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TF, Thompson CB: Apoptosis meets signal transduction: elimination of a BAD influence. Cell 1996, 87:589–592.PubMedCrossRef 26. Zhang K, Kaufman RJ: From endoplasmic-reticulum stress to the inflammatory response. Nature 2008, 454:455–462.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions In our study, all authors are in agreement with the content of the manuscript. Each author’s contribution to the paper: BC: First author, Participated A-1210477 price in research design, the writing of the paper, the performance of the research and data analysis. JQW: Corresponding author, research instruction, data analysis, development of final

manuscript. XLW: the performance of the research and data analysis. WHZ: research instruction, development of final manuscript.”
“Introduction Multidrug resistance (MDR) is a major cause of treatment failure and mortality in cancer patients. Breast cancer is the most prevalent cancer among women and the second leading cause of death in cancer. The most widely used treatment of breast cancer is chemotherapy, while the success of chemotherapy in breast cancer patients is also seriously limited by the development of MDR [1]. One well-known mechanism of MDR is the over-expression of ATP-binding cassette transporters such as multidrug resistance gene 1 (MDR1), multidrug resistance-associated protein 1 (MRP1), Sunitinib lung resistance protein (LRP)

and the breast cancer resistance protein (BCRP) [2–7]. P-glycoprotein (P-gp), which is encoded by the MDR1, is the most extensively studied drug transporter. It is an integral membrane glycoprotein with a molecular mass of 170 kDa and has been postulated to function as a pump that removes hydrophobic anticancer agents from drug-resistant cells, thus promoting MDR [8]. The novel gene HA117 (Gene Bank accession number: AY230154), which was screened and cloned from the ATRA-resistant acute myeloid leukemia cell line HL-60/ATRA using differential hybridization and gene chip assays [9], was shown to promote MDR in the chronic myelogenous myeloid leukemia cell line K562 [10]. However, the strength and mechanism of the MDR of HA117 have not yet been elucidated, especially in solid tumor cells.

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