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. 2022 Dec 3;20:559. doi: 10.1186/s12967-022-03780-2

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 8 — TEMo-secreted miR-181a activates AKT signaling partly by inhibiting PTEN in BC cells. A Western blot analysis showed up-regulation of the phosphorylated levels of AKT and mTOR in MDA-MB-231 BC cells, 48 h after treatment with 100 μg/mL TEMo-Exo compared with the corresponding control cells. Results indicated that the promoting effects of TEMo-Exo on Akt–mTOR signaling were partially abolished when the cells were transfected with the miR-181a inhibitor. B Western blot analysis revealed that when MDA-MB-231 BC cells were incubated with the AKT inhibitor MK-2206, the activation of the Akt–mTOR signaling caused by miR-181a was suppressed. Actin was used as an endogenous loading control. Western blot images are representative of at least three independent experiments. C BC cells displayed the lowest rate of proliferation when treated with MK-2206 at the indicated time points. Although transfection of miR-181a mimic considerably increased the proliferation rate of MDA-MB-231 BC cells compared to control cells, miR-181a did not increase BC cell proliferation in the cell group treated with MK-2206. Points, mean of three different experiments; bars, SD. **P-value < 0.01. D, E Representative photomicrographs (D) and bar graphs (E) illustrated that MK-2206 abrogated the promoting effect of miR-181a on BC cell migration. F Transfection of miR-181a mimic caused a significant reduction of PTEN expression at both mRNA and protein levels in MDA-MB-231 BC cells, suggesting that miR-181a may regulate PTEN in BC cells. G The mean normalized ratio for PTEN mRNA levels were measured by RT-qPCR in different conditions, 48 h after incubation. Results demonstrated that PTEN mRNA levels were considerably decreased in MDA-MB-231 BC cells incubated with 100 μg/mL TEMo-Exo compared to those cells incubated with exosomes derived from control monocytes or NEMo. In contrast, inhibition of miR-181a in MDA-MB-231 BC cells partially prevented the inhibitory effect of TEMo-Exo on PTEN expression. Columns, mean of three different experiments; bars, SD. *P-value < 0.05, **P-value < 0.01, ***P-value < 0.001