Wen-Li et al. Journal of Experimental & Clinical Cancer Research 2012, 31:92 http://www.jeccr.com/content/31/1/92 Page 8 of 9 synthase co-immunoprecipitates with Hsp90 and Hsp90- client proteins in cell lysate from MCF-7, T47D, MDA- MB-453 and HT-29 cancer cells [37]. Heat shock pro- teins are often overexpressed in human malignancies, including AML. Hsp90 is the major chaperone required for stabilization of the multiple oncogenic kinases involved in the development of AML [38]. Hsp90 client proteins are also involved in the regulation of apoptosis, proliferation, autophagy and cell cycle progression, and several hsp90 client proteins are considered to be pos- sible therapeutic targets for the treatment of AML [39]. Hsp90 inhibitors could be used as single agents or po- tentially, in combination with other targeted treatments such as a functional ATP synthase β subunit antibody. This study indicates that clinical focus of hsp90 inhibi- tors and F1F0-ATP β subunit synthase functional anti- bodies should be directed towards hematological malignancies, as well as solid tumors and malignant melanoma. Conclusions This study demonstrates that the β subunit of F1F0 ATPase is expressed on the cell surface of several leukemia cell lines with between 0.1% and 56% of cells expressing the ecto-F1F0-ATPase β subunit. We pre- pared a McAb against the ecto-F1F0-ATPase β subunit, which significantly inhibited proliferation and induced apoptosis in cell lines derived from AML in vitro. These findings indicate that expression of the ecto-F1F0- ATPase β subunit is a cancer-associated antigen in hematological malignancies. The ecto-F1F0-ATPase β subunit provides a potential target for immunotherapy in AML and other hematological malignancies. Abbreviations ELISA: Enzyme-linked immunosorbent assay; McAb: Monoclonal antibody; AML: Acute myeloid leukemia. Competing interests The authors have no conflicts of interest to disclose. Authors’ contributions PJ designed and directed the study. ZWL, WJ and TYF finished the most of the experiments. FX and LYH drafted this manuscript. ZXM and ZM participated in the cell culture. NJ participated in study design and coordination, data analysis and interpretation and drafted the manuscript. All authors read and approved the final manuscript. Acknowledgements We thank Professor Zhi-Hua Yang (Cancer Institute/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China) for her kindly instruction. This work was supported by grants from the National Key Basic Research Program No. 2010CB933902, National Natural Science Foundation for youth No. 81100371, Natural Science Foundation of Jiangsu Province No. BK2011308, Universities Natural Science Foundation of Jiangsu Province No. 11KJB320014 and Talent’s subsidy project in science and education of department of public health of Suzhou City No. SWKQ1020. Medical innovation team and leading talent of Jiangsu Province. No. LJ201126. Major scientific and technological special project for “significant new drugs creation” No. 2012ZX09103301-040. Author details 1Department of Hematology and Oncology, Children’s Hospital of Soochow University, Suzhou, China. 2Translational Research Center, Second Hospital, The Second Clinical School, Nanjing Medical University, Nanjing, China. Received: 7 August 2012 Accepted: 5 November 2012 Published: 9 November 2012 References 1. 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