., Chen Z, Van Waes C. NF-kB in carcinoma therapy and prevention. Exp Opin Ther Targets 2008; 12:1109-22.
16. Garcia H, Miecznikowski JC, Safina A, Commane M., Ruusulehto A, Kilpinen S, et al. Facilitates Chromatin Transcription Complex is an "accelerator" of tumor transformation and potential marker and target of aggressive cancers. Cell Rep 2013; 4:159-73.
17. van Meerloo J, Kaspers GJ, Cloos J. Cell sensitivity assays: the MTT assay. Methods Mol Biol 2011; 731:237-45.
18. Chou TC. Drug combination studies and their synergy quantification using the Chou-Talalay method. Cancer Res 2010; 70:440-6.
19. Chou TC, Talalay P. Quantitative analysis of dose-effect relationships: the combined effects of multiple drugs or enzyme inhibitors. Adv Enzyme Regul 1984; 22:27-55.
20. Gasparian AV, Guryanova OA, Chebotaev D.V., Shishkin AA, Yemelya-nov AY, Budunova IV. Targeting transcription factor NF-kB: comparative analysis of proteasome and IKK inhibitors. Cell Cycle 2009; 8: 1559-66.
21. Ishwaran H, Rao JS, Kogalur UB. BAMarray: Java software for Bayes-ian analysis of variance for microarray data. BMC Bioinformatics 2006; 7:59.
22. Ernst J, Bar-Joseph Z. STEM: a tool for analysis of short time series gene expression data. BMC Bioinformatics 2006; 7:191.
23. Sherman BT, Huang DW, Lempicki RA. Systemic and integrative analysis of large gene lists using DAVID bioinformatics resources. Nat Protoc 2009; 4:44-57.
24. Ho Sui SJ, Mortimer JR, Arenillas D.J., Brumm J., Walsh CJ, Kennedy BP, et al. oPOSSUM: identification of over-represented transcription factor binding sites in co-expressed genes. Nucleic Acid Res 2005; 33:3154-64.
25. Gyorffy B, Surowiak P, Budczies J, Lánczky A. Online survival analysis software to assess the prognostic value of biomarkers using tran-scriptomic data in non-small-cell lung cancer. PLoS ONE 2013; 8: e82241.
26. Hidalgo M, Siu LL, Neumunaitis J, Rizzo J, Hammond LA, Takimoto C, et al. Phase I and pharmacologic study of OSI-774, an epidermal growth factor receptor tyrosine kinase inhibitor, in patients with advanced solid malignancies. J Clin Oncol 2001; 19:3267-79.
27. Lu JF, Eppler SM, Wolf J, Hamilton M, Rakhit A, Bruno R, et al. Clinical pharmacokinetics of erlotinib in patients with solid tumors and exposure-safety relationship in patients with non-small cell lung cancer. Clin Pharmacol Ther 2006; 80:136-45.
28. Sharma SV, Bell DW, Settleman J, Haber DA. Epidermal growth factor receptor mutations in lung cancer. Nat Rev Cancer 2007; 7:169-81.
29. Zou Y, Ling YH, Sironi J, Schwartz E.L., Perez-Soler R, Piperdi B. The autophagy inhibitor chloroquine overcomes the innate resistance of wild-type EGFR non-small-cell-lung cancer cells to erlotinib. JThorac Oncol 2013; 8:693-702.
30. Kimmelman AC. The dynamic nature of autophagy in cancer. Genes Dev 2011; 25:1999-2010.
31. Bolte J, Demuynck C, Lhomme M.F., Lhomme J., Barbet J, Roques BP. Synthetic models related to DNA intercalating molecules: comparison between quinacrine and chloroquine in their ring-ring interaction with adenine and thymine. J Am Chem Soc 1982; 104:760-65.
32. Garraway LA, Lander ES. Lessons from the cancer genome. Cell 2013; 153:17-37.