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. 2021 Nov 19;11:671082. doi: 10.3389/fonc.2021.671082

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Copyright © 2021 Chi, Xin and Liu

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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HPSC-EXO facilitates Gem resistance and tumorigenesis of pancreatic cancer cells. (A), Viability of PANC-1 cells treated with PSC-EXO and HPSC-EXO was detected by MTT assay. (B), Flow cytometric analysis of apoptosis of PANC-1 cells treated with PSC-EXO and HPSC-EXO. (C), Apoptosis of PANC-1 cells treated with PSC-EXO and HPSC-EXO was detected by TUNEL staining. (D), Cleaved caspase 3 protein expression in PANC-1 cells treated with PSC-EXO and HPSC-EXO was detected by Western blot. (E), Migration of PANC-1 cells treated with PSC-EXO and HPSC-EXO was detected by Transwell assay. (F), Invasion of PANC-1 cells treated with PSC-EXO and HPSC-EXO was detected by Transwell assay. (G), Gem sensitivity of PANC-1 cells treated with PSC-EXO and HPSC-EXO was detected by MTT assay. (H), Tumor volume of mice treated with PSC-EXO and HPSC-EXO after injection of Gem. (I), Tumor weight of mice treated with PSC-EXO and HPSC-EXO after injection of Gem. (J), The positive expression rate of Ki67 in tumor tissues of mice treated with PSC-EXO and HPSC-EXO after injection of Gem was detected by immunohistochemistry. *p < 0.05. Measurement data were expressed as mean ± standard deviation. The data comparison among multiple groups was performed using one-way ANOVA, followed by the Tukey’s post hoc test. The data at different time points were compared by repeated measures ANOVA, followed by Bonferroni’s post hoc test. The cell experiment was repeated three times. n = 8 for mice following each treatment.