Published December 2, 2013 - More info
Platinum compounds display clinical activity against a wide variety of solid tumors; however, resistance to these agents is a major limitation in cancer therapy. Reduced platinum uptake and increased platinum export are examples of resistance mechanisms that limit the extent of DNA damage. Here, we report the discovery and characterization of the role of ATP11B, a P-type ATPase membrane protein, in cisplatin resistance. We found that
Myrthala Moreno-Smith, J.B. Halder, Paul S. Meltzer, Tamas A. Gonda, Lingegowda S. Mangala, Rajesha Rupaimoole, Chunhua Lu, Archana S. Nagaraja, Kshipra M. Gharpure, Yu Kang, Cristian Rodriguez-Aguayo, Pablo E. Vivas-Mejia, Behrouz Zand, Rosemarie Schmandt, Hua Wang, Robert R. Langley, Nicholas B. Jennings, Cristina Ivan, Jeremy E. Coffin, Guillermo N. Armaiz, Justin Bottsford-Miller, Sang Bae Kim, Margaret S. Halleck, Mary J.C. Hendrix, William Bornman, Menashe Bar-Eli, Ju-Seog Lee, Zahid H. Siddik, Gabriel Lopez-Berestein, Anil K. Sood
Original citation: J Clin Invest. 2013;123(5):2119–2130. doi:10.1172/JCI65425.
Citation for this corrigendum: J Clin Invest. 2013;123(12):5411. doi:10.1172/JCI73904.
The legend for Figure 5 did not disclose that the images presented in part A were duplicated as the no treatment control for the cisplatin experiment shown in parts D and E. The authors wish to add the correction below to the legend for Figure 5.
The merged immunofluorescence images showing colocalization of ATP11B and STX6 in A2780-PAR and A2780-CP20 cells in A are shown again in D and E to demonstrate localization of ATP11B and STX6 in the absence of cisplatin in A2780-PAR and A2780-CP20 cells.
The authors regret the error.