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CLC number: R73

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Received: 2009-08-29

Revision Accepted: 2009-09-22

Crosschecked: 2009-10-12

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Journal of Zhejiang University SCIENCE B 2009 Vol.10 No.11 P.796~804

10.1631/jzus.B0910009


Knockdown of OLA1, a regulator of oxidative stress response, inhibits motility and invasion of breast cancer cells


Author(s):  Jia-wei ZHANG, Valentina RUBIO, Shu ZHENG, Zheng-zheng SHI

Affiliation(s):  Cancer Institute (National Ministry of Education Key Laboratory of Cancer Prevention and Intervention), the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China; more

Corresponding email(s):   zhengshu@zju.edu.cn, zshi@tmhs.org

Key Words:  Reactive oxygen species, Cell migration, Cancer metastasis, RNA interference


Jia-wei ZHANG, Valentina RUBIO, Shu ZHENG, Zheng-zheng SHI. Knockdown of OLA1, a regulator of oxidative stress response, inhibits motility and invasion of breast cancer cells[J]. Journal of Zhejiang University Science B, 2009, 10(11): 796~804.

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author="Jia-wei ZHANG, Valentina RUBIO, Shu ZHENG, Zheng-zheng SHI",
journal="Journal of Zhejiang University Science B",
volume="10",
number="11",
pages="796~804",
year="2009",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B0910009"
}

%0 Journal Article
%T Knockdown of OLA1, a regulator of oxidative stress response, inhibits motility and invasion of breast cancer cells
%A Jia-wei ZHANG
%A Valentina RUBIO
%A Shu ZHENG
%A Zheng-zheng SHI
%J Journal of Zhejiang University SCIENCE B
%V 10
%N 11
%P 796~804
%@ 1673-1581
%D 2009
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B0910009

TY - JOUR
T1 - Knockdown of OLA1, a regulator of oxidative stress response, inhibits motility and invasion of breast cancer cells
A1 - Jia-wei ZHANG
A1 - Valentina RUBIO
A1 - Shu ZHENG
A1 - Zheng-zheng SHI
J0 - Journal of Zhejiang University Science B
VL - 10
IS - 11
SP - 796
EP - 804
%@ 1673-1581
Y1 - 2009
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B0910009


Abstract: 
To explore the role of a novel Obg-like ATPase 1 (OLA1) in cancer metastasis, small interference RNA (siRNA) was used to knockdown the protein, and the cells were subjected to in vitro cell migration and invasion assays. Knockdown of OLA1 significantly inhibited cell migration and invasion in breast cancer cell line MDA-MB-231. The knockdown caused no changes in cell growth but affected ROS production. In wound-healing assays, decreased ROS in OLA1-knockdown cells were in situ associated with the cells’ decreased motile morphology. Further, treatment of N-acetylcysteine, a general ROS scavenger, blunted the motility and invasiveness of MDA-MB-231 cells, similar to the effect of OLA1-knockdown. These results suggest that knockdown of OLA1 inhibits breast cancer cell migration and invasion through a mechanism that involves the modulation of intracellular ROS levels.

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Reference

[1] Alexandrova, A.Y., Kopnin, P.B., Vasiliev, J.M., Kopnin, B.P., 2006. ROS up-regulation mediates Ras-induced changes of cell morphology and motility. Exp. Cell Res., 312(11): 2066-2073.

[2] Chène, P., 2002. ATPases as drug targets: learning from their structure. Nat. Rev. Drug Discov., 1(9):665-673.

[3] Ferraro, D., Corso, S., Fasano, E., Panieri, E., Santangelo, R., Borrello, S., Giordano, S., Pani, G., Galeotti, T., 2006. Pro-metastatic signaling by c-Met through RAC-1 and reactive oxygen species (ROS). Oncogene, 25(26): 3689-3698.

[4] Fini, M.A., Orchard-Webb, D., Kosmider, B., Amon, J.D., Kelland, R., Shibao, G., Wright, R.M., 2008. Migratory activity of human breast cancer cells is modulated by differential expression of xanthine oxidoreductase. J. Cell. Biochem., 105(4):1008-1026.

[5] Gradia, D.F., Rau, K., Umaki, A.C., de Souza, F.S., Probst, C.M., Correa, A., Holetz, F.B., Avila, A.R., Krieger, M.A., Goldenberg, S., et al., 2009. Characterization of a novel Obg-like ATPase in the protozoan Trypanosoma cruzi. Int. J. Parasitol., 39(1):49-58.

[6] Hortobagyi, G.N., de la Garza Salazar, J., Pritchard, K., Amadori, D., Haidinger, R., Hudis, C.A., Khaled, H., Liu, M.C., Martin, M., Namer, M., et al., 2005. The global breast cancer burden: variations in epidemiology and survival. Clin. Breast Cancer, 6(5):391-401.

[7] Huo, Y., Qiu, W.Y., Pan, Q., Yao, Y.F., Xing, K., Lou, M.F., 2009. Reactive oxygen species (ROS) are essential mediators in epidermal growth factor (EGF)-stimulated corneal epithelial cell proliferation, adhesion, migration, and wound healing. Exp. Eye Res., in press [Epub ahead of print].

[8] Ikeda, S., Yamaoka-Tojo, M., Hilenski, L., Patrushev, N.A., Anwar, G.M., Quinn, M.T., Ushio-Fukai, M., 2005. IQGAP1 regulates reactive oxygen species-dependent endothelial cell migration through interacting with Nox2. Arterioscler. Thromb. Vasc. Biol., 25(11):2295-2300.

[9] Koller-Eichhorn, R., Marquardt, T., Gail, R., Wittinghofer, A., Kostrewa, D., Kutay, U., Kambach, C., 2007. Human OLA1 defines an ATPase subfamily in the Obg family of GTP-binding proteins. J. Biol. Chem., 282(27):19928-19937.

[10] Moldovan, L., Moldovan, N.I., Sohn, R.H., Parikh, S.A., Goldschmidt-Clermont, P.J., 2000. Redox changes of cultured endothelial cells and actin dynamics. Circ. Res., 86(5):549-557.

[11] Moldovan, L., Mythreye, K., Goldschmidt-Clermont, P.J., Satterwhite, L.L., 2006. Reactive oxygen species in vascular endothelial cell motility. Roles of NAD(P)H oxidase and Rac1. Cardiovasc. Res., 71(2):236-246.

[12] Nishikawa, M., 2008. Reactive oxygen species in tumor metastasis. Cancer Lett., 266(1):53-59.

[13] Olson, M.F., Sahai, E., 2009. The actin cytoskeleton in cancer cell motility. Clin. Exp. Metastasis, 26(4):273-287.

[14] Pendyala, S., Gorshkova, I.A., Usatyuk, P., He, D., Pennathur, A., Lambeth, J.D., Thannickal, V.J., Natarajan, V., 2008. Role of Nox4 and Nox2 in hyperoxia-induced reactive oxygen species generation and migration of human lung endothelial cells. Antioxid. Redox Signal, 11(4):747-764.

[15] Radisky, D.C., Levy, D.D., Littlepage, L.E., Liu, H., Nelson, C.M., Fata, J.E., Leake, D., Godden, E.L., Albertson, D.G., Nieto, M.A., et al., 2005. Rac1b and reactive oxygen species mediate MMP-3-induced EMT and genomic instability. Nature, 436(7047):123-127.

[16] Shim, H., Shim, E., Lee, H., Hahn, J., Kang, D., Lee, Y.S., Jeoung, D., 2006. CAGE, a novel cancer/testis antigen gene, promotes cell motility by activation ERK and p38 MAPK and downregulating ROS. Mol. Cells, 21(3): 367-375.

[17] Steeg, P.S., 2006. Tumor metastasis: mechanistic insights and clinical challenges. Nat. Med., 12(8):895-904.

[18] Storz, P., 2005. Reactive oxygen species in tumor progression. Front. Biosci., 10(1-3):1881-1896.

[19] Valko, M., Leibfritz, D., Moncol, J., Cronin, M.T., Mazur, M., Telser, J., 2007. Free radicals and antioxidants in normal physiological functions and human disease. Int. J. Biochem. Cell Biol., 39(1):44-84.

[20] Weigelt, B., Peterse, J.L., van't Veer, L.J., 2005. Breast cancer metastasis: markers and models. Nat. Rev. Cancer, 5(8): 591-602.

[21] Wu, W.S., 2006. The signaling mechanism of ROS in tumor progression. Cancer Metastasis Rev., 25(4):695-705.

[22] Zhang, J., Rubio, V., Lieberman, M.W., Shi, Z.Z., 2009. OLA1, an Obg-like ATPase, suppresses antioxidant response via nontranscriptional mechanisms. Proc. Natl. Acad. Sci. USA, 106(36):15356-15361.

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