Mitochondrial dysfunction and reactive oxygen species imbalance promote breast cancer cell motility through a CXCL14-mediated mechanism

Cancer Research

Volumn 69, Issue 6, 2009, Pages 2375-2383

  Pelicano, Helene ^a   Lu, Weiqin ^a   Zhou, Yan ^a   Zhang, Wan ^a   Chen, Zhao ^a   Hu, Yumin ^a   Huang, Peng ^a,b  

^a UNIVERSITY OF TEXAS   (United States)

^b UNIVERSITY OF TEXAS MD ANDERSON CANCER CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM ION; CXCL14 CHEMOKINE; INOSITOL 1,4,5 TRISPHOSPHATE RECEPTOR; REACTIVE OXYGEN METABOLITE; TRANSCRIPTION FACTOR AP 1; ALPHA CHEMOKINE; CALCIUM; CXCL14 PROTEIN, HUMAN;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BREAST CANCER; CANCER CELL; CELL CLONE; CELL INVASION; CELL MOTILITY; CELL PROLIFERATION; ENDOPLASMIC RETICULUM; FEMALE; GENE EXPRESSION; HUMAN; HUMAN CELL; IN VITRO STUDY; IN VIVO STUDY; MICROARRAY ANALYSIS; MITOCHONDRION; MOUSE; NONHUMAN; PRIORITY JOURNAL; RECEPTOR BINDING; RESPIRATORY CHAIN; SIGNAL TRANSDUCTION; UPREGULATION; ANIMAL; BAGG ALBINO MOUSE; BREAST TUMOR; CANCER INVASION; CELL MOTION; CYTOSOL; METABOLISM; OXYGEN CONSUMPTION; PATHOLOGY; PHYSIOLOGY; TUMOR CELL LINE;

ANIMALS; BREAST NEOPLASMS; CALCIUM; CELL LINE, TUMOR; CELL MOVEMENT; CHEMOKINES, CXC; CYTOSOL; FEMALE; HUMANS; MICE; MICE, INBRED BALB C; MITOCHONDRIA; NEOPLASM INVASIVENESS; OXYGEN CONSUMPTION; REACTIVE OXYGEN SPECIES; SIGNAL TRANSDUCTION; TRANSCRIPTION FACTOR AP-1;

EID: 65549142759     PISSN: 00085472     EISSN: 15387445     Source Type: Journal    
DOI: 10.1158/0008-5472.CAN-08-3359     Document Type: Article

References (41)

1. Storz P. Reactive oxygen species in tumor progression. Front Riosci 2005;10:1881-96.
2. 2.Radisky DC, Levy DD, Littlepage LE, et al, Raclb and reactive oxygen species mediate MMP-3-induced EMT and genomic instability. Nature 2005;436:123-27.
3. Ristow M, Oxidative metabolism In cancer growth, Curr Opin Clin Nutr Metab Care 2006;9:339-45.
4. Wu M, Neilson A, Swift AL, et al. Multiparameter metabolic analysis reveals a close link between attenuated mitochondrial bioenergetic function and enhanced glycolysis dependency in human tumor cells. Am j Physiol Cell Physiol 2007;292:C125-36.
5. Pelicano H, Carney D( Huang P. ROS stress in cancer cells and therapeutic implications. Drug Resist Updat 2004;7:97-110.
6. Pelicano H, Martin DS, Xu RH, Huang P. Glycolysis inhibition for anticancer treatment. Oncogene 2006;25: 4633-46.
7. Moreno-Sanchez R, Rodriguez- Enriquez S, Marin- Hernandez A, Saavedra E. Energy metabolism in tumor cells. FEBS j 2007;274:1393-418.
8. Suh YA, Arnold RS, Lassegue R, et al. Cell transformation by the superoxide-generating oxidase Moxl. Nature 1999;401:79-82.
9. Huang P, Feng L, Oldham EA, Keating Mj, Plunkett W. Superoxide dismutase as a target for the selective killing of cancer cells. Nature 2000;407:309-11.
10. Droge W. Free radicals in the physiological control of cell fonction. Physiol Rev 2002;82:47-95.
11. Klaunig JE, Kamendulis LM, The role of oxidative stress in carcinogenesis. Annu Rev Pharmacol Toxicol 2004;44:239-67.
12. Hanahan, D, Weinberg RA. The hallmarks of cancer. Cell 2000;100:57-70.
13. Kemoto S, Takeda K, Yu ZX, Ferrans V], Finkel T. Role for mitochondrial oxidants as regulators of cellular metabolism. Mol Cell Riol 2000;20:7311-8.
14. Samper E, Nicholls DG, Melov S. Mitochondrial oxidative stress causes chromosomal Instability of mouse embryonic fibroblasts. Aging Cell 2003;2:277-85.
15. Warburg O. On the origin of cancer cells. Science 1956;123:309-14.
16. Alirol E, Mart in ou JC. Mitochondria and cancer: is there a morphological connection? Oncogene 2006;25: 4706-16.
17. Chatterjee A, Mamho E, Sidransky D. Mitochondrial DNA mutations in human cancer. Oncogene 2006;25: 4663-74.
18. Pelicano H, Feng L, Zhou Y, et al. Inhibition of mitochondrial respiration: a novel strategy to enhance drag-induced apoptosis in human leukemia cells by a reactive oxygen species-mediated mechanism, j Biol Chem 2003;278:37832-9.
19. Xu RFf, Pelicano H, Zhou Y, et al. Inhibition of glycolysis in cancer cells: a novel strategy to overcome drag resistance associated with mitochondrial respiratory defect and hypoxia. Cancer Res 2005;65:613-21.
20. Robinson JP, Darzynkiewdcz Z, Dean PN, et al. Current protocols in cytometry. Supplement 14. New York: John Wiley & Sons, inc.; 2000.
21. Pines A, Perrone L, Bivi N, et al. Activation of APE1/ Ref-1 is dependent on reactive oxygen species generated after purinergic receptor stimulation by ATP. Nucleic- Acids Res 2005;33:4379-94.
22. Morimoto T, Sabatini DD, Doda JN. Subcellular fractionation. In: Spector DL, Goldman RD, Leinwand LA, editors. Cells: a laboratory manual, culture of cells and biochemical analysis. New York: Cold Spring Harbor Laboratory; 1998. p. 34.1-41.4.
23. Guillemette G, Ralla T, Baukal Aj( Catt Kj. Characterization of inositol 1,4,5-trisphosphate receptors and calcium mobilization in a hepatic plasma membrane fraction. J Biol Chem 1988;263:4541-8.
24. Lee HC, Yin PH, Lu CY, Chi CW, Wei YH. Increase of mitochondria and mitochondrial DMA in response to oxidative stress In human cells. Bioehem j 2000;348: 425-32.
25. Finkel T, Oxidant signals and oxidative stress. Curr Opin Cell Biol 2003;15:247-54.
26. Mori K, Shibanuma M, Nose K, Invasive potential induced under long-term oxidative stress in mammary epithelial cells. Cancer Res 2004;64:7464-72.
27. Berridge MJ, Bootman MD, Roderick HL. Calcium signalling dynamics, homeostasis and remodelling. Nat Rev Mol Cell Biol 2003;4:517-29.
28. Berridge Mj. Elementary and global aspects of calcium signalling. J Physiol 1997;499:291-306.
29. Maruyama T, Kanaji T, Nakade S, Kanno T, Mikoshiba K, 2APB, 2-aminoethoxydiphenyl borate, a membrane- penetrable modulator of Ins(l,4,5)P3-induced Cai+ release.] Bioehem (Tokyo) 1997;122:498-505.
30. Ishikawa K, Takenaga K, Akimoto M, et al. ROS- generating mitochondrial DMA mutations can regulate tumor cell metastasis. Science 2008:320:661 -4.
31. Frederick Mj, Henderson Y, Xu X, et al. In vivo expression of the novel CXC chemokine BRAK in normal and cancerous human tissue. Am J Pathol 2000;156: 1937-50.
32. Hromas K, Rroxmeyer HE, Kim C, et al. Cloning of BRAK, a novel divergent CXC chemokine preferentially expressed in normal versus malignant cells. Biochem Riophys Res Commun 1999;255:703-6.
33. Schwarze SR, Luo j, Isaacs WB, Jarrard DF. Modulation of CXCL14 (BRAK) expression in prostate cancer. Prostate 2005;64:67-74.
34. Kurth I, Willimami K, Schaerli P, Hunziker T, Clark- Lewis I, Moser R. Monocyte selectivity and tissue localization suggests a role for breast and kidneyexpressed chemokine (BRAK) in macrophage development, j Exp Med 2001;194:855-61.
35. 35.Shellenberger TD, Wang M, Gujrati M, et al. BRAK/ CXCL14 Is a potent inhibitor of angiogenesis and is a chemotactic factor for immature dendritic cells. Cancer Res 2004;64:8262-70.
36. Shurin GV, Ferris RE, Tourkova IL, et al. Loss of new chemokine CXCL14 in tumor tissue is associated with low infiltration by dendritic cells (DC), while restoration of human CXCL14 expression in tumor cells causes attraction of DC both in vitro and in vivo. J Immunol 2005;174:5490-8.
37. Allinen M, Beroukhim R, Cai L, et al. Molecular characterization of the tumor microenvironment in breast cancer. Cancer Cell 2004;6:17-32.
38. Chiu SH, Chen CC, Lin TH. Using support vector regression to model the correlation between the clinical metastases time and gene expression profile for breast cancer. Artif Intell Med 2008;44:221-31. 39- Wente MN, Mayer C, Gaida MM, et al. CXCL14 expression and potential function In pancreatic cancer. Cancer Lett 2008;259:209-17.
39. Philips A, Teyssier C, Galtier F, et al. FRA-1 expression level modulates regulation of activator protein-1 activity by estradiol in breast cancer cells. Mol Endocrinol 1998;12:973-85.
40. Crowe DL, Tsang Kj, Shemirani B. jun N- terminal kinase 1 mediates transcriptional induction of matrix met alio pr o t ei nase 9 expression. Neoplasia 2001;3:27-32.
41. Vleugel MM, Greijer E, Bos R, van der Wall E, van Diest Pj. c-Jun activation is associated with proliferation and angiogenesis in invasive breast cancer. Hum Pathol 2006;37:668-74.