Relevant Research of Reactive oxygen species and tumor stem cell

doi:10.3877/cma.j.issn.1674-0785.2017.23.008

Abstract

Abstract:

Reactive Oxygen Species (ROS) are widely present in the body's metabolic response, but their concentrations in tumor cells of different differentiation are significantly different. Oxidative stress is caused by the imbalance of the oxidation system and the antioxidant system of the human body. In contrast to general cancer cells in which ROS levels are increased, cancer stem cells (CSCs) exhibit lower levels of ROS. CSCs have attracted much attention of the research community in recent years, since they are the key to tumor genesis and development, and their unique metabolic characteristics may be the key to their drug resistance. It is possible to selectively kill CSCs by increasing the concentration of ROS in CSCs or to increase the sensitivity of CSCs to radiotherapy and chemotherapy

Key words: Cancer stem cells, Reactive oxygen species, Glycolysis, Oxidative phosphorylation

Hua Ji, Mingwei Chen. Relevant Research of Reactive oxygen species and tumor stem cell[J]. Chinese Journal of Clinicians(Electronic Edition), 2017, 11(23): 2462-2465.

/ / Recommend

Add to citation manager EndNote|Ris|BibTeX

URL: https://zhlcyszz.cma-cmc.com.cn/EN/10.3877/cma.j.issn.1674-0785.2017.23.008

https://zhlcyszz.cma-cmc.com.cn/EN/Y2017/V11/I23/2462

References 44

[1]	Diehn M,Cho RW,Lobo NA, et al. Association of reactive oxygen species levels and radioresistance in cancer stem cells[J]. Nature, 2009, 458(7239): 780-783.
[2]	Zhou D,Shao L,Spitz DR. Reactive oxygen species in normal and tumor stem cells[J]. Adv Cancer Res, 2014, 122: 1-67.
[3]	Ji Y,Yang C,Tang Z, et al. Adenylate kinase hCINAP determines self-renewal of colorectal cancer stem cells by facilitating LDHA phosphorylation[J]. Nat Commun, 2017, 8: 15308.
[4]	李国林, 印大中. ROS介导的蛋白质氧化的生化机制[J]. 生命的化学, 2007, 27(6): 516-520.
[5]	Hoffmann MJ,Schulz WA. Causes and consequences of DNA hypomethylation in human cancer[J]. Biochem Cell Biol, 2005, 83(3): 296-321.
[6]	Van De Voorde L,Speeckaert R,Van Gestel D, et al. DNA methylation-based biomarkers in serum of patients with breast cancer[J]. Mutat Res, 2012, 751(2): 304-325.
[7]	Donkena KV,Young CY,Tindall DJ. Oxidative stress and DNA methylation in prostate cancer[J]. Obstet Gynecol Int, 2010, 2010: 302051.
[8]	Franco R,Schoneveld O,Georgakilas AG, et al. Oxidative stress, DNA methylation and carcinogenesis[J]. Cancer Lett, 2008, 266(1): 6-11.
[9]	Kryston TB,Georgiev AB,Pissis P, et al. Role of oxidative stress and DNA damage in human carcinogenesis[J]. Mutat Res, 2011, 711(1-2): 193-201.
[10]	Young IS,McEneny J. Lipoprotein oxidation and atherosclerosis[J]. Biochem Soc Trans, 2001, 29(Pt2): 358-362.
[11]	Niedernhofer LJ,Daniels JS,Rouzer CA, et al. Malondialdehyde, a product of lipid peroxidation, is mutagenic in human cells[J]. J Biol Chem, 2003, 278(33): 31426-31433.
[12]	Velasco-Velazquez MA,Homsi N,De La Fuente M, et al. Breast cancer stem cells[J]. Int J Biochem Cell Biol, 2012, 44(4) :573-577.
[13]	Salmanzadeh A,Romero L,Shafiee H, et al. Isolation of prostate tumor initiating cells (TICs) through their dielectrophoretic signature[J].Lab Chip, 2012, 12(1): 182-189.
[14]	O′Brien CA,Pollett A,Gallinger S. A human colon cancer cell capable of initiating tumour growth in immunodeficient mice[J]. Nature, 2007, 445(7123): 106-110.
[15]	Chiba T,Kita K,Zheng YW, et al. Side population purified from hepatocellular carcinoma cells harbors cancer stem cell-like properties[J]. Hepatology, 2006, 44(1): 240-251.
[16]	李士亭, 陶文成. 肿瘤干细胞表面标记物CD44在胃癌浸润和淋巴结转移中的作用[J].中国组织工程研究, 2015, 19(23): 3669-3673.
[17]	Sahlberg SH,Spiegelberg D,Glimelius B, et al. Evaluation of cancer stem cell markers CD133, CD44, CD24: association with AKT isoforms and radiation resistance in colon cancer cells[J]. PloS one, 2014, 9(4): e94621.
[18]	Ciavardelli D,Rossi C,Barcaroli D, et al. Breast cancer stem cells rely on fermentative glycolysis and are sensitive to 2-deoxyglucose treatment[J]. Cell death Dis, 2014, 5: e1336.
[19]	Emmink BL,Verheem A,Van Houdt WJ, et al. The secretome of colon cancer stem cells contains drug-metabolizing enzymes[J]. J Proteomics, 2013, 91: 84-96.
[20]	Liao J,Qian F,Tchabo N, et al. Ovarian cancer spheroid cells with stem cell-like properties contribute to tumor generation, metastasis and chemotherapy resistance through hypoxia-resistant metabolism[J].PloS one, 2014, 9(1): e84941.
[21]	Palorini R,Votta G,Balestrieri C, et al. Energy metabolism characterization of a novel cancer stem cell-like line 3AB-OS[J]. J Cell Biochem, 2014, 115(2): 368-379.
[22]	Zhou Y,Zhou Y,Shingu T, et al. Metabolic alterations in highly tumorigenic glioblastoma cells: preference for hypoxia and high dependency on glycolysis[J]. J Biol Chem, 2011, 286(37): 32843-32853.
[23]	Dando I,Cordani M,Dalla Pozza E, et al. Antioxidant mechanisms and ROS-related microRNAs in cancer stem cells[J]. Oxid Med Cell Longev, 2015, 2015: 425708.
[24]	Ciavardelli D,Rossi C,Barcaroli D, et al. Breast cancer stem cells rely on fermentative glycolysis and are sensitive to 2-deoxyglucose treatment[J]. Cell Death Dis, 2014, 5: e1336.
[25]	Emmink BL,Verheem A,Van Houdt WJ, et al. The secretome of colon cancer stem cells contains drug-metabolizing enzymes[J]. J Proteomics, 2013, 91: 84-96.
[26]	Tamada M,Nagano O,Tateyama S, et al. Modulation of glucose metabolism by CD44 contributes to antioxidant status and drug resistance in cancer cells[J]. Cancer Res, 2012, 72(6): 1438-1448.
[27]	De Luca A,Fiorillo M,Peiris-Pagès M, et al. Mitochondrial biogenesis is required for the anchorage-independent survival and propagation of stem-like cancer cells[J]. Oncotarget, 2015, 6(17): 14777-14795.
[28]	Cipolleschi MG,Marzi I,Santini R, et al. Hypoxia-resistant profile implies vulnerability of cancer stem cells to physiological agents, which suggests new therapeutic targets[J]. Cell Cycle, 2014, 13(2): 268-278.
[29]	Vlashi E,Lagadec C,Vergnes L, et al. Metabolic state of glioma stem cells and nontumorigenic cells[J]. Proc Natl Acad Sci U S A, 2011, 108(38): 16062-16067.
[30]	Viale A,Pettazzoni P,Lyssiotis CA, et al. Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function[J].Nature, 2014, 514(7524): 628-632.
[31]	Pastò A,Bellio C,Pilotto G, et al. Cancer stem cells from epithelial ovarian cancer patients privilege oxidative phosphorylation, and resist glucose deprivation[J]. Oncotarget, 2014, 5(12): 4305-4319.
[32]	Flavahan WA,Wu Q,Hitomi M, et al. Brain tumor initiating cells adapt to restricted nutrition through preferential glucose uptake[J]. Nat neurosci, 2013, 16(10): 1373-1382.
[33]	Dong C,Yuan T,Wu Y, et al. Loss of FBP1 by Snail-mediated repression provides metabolic advantages in basal-like breast cancer[J]. Cancer cell, 2013, 23(3): 316-331.
[34]	Ishimoto T,Nagano O,Yae T, et al. CD44 variant regulates redox status in cancer cells by stabilizing the xCT subunit of system xc(-) and thereby promotes tumor growth[J]. Cancer cell, 2011, 19(3): 387-400.
[35]	Kawano Y,Iwama E,Tsuchihashi K, et al. CD44 variant-dependent regulation of redox balance in EGFR mutation-positive non-small cell lung cancer: A target for treatment[J]. Lung Cancer, 2017, 113: 72-78.
[36]	Kim HM,Haraguchi N,Ishii H, et al. Increased CD13 expression reduces reactive oxygen species, promoting survival of liver cancer stem cells via an epithelial-mesenchymal transition-like phenomenon[J] .Ann Surg Oncol, 2012, 19 Suppl 3: S539-S548.
[37]	Haraguchi N,Ishii H,Mimori K, et al. CD13 is a therapeutic target in human liver cancer stem cells[J]. J Clin Invest, 2010, 120(9): 3326-3339.
[38]	Wu WJ,Zhang Y,Zeng ZL, et al. β-phenylethyl isothiocyanate reverses platinum resistance by a GSH-dependent mechanism in cancer cells with epithelial-mesenchymal transition phenotype[J]. Biochem Pharmacol, 2013, 85(4): 486-496.
[39]	Yuan S,Wang F,Chen G, et al. Effective elimination of cancer stem cells by a novel drug combination strategy[J]. Stem Cells, 2013, 31(1): 23-34.
[40]	Liu PP,Liao J,Tang ZJ, et al. Metabolic regulation of cancer cell side population by glucose through activation of the Akt pathway[J]. Cell Death Differ, 2014, 21(1): 124-135.
[41]	Mayer MJ,Klotz LH. Metformin and prostate cancer stem cells: a novel therapeutic target[J]. Prostate Cancer Prostatic Dis, 2015, 18(4): 303-309.
[42]	Cheong JH,Park ES,Liang J, et al. Dual inhibition of tumor energy pathway by 2-deoxyglucose and metformin is effective against a broad spectrum of preclinical cancer models[J]. Mol Cancer Ther, 2011, 10(12): 2350-2362.
[43]	Sancho P,Burgos-Ramos E,Tavera A, et al. MYC/PGC-1α balance determines the metabolic phenotype and plasticity of pancreatic cancer stem cells[J]. Cell Metab, 2015, 22(4): 590-605.
[44]	Li D,Fu Z,Chen R, et al. Inhibition of glutamine metabolism counteracts pancreatic cancer stem cell features and sensitizes cells to radiotherapy[J]. Oncotarget, 2015, 6(31): 31151-31163.

Please choose a citation manager

Content to export