[1] Maier VK, Chioda M, Becker PB. ATP-dependent chromatosome remodeling. Biol Chem, 2008, 389(4): 345-352.[2] Clapier CR, Cairns BR. The biology of chromatin remodeling complexes. Annu Rev Biochem, 2009, 78(1): 273-304.[3] Reisman D, Glaros S, Thompson EA. The SWI/SNF complex and cancer. Oncogene, 2009, 28(14): 1653-1668.[4] Wang GG, Allis CD, Chi P. Chromatin remodeling and cancer, Part II: ATP-dependent chromatin remodeling. Trends Mol Med, 2007, 13(9): 373-380.[5] Wiegand KC, Shah SP, Al-Agha OM, Zhao YJ, Tse K, Zeng T, Senz J, McConechy MK, Anglesio MS, Kalloger SE, Yang W, Heravi-Moussavi A, Giuliany R, Chow C, Fee J, Zayed A, Prentice L, Melnyk N, Turashvili G, Delaney AD, Madore J, Yip S, McPherson AW, Ha G, Bell L, Fereday S, Tam A, Galletta L, Tonin PN, Provencher D, Miller D, Jones SJ, Moore RA, Morin GB, Oloumi A, Boyd N, Aparicio SA, Shih IeM, Mes-Masson AM, Bow-tell DD, Hirst M, Gilks B, Marra MA, Huntsman DG. ARID1A mutations in endometriosis-associated ovarian carcinomas. N Engl J Med, 2010, 363(16): 1532-1543.[6] Jones S, Wang TL, Shih IM, Mao TL, Nakayama K, Roden R, Glas R, Slamon D, Diaz LA Jr, Vogelstein B, Kinzler KW, Velculescu VE, Papadopoulos N. Frequent mutations of chromatin remodeling gene ARID1A in ovarian clear cell carcinoma. Science, 2010, 330(6001): 228-231.[7] Gui YT, Guo GW, Huang Y, Hu XD, Tang AF, Gao SJ, Wu RH, Chen C, Li XX, Zhou L, He MH, Li ZS, Sun XJ, Jia WL, Chen JN, Yang SM, Zhou FJ, Zhao XK, Wan SQ, Ye R, Liang CZ, Liu ZS, Huang PD, Liu CX, Jiang H, Wang Y, Zheng HC, Sun L, Liu XW, Jiang ZM, Feng DF, Chen J, Wu S, Zou J, Zhang ZF, Yang RL, Zhao J, Xu CJ, Yin WH, Guan ZC, Ye JX, Zhang H, Li JX, Kristiansen K, Nicker-son ML, Theodorescu D, Li YR, Zhang XQ, Li SG, Wang J, Yang HM, Wang J, Cai ZM. Frequent mutations of chro-matin remodeling genes in transitional cell carcinoma of the bladder. Nat Genet, 2011, 43(9): 875-878.[8] Wang K, Kan JS, Yuen ST, Shi ST, Chu KM, Law S, Chan TL, Kan ZY, Chan ASY, Tsui WY, Lee SP, Ho SL, Chan AKW, Cheng GHW, Roberts PC, Rejto PA, Gibson NW, Pocalyko DJ, Mao M, Xu JC, Leung SY. Exome sequencing identifies frequent mutation of ARID1A in molecular subtypes of gastric cancer. Nat Genet, 2011, 43(12): 1219-1223.[9] Takeuchi T, Chen BK, Qiu Y, Sonobe H, Ohtsuki Y. Mo-lecular cloning and expression of a novel human cDNA containing CAG repeats. Gene, 1997, 204(1-2): 71-77.[10] Nie ZQ, Xue YT, Yang DF, Zhou S, Deroo BJ, Archer TK, Wang WD. A specificity and targeting subunit of a human SWI/SNF family-related chromatin-remodeling complex. Mol Cell Biol, 2000, 20(23): 8879-8888.[11] Dallas PB, Pacchione S, Wilsker D, Bowrin V, Kobayashi R, Moran E. The human SWI-SNF complex protein p270 is an ARID family member with non-sequence-specific DNA binding activity. Mol Cell Biol, 2000, 20(9): 3137-3146.[12] Kozmik Z, Machon O, Králová J, Kreslová J, Pa?es J, Vl?ek C. Characterization of mammalian orthologues of the Drosophila osa gene: cDNA cloning, expression, chromosomal localization, and direct physical interaction with Brahma chromatin-remodeling complex. Genomics, 2001, 73(2): 140-148.[13] Wilsker D, Patsialou A, Zumbrun SD, Kim S, Chen Y, Dallas PB, Moran E. The DNA-binding properties of the ARID-containing subunits of yeast and mammalian SWI/ SNF complexes. Nucleic Acids Res, 2004, 32(4): 1345-1353.[14] Patsialou A, Wilsker D, Moran E. DNA-binding properties of ARID family proteins. Nucleic Acids Res, 2005, 33(1): 66-80.[15] Kim S, Zhang ZM, Upchurch S, Isern N, Chen Y. Struc-ture and DNA-binding sites of the SWI1 AT-rich interaction domain (ARID) suggest determinants for sequence- specific DNA recognition. J Biol Chem, 2004, 279(16): 16670-16676.[16] Tang L, Nogales E, Ciferri C. Structure and function of SWI/SNF chromatin remodeling complexes and mechanistic implications for transcription. Prog Biophys Mol Biol, 2010, 102(2-3): 122-128.[17] Shain AH, Giacomini CP, Matsukuma K, Karikari CA, Bashyam MD, Hidalgo M, Maitra A, Pollack JR. Convergent structural alterations define SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeler as a central tumor suppressive complex in pancreatic cancer. Proc Natl Acad Sci USA, 2012, 109(5): E252-E259.[18] Racki LR, Narlikar GJ. ATP-dependent chromatin remodeling enzymes: two heads are not better, just different. Curr Opin Genet Dev, 2008, 18(2): 137-144.[19] Wang X, Nagl NG, Wilsker D, Van Scoy M, Pacchione S, Yaciuk P, Dallas PB, Moran E. Two related ARID family proteins are alternative subunits of human SWI/SNF complexes. Biochem J, 2004, 383(Pt 2): 319-325.[20] Inoue H, Furukawa T, Giannakopoulos S, Zhou S, King DS, Tanese N. Largest subunits of the human SWI/SNF chromatin-remodeling complex promote transcriptional activation by steroid hormone receptors. J Biol Chem, 2002, 277(44): 41674-41685.[21] Yamamoto S, Tsuda H, Takano M, Tamai S, Matsubara O. Loss of ARID1A protein expression occurs as an early event in ovarian clear-cell carcinoma development and frequently coexists with PIK3CA mutations. Mod Pathol, 2012, 25(4): 615-624.[22] Lowery WJ, Schildkraut JM, Akushevich L, Bentley R, Marks JR, Huntsman D, Berchuck A. Loss of ARID1A- associated protein expression is a frequent event in clear cell and endometrioid ovarian cancers. Int J Gynecol Cancer, 2012, 22(1): 9-14.[23] Yamamoto S, Tsuda H, Takano M, Tamai S, Matsubara O. PIK3CA mutations and loss of ARID1A protein expression are early events in the development of cystic ovarian clear cell adenocarcinoma. Virchows Arch, 2012, 460(1): 77-87.[24] Fadare O, Renshaw IL, Liang SX. Does the Loss of ARID1A (BAF-250a) Expression in Endometrial Clear Cell Carcinomas Have Any Clinicopathologic Signifi-cance? A Pilot Assessment. J Cancer, 2012, 3: 129-136.[25] Katagiri A, Nakayama K, Rahman MT, Rahman M, Katagiri H, Nakayama N, Ishikawa M, Ishibashi T, Iida K, Kobayashi H, Otsuki Y, Nakayama S, Miyazaki K. Loss of ARID1A expression is related to shorter progression-free survival and chemoresistance in ovarian clear cell carcinoma. Mod Pathol, 2012, 25(2): 282-288.[26] Guan B, Mao TL, Panuganti PK, Kuhn E, Kurman RJ, Maeda D, Chen E, Jeng YM, Wang TL, Shih IM. Mutation and loss of expression of ARID1A in uterine low-grade endometrioid carcinoma. Am J Surg Pathol, 2011, 35(5): 625-632.[27] Maeda D, Mao TL, Fukayama M, Nakagawa S, Yano T, Taketani Y, Shih IM. Clinicopathological significance of loss of ARID1A Immunoreactivity in ovarian clear cell carcinoma. Int J Mol Sci, 2010, 11(12): 5120-5128.[28] Katagiri A, Nakayama K, Rahman MT, Rahman M, Katagiri H, Ishikawa M, Ishibashi T, Iida K, Otsuki Y, Nakayama S, Miyazaki K. Frequent loss of tumor sup-pressor ARID1A protein expression in adenocarcino-mas/adenosquamous carcinomas of the uterine cervix. Int J Gynecol Cancer, 2012, 22(2): 208-212.[29] Zang ZJ, Cutcutache I, Poon SL, Zhang SL, McPherson JR, Tao J, Rajasegaran V, Heng HL, Deng N, Gan A, Lim KH, Ong CK, Huang D, Chin SY, Tan IB, Ng CC, Yu W, Wu Y, Lee M, Wu J, Poh D, Wan WK, Rha SY, So J, Salto-Tellez M, Yeoh KG, Wong WK, Zhu YJ, Futreal PA, Pang B, Ruan Y, Hillmer AM, Bertrand D, Nagarajan N, Rozen S, Teh BT, Tan P. Exome sequencing of gastric adenocarci-noma identifies recurrent somatic mutations in cell adhe-sion and chromatin remodeling genes. Nat Genet, 2012, 44(5): 570-574.[30] Fujimoto A, Totoki Y, Abe T, Boroevich KA, Hosoda F, Nguyen HH, Aoki M, Hosono N, Kubo M, Miya F, Arai Y, Takahashi H, Shirakihara T, Nagasaki M, Shibuya T, Na-kano K, Watanabe-Makino K, Tanaka H, Nakamura H, Kusuda J, Ojima H, Shimada K, Okusaka T, Ueno M, Shigekawa Y, Kawakami Y, Arihiro K, Ohdan H, Gotoh K, Ishikawa O, Ariizumi S, Yamamoto M, Yamada T, Cha-yama K, Kosuge T, Yamaue H, Kamatani N, Miyano S, Nakagama H, Nakamura Y, Tsunoda T, Shibata T, Naka-gawa H. Whole-genome sequencing of liver cancers iden-tifies etiological influences on mutation patterns and re-current mutations in chromatin regulators. Nat Genet, 2012, 44(7): 760-764.[31] Tsurusaki Y, Okamoto N, Ohashi H, Kosho T, Imai Y, Hibi-Ko Y, Kaname T, Naritomi K, Kawame H, Wakui K, Fukushima Y, Homma T, Kato M, Hiraki Y, Yamagata T, Yano S, Mizuno S, Sakazume S, Ishii T, Nagai T, Shiina M, Ogata K, Ohta T, Niikawa N, Miyatake S, Okada I, Mi-zuguchi T, Doi H, Saitsu H, Miyake N, Matsumoto N. Mutations affecting components of the SWI/SNF complex cause Coffin-Siris syndrome. Nat Genet, 2012, 44(4): 376-378.[32] Wang XM, Nagl NG Jr, Flowers S, Zweitzig D, Dallas PB, Moran E. Expression of p270 (ARID1A), a component of human SWI/SNF complexes, in human tumors. Int J Cancer, 2004, 112(4): 636-642.[33] Huang JM, Zhao YL, Li Y, Fletcher JA, Xiao S. Genomic and functional evidence for an ARID1A tumor suppressor role. Genes Chromosomes Cancer, 2007, 46(8): 745-750.[34] Nissenblatt M. Endometriosis-associated ovarian carcinomas. N Engl J Med, 2011, 364(5): 482-483.[35] Jones S, Li M, Parsons DW, Zhang XS, Wesseling J, Kristel P, Schmidt MK, Markowitz S, Yan H, Bigner D, Hruban RH, Eshleman JR, Iacobuzio-Donahue CA, Goggins M, Maitra A, Malek SN, Powell S, Vogelstein B, Kinzler KW, Velculescu VE, Papadopoulos N. Somatic mutations in the chromatin remodeling gene ARID1A oc-cur in several tumor types. Hum Mutat, 2012, 33(1): 100-103.[36] Wiegand KC, Lee AF, Al-Agha OM, Chow C, Kalloger SE, Scott DW, Steidl C, Wiseman SM, Gascoyne RD, Gilks B, Huntsman DG. Loss of BAF250a (ARID1A) is frequent in high-grade endometrial carcinomas. J Pathol, 2011, 224(3): 328-333.[37] Wu JI. Diverse functions of ATP-dependent chromatin remodeling complexes in development and cancer. Acta Biochim Biophys Sin (Shanghai), 2012, 44(1): 54-69.[38] Keenen B, de la Serna IL. Chromatin remodeling in em-bryonic stem cells: regulating the balance between pluri-potency and differentiation. J Cell Physiol, 2009, 219(1): 1-7.[39] Gao XL, Tate P, Hu P, Tjian R, Skarnes WC, Wang Z. ES cell pluripotency and germ-layer formation require the SWI/SNF chromatin remodeling component BAF250a. Proc Natl Acad Sci USA, 2008, 105(18): 6656-6661.[40] Yan ZJ, Wang Z, Sharova L, Sharov AA, Ling C, Piao YL, Aiba K, Matoba R, Wang WD, Ko MSH. BAF250B-asso-ciated SWI/SNF chromatin-remodeling complex is required to maintain undifferentiated mouse embryonic stem cells. Stem Cells, 2008, 26(5): 1155-1165.[41] Wilsker D, Patsialou A, Dallas PB, Moran E. ARID proteins: a diverse family of DNA binding proteins implicated in the control of cell growth, differentiation, and development. Cell Growth Differ, 2002, 13(3): 95-106.[42] Flores-Alcantar A, Gonzalez-Sandoval A, Escalante-Alcalde D, Lomelí H. Dynamics of expression of ARID1A and ARID1B subunits in mouse embryos and in cells during the cell cycle. Cell Tissue Res, 2011, 345(1): 137-148.[43] Nagl NG Jr, Patsialou A, Haines DS, Dallas PB, Beck GR Jr, Moran E. The p270 (ARID1A/SMARCF1) sub-unit of mammalian SWI/SNF-related complexes is essen-tial for normal cell cycle arrest. Cancer Res, 2005, 65(20): 9236-9244.[44] Nagl NG Jr, Zweitzig DR, Thimmapaya B, Beck GR Jr, Moran E. The c-myc gene is a direct target of mammalian SWI/SNF-related complexes during differentiation-associated cell cycle arrest. Cancer Res, 2006, 66(3): 1289-1293.[45] Nagl NG Jr, Wang XM, Patsialou A, Van Scoy M, Moran E. Distinct mammalian SWI/SNF chromatin remodeling complexes with opposing roles in cell-cycle control. EMBO J, 2007, 26(3): 752-763.[46] Van Rechem C, Boulay G, Leprince D. HIC1 interacts with a specific subunit of SWI/SNF complexes, ARID1A/ BAF250A. Biochem Biophys Res Commun, 2009, 385(4): 586-590.[47] Guan B, Wang TL, Shih IM. ARID1A, a factor that pro-motes formation of SWI/SNF-mediated chromatin remodeling, is a tumor suppressor in gynecologic cancers. Cancer Res, 2011, 71(21): 6718-6727.[48] Lans H, Marteijn JA, Vermeulen W. ATP-dependent chromatin remodeling in the DNA-damage response. Epigenetics Chromatin, 2012, 5: 4.[49] Matsuoka S, Ballif BA, Smogorzewska A, McDonald ER 3rd, Hurov KE, Luo J, Bakalarski CE, Zhao ZM, Solimini N, Lerenthal Y, Shiloh Y, Gygi SP, Elledge SJ. ATM and ATR substrate analysis reveals extensive protein networks responsive to DNA damage. Science, 2007, 316(5828): 1160-1166.[50] Hargreaves DC, Crabtree GR. ATP-dependent chromatin remodeling: genetics, genomics and mechanisms. Cell Res, 2011, 21(3): 396-420.[51] Bartlett C, Orvis TJ, Rosson GS, Weissman BE. BRG1 mutations found in human cancer cell lines inactivate Rb-mediated cell-cycle arrest. J Cell Physiol, 2011, 226(8): 1989-1997.[52] Naidu SR, Love IM, Imbalzano AN, Grossman SR, An-drophy EJ. The SWI/SNF chromatin remodeling subunit BRG1 is a critical regulator of p53 necessary for proliferation of malignant cells. Oncogene, 2009, 28(27): 2492-2501.[53] Wilson BG, Roberts CW. SWI/SNF nucleosome remodel-lers and cancer. Nat Rev Cancer, 2011, 11(7): 481-492. |