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Exosomal microRNA‑146a derived from mesenchymal stem cells increases the sensitivity of ovarian cancer cells to docetaxel and taxane via a LAMC2‑mediated PI3K/Akt axis

Qiu, Liya, Wang, Jiakun, Chen, Mei, Chen, Fengyun, Tu, Wenluo·2020·International Journal of Molecular Medicine
DOI 10.3892/ijmm.2020.4634PMC PMC7307828
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Figure 1 Identification of hUCMSCs and their derived exosomes. (A) Expression of MSCs surface markers, including CD29, CD44, CD73, CD90, CD105, CD14, CD34, CD45 and HLA-DR, analyzed by flow cytometry. (B) hUCMSC morphology at passage 3 observed under a light microscope. Scale bar, 100 µm. (C) Representative images of osteogenic differentiation of hUCMSCs using Alizarin Red staining. Scale bar, 100 µm. (D) Representative images of adipogenic differentiation of hUCMSCs using Oil red O staining. Scale bar, 100 µm. (E) Morphological analysis of hUCMSC by transmission electronic microscopy. Scale bar, 200 nm. (F) Detection of exosomal marker expression in hUCMSC-released exosomes by western blotting. (G) Internalization of PKH26-labeled exosomes by SKOV3 and A2780 cells was observed under a fluorescence microscope. Scale bar, 50 µm. hUCMSCs, human umbilical cord mesenchymal stem cells.
Figure 1 Identification of hUCMSCs and their derived exosomes. (A) Expression of MSCs surface markers, including CD29, CD44, CD73, CD90, CD105, CD14, CD34, CD45 and HLA-DR, analyzed by flow cytometry. (B) hUCMSC morphology at passage 3 observed under a light microscope. Scale bar, 100 µm. (C) Representative images of osteogenic differentiation of hUCMSCs using Alizarin Red staining. Scale bar, 100 µm. (D) Representative images of adipogenic differentiation of hUCMSCs using Oil red O staining. Scale bar, 100 µm. (E) Morphological analysis of hUCMSC by transmission electronic microscopy. Scale bar, 200 nm. (F) Detection of exosomal marker expression in hUCMSC-released exosomes by western blotting. (G) Internalization of PKH26-labeled exosomes by SKOV3 and A2780 cells was observed under a fluorescence microscope. Scale bar, 50 µm. hUCMSCs, human umbilical cord mesenchymal stem cells.CC BY-NC-ND · PubMed Central
Figure 2 hUCMSC-derived exosomes inhibit OC cell drug resistance. SKOV3/DTX and A2780/TAX cells were induced by the exposure to gradient concentrations of drugs. (A) Cell survival rate examined by CCK-8 cell survival assays. Subsequently, the parental or drug-resistant OC cells were treated with 20 µg/ml MSCs-derived exosomes or PBS as a negative control. Exosome-treated parental or drug-resistant OC cells were exposed to 2 µM DTX or 5 µM TAX for 2 h, respectively. *P<0.05 vs. parental SKOV3 cells, #P<0.05 vs. parental A2780 cells. (B) Cell viability evaluated by CCK-8 cell viability assays. (C) EdU staining for cell proliferation. Scale bar, 25 µm. (D) Flow cytometry analysis for cells labelled with PI/Annexin V. (E) Hoechst 33258 staining for cell apoptosis. Scale bar, 25 µm. Data are presented as the mean ± SD. One-way (panels C, D and E) or two-way (panel A) ANOVA followed by Tukey's multiple comparisons test was used to determine statistical significance. Each assessment was performed in triplicate with three repetitions to ensure minimum deviation. In panels B, C, D and E: *P<0.05 vs. parental SKOV3 cells treated with PBS; #P<0.05 vs. SKOV3/DTX cells treated with PBS; @P<0.05 vs. parental A2780 cells treated with PBS, &P<0.05 vs. A2780/TAX cells treated with PBS. CCK-8, Cell Counting Kit-8; DTX, docetaxel; hUCMSCs, human umbilical cord mesenchymal stem cells; OC, ovarian cancer; PI, propidium iodide; TAX, taxane.
Figure 2 hUCMSC-derived exosomes inhibit OC cell drug resistance. SKOV3/DTX and A2780/TAX cells were induced by the exposure to gradient concentrations of drugs. (A) Cell survival rate examined by CCK-8 cell survival assays. Subsequently, the parental or drug-resistant OC cells were treated with 20 µg/ml MSCs-derived exosomes or PBS as a negative control. Exosome-treated parental or drug-resistant OC cells were exposed to 2 µM DTX or 5 µM TAX for 2 h, respectively. *P<0.05 vs. parental SKOV3 cells, #P<0.05 vs. parental A2780 cells. (B) Cell viability evaluated by CCK-8 cell viability assays. (C) EdU staining for cell proliferation. Scale bar, 25 µm. (D) Flow cytometry analysis for cells labelled with PI/Annexin V. (E) Hoechst 33258 staining for cell apoptosis. Scale bar, 25 µm. Data are presented as the mean ± SD. One-way (panels C, D and E) or two-way (panel A) ANOVA followed by Tukey's multiple comparisons test was used to determine statistical significance. Each assessment was performed in triplicate with three repetitions to ensure minimum deviation. In panels B, C, D and E: *P<0.05 vs. parental SKOV3 cells treated with PBS; #P<0.05 vs. SKOV3/DTX cells treated with PBS; @P<0.05 vs. parental A2780 cells treated with PBS, &P<0.05 vs. A2780/TAX cells treated with PBS. CCK-8, Cell Counting Kit-8; DTX, docetaxel; hUCMSCs, human umbilical cord mesenchymal stem cells; OC, ovarian cancer; PI, propidium iodide; TAX, taxane.CC BY-NC-ND · PubMed Central
Figure 3 miR-146a is enriched in hUCMSC-derived exosomes. (A) Heatmap of 15 ectopic expressed miRNAs in hUCMSC-derived exosomes. (B) miR-146a expression in exosome-treated ovarian cancer cells. *P<0.05 vs. parental SKOV3 cells treated with PBS; #P<0.05 vs. SKOV3/DTX cells treated with PBS; @P<0.05 vs. parental A2780 cells treated with PBS; &P<0.05 vs. A2780/TAX cells treated with PBS. (C) miR-146a expression pattern in SKOV3 and A2780 cells treated with miR-146a inhibitor or inhibitor control and co-cultured with exosomes extracted from hUCMSCs. *P<0.05 vs. exosomes co-cultured with parental SKOV3 cells transfected with InC; #P<0.05 vs. exosomes co-cultured with SKOV3/DTX cells transfected with InC; @P<0.05 vs. exosomes co-cultured with parental A2780 cells transfected with InC; &P<0.05 vs. exosomes co-cultured with A2780/TAX cells transfected with InC. Data are presented as the mean ± SD. One-way ANOVA and Tukey's multiple comparisons test were used to determine statistical significance. Each assessment was performed in triplicate with three repetitions to ensure minimum deviation. hUCMSCs, human umbilical cord mesenchymal stem cells; inhi, inhibitor; InC, inhibitor control; miR, microRNA.
Figure 3 miR-146a is enriched in hUCMSC-derived exosomes. (A) Heatmap of 15 ectopic expressed miRNAs in hUCMSC-derived exosomes. (B) miR-146a expression in exosome-treated ovarian cancer cells. *P<0.05 vs. parental SKOV3 cells treated with PBS; #P<0.05 vs. SKOV3/DTX cells treated with PBS; @P<0.05 vs. parental A2780 cells treated with PBS; &P<0.05 vs. A2780/TAX cells treated with PBS. (C) miR-146a expression pattern in SKOV3 and A2780 cells treated with miR-146a inhibitor or inhibitor control and co-cultured with exosomes extracted from hUCMSCs. *P<0.05 vs. exosomes co-cultured with parental SKOV3 cells transfected with InC; #P<0.05 vs. exosomes co-cultured with SKOV3/DTX cells transfected with InC; @P<0.05 vs. exosomes co-cultured with parental A2780 cells transfected with InC; &P<0.05 vs. exosomes co-cultured with A2780/TAX cells transfected with InC. Data are presented as the mean ± SD. One-way ANOVA and Tukey's multiple comparisons test were used to determine statistical significance. Each assessment was performed in triplicate with three repetitions to ensure minimum deviation. hUCMSCs, human umbilical cord mesenchymal stem cells; inhi, inhibitor; InC, inhibitor control; miR, microRNA.CC BY-NC-ND · PubMed Central
Figure 4 Exosomes from hUCMSCs promote OC cell chemosensitivity partly by transferring miR-146a. hUCMSC-derived exosome-treated parental or drug resistant OC cells were exposed to 2 µM DTX or 5 µM TAX for 2 h, respectively. (A) Cell viability assessed by Cell Counting Kit-8 cell viability assays. (B) EdU staining for cell proliferation. Scale bar, 25 µm. (C) Flow cytometry analysis for cells labelled with PI/Annexin V. (D) Hoechst 33258 staining for cell apoptosis. Scale bar, 25 µm. Data are presented as the mean ± SD. One-way (panels C, D and E) or two-way (panel A) ANOVA followed by Tukey's post hoc test was used to determine statistical significance. Each assessment was performed in triplicate with three repetitions to ensure minimum deviation. *P<0.05 vs. parental cells co-cultured with exosomes derived from InC-transfected MSCs. DTX, docetaxel; hUCMSCs, human umbilical cord mesenchymal stem cells; inhi, inhibitor; InC, inhibitor control; miR, microRNA; OC, ovarian cancer; PI, propidium iodide; TAX, taxane.
Figure 4 Exosomes from hUCMSCs promote OC cell chemosensitivity partly by transferring miR-146a. hUCMSC-derived exosome-treated parental or drug resistant OC cells were exposed to 2 µM DTX or 5 µM TAX for 2 h, respectively. (A) Cell viability assessed by Cell Counting Kit-8 cell viability assays. (B) EdU staining for cell proliferation. Scale bar, 25 µm. (C) Flow cytometry analysis for cells labelled with PI/Annexin V. (D) Hoechst 33258 staining for cell apoptosis. Scale bar, 25 µm. Data are presented as the mean ± SD. One-way (panels C, D and E) or two-way (panel A) ANOVA followed by Tukey's post hoc test was used to determine statistical significance. Each assessment was performed in triplicate with three repetitions to ensure minimum deviation. *P<0.05 vs. parental cells co-cultured with exosomes derived from InC-transfected MSCs. DTX, docetaxel; hUCMSCs, human umbilical cord mesenchymal stem cells; inhi, inhibitor; InC, inhibitor control; miR, microRNA; OC, ovarian cancer; PI, propidium iodide; TAX, taxane.CC BY-NC-ND · PubMed Central
Figure 5 miR-146a blocks the PI3K signaling pathway by inhibiting LAMC2. (A) Possible miR-146 binding sites in the LAMC2 3' untranslated region. (B) Impact of miR-146a on the luciferase activity of LAMC2-WT and LAMC2-MT evaluated by dual luciferase assays. *P<0.05 vs. LAMC2 MT. (C) LAMC2 expression in The Cancer Genome Atlas-ovarian cancer dataset (n=426 for tumor samples and n=88 for normal tissues) predicted by gene expression profiling interactive analysis. *P<0.05. (D) LAMC2 expression in SKOV3 and A2780 cells determined by RT-qPCR. *P<0.05 vs. cells treated with PBS; #P<0.05 vs. cells co-cultured with exosomes extracted from InC-treated MSCs. (E) Protein expression levels of PI3K measured by ELISA. *P<0.05 vs. cells treated with PBS; #P<0.05 vs. cells co-cultured with exosomes extracted from InC-treated MSCs. (F) LAMC2 expression in SKOV3/DTX and A2780/TAX cells determined by RT-qPCR. Data are presented as the mean ± SD. *P<0.05 vs. cells transfected with EV. One-way (panels D, E and F) or two-way (panel B) ANOVA and Tukey's multiple comparisons test were used to determine statistical significance. Each assessment was performed in triplicate with three repetitions to ensure minimum deviation. DTX, docetaxel; InC, inhibitor control; inhi, inhibitor; LAMC2, laminin γ2; miR, microRNA; MSCs, mesenchymal stem cells; MT, mutant; RT-qPCR, reverse transcription-quantitative PCR; TAX, taxane; WT, wild type.
Figure 5 miR-146a blocks the PI3K signaling pathway by inhibiting LAMC2. (A) Possible miR-146 binding sites in the LAMC2 3' untranslated region. (B) Impact of miR-146a on the luciferase activity of LAMC2-WT and LAMC2-MT evaluated by dual luciferase assays. *P<0.05 vs. LAMC2 MT. (C) LAMC2 expression in The Cancer Genome Atlas-ovarian cancer dataset (n=426 for tumor samples and n=88 for normal tissues) predicted by gene expression profiling interactive analysis. *P<0.05. (D) LAMC2 expression in SKOV3 and A2780 cells determined by RT-qPCR. *P<0.05 vs. cells treated with PBS; #P<0.05 vs. cells co-cultured with exosomes extracted from InC-treated MSCs. (E) Protein expression levels of PI3K measured by ELISA. *P<0.05 vs. cells treated with PBS; #P<0.05 vs. cells co-cultured with exosomes extracted from InC-treated MSCs. (F) LAMC2 expression in SKOV3/DTX and A2780/TAX cells determined by RT-qPCR. Data are presented as the mean ± SD. *P<0.05 vs. cells transfected with EV. One-way (panels D, E and F) or two-way (panel B) ANOVA and Tukey's multiple comparisons test were used to determine statistical significance. Each assessment was performed in triplicate with three repetitions to ensure minimum deviation. DTX, docetaxel; InC, inhibitor control; inhi, inhibitor; LAMC2, laminin γ2; miR, microRNA; MSCs, mesenchymal stem cells; MT, mutant; RT-qPCR, reverse transcription-quantitative PCR; TAX, taxane; WT, wild type.CC BY-NC-ND · PubMed Central
Figure 6 LAMC2 is involved in miR-146a-mediated OC cell sensitivity. hUCMSCs-derived exosome-treated parental or drug resistant OC cells were exposed to 2 µM DTX or 5 µM TAX for 2 h, respectively. (A) LAMC2 mRNA expression measured by reverse transcription-quantitative PCR. (B) Cell viability examined by Cell Counting Kit-8 cell viability assays. (C) EdU staining of OC cells. Scale bar, 25 µm. (D) Flow cytometry analysis for cells labelled with propidium iodide/Annexin V. Scale bar, 25 µm. (E) Hoechst 33258 staining for cell apoptosis. Data are presented as the mean ± SD. One-way (panels A, C, D and E) or two-way (panel B) ANOVA followed by Tukey's multiple comparisons test was used. *P<0.05 vs. cells transfected with EV. Each assessment was performed in triplicate with three repetitions to ensure minimum deviation. DTX, docetaxel; EV, empty vector; hUCMSCs, human umbilical cord mesenchymal stem cells; LAMC2, laminin γ2; miR, microRNA; OC, ovarian cancer; TAX, taxane.
Figure 6 LAMC2 is involved in miR-146a-mediated OC cell sensitivity. hUCMSCs-derived exosome-treated parental or drug resistant OC cells were exposed to 2 µM DTX or 5 µM TAX for 2 h, respectively. (A) LAMC2 mRNA expression measured by reverse transcription-quantitative PCR. (B) Cell viability examined by Cell Counting Kit-8 cell viability assays. (C) EdU staining of OC cells. Scale bar, 25 µm. (D) Flow cytometry analysis for cells labelled with propidium iodide/Annexin V. Scale bar, 25 µm. (E) Hoechst 33258 staining for cell apoptosis. Data are presented as the mean ± SD. One-way (panels A, C, D and E) or two-way (panel B) ANOVA followed by Tukey's multiple comparisons test was used. *P<0.05 vs. cells transfected with EV. Each assessment was performed in triplicate with three repetitions to ensure minimum deviation. DTX, docetaxel; EV, empty vector; hUCMSCs, human umbilical cord mesenchymal stem cells; LAMC2, laminin γ2; miR, microRNA; OC, ovarian cancer; TAX, taxane.CC BY-NC-ND · PubMed Central
Figure 7 Regulatory mechanism of hUCMSC-derived exosomal miR-146a involved in OC cell proliferation and drug resistance. hUCMSC-derived exosomal miR-146a impeded the proliferation and drug resistance of OC cells by targeting LAMC2 to regulate the PI3K/Akt signaling pathway. hUCMSCs, human umbilical cord mesenchymal stem cells; miR, microRNA; OC, ovarian cancer.
Figure 7 Regulatory mechanism of hUCMSC-derived exosomal miR-146a involved in OC cell proliferation and drug resistance. hUCMSC-derived exosomal miR-146a impeded the proliferation and drug resistance of OC cells by targeting LAMC2 to regulate the PI3K/Akt signaling pathway. hUCMSCs, human umbilical cord mesenchymal stem cells; miR, microRNA; OC, ovarian cancer.CC BY-NC-ND · PubMed Central

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Metadata

Authors
Qiu, L., Wang, J., Chen, M., Chen, F., & Tu, W.
Venue
International Journal of Molecular Medicine
Publisher
Spandidos Publications
Published
2020-06-05
Volume
46
Issue
2
Pages
609-620
ISSN
  • 1107-3756
  • 1791-244X
DOI
10.3892/ijmm.2020.4634
PMC
PMC7307828
Cited by
88
References
2

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CoChat. (2026). Citation check: Exosomal microRNA‑146a derived from mesenchymal stem cells increases the sensitivity of ovarian cancer cells to docetaxel and taxane via a LAMC2‑mediated PI3K/Akt axis. https://app.cochat.ai/papers/10.3892/ijmm.2020.4634
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Qiu, L., Wang, J., Chen, M., Chen, F., & Tu, W. (2020). Exosomal microRNA‑146a derived from mesenchymal stem cells increases the sensitivity of ovarian cancer cells to docetaxel and taxane via a LAMC2‑mediated PI3K/Akt axis. International Journal of Molecular Medicine. https://doi.org/10.3892/ijmm.2020.4634