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. 2019 Nov 28;68(1):45–51. doi: 10.1136/jim-2019-001010

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© American Federation for Medical Research 2020. Re-use permitted under CC BY-NC. No commercial re-use. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, an indication of whether changes were made, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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MM cell-derived exosomes induced IL-6 secretion of BMSCs via the Ape1/NF-kB pathway. (A) The level of IL-6 in BMSC and culture media in RPMI-8226 cell-derived exosomes group (200 μg/mL) was significantly higher than the BMSC alone. (B, C) The messenger RNA levels of IL-6 and Ape1 in BMSC and RPMI-8226 cell-derived exosomes (200 μg/mL) coculture were higher than the BMSC alone. (D) RPMI-8226 cell-derived exosomes (200 μg/mL) inhibit the expression of Ape1 and NF-kB. The level of NF-kB was downregulated, followed by a decrease in Ape1 siRNA. BMSC, bone marrow stromal cell; Exo, exosome; IL-6, interleukin 6; MM, multiple myeloma;GAPDH, glyceraldehyde-3-phosphate dehydrogenase; siRNA, small interfering RNA.