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Cited by 19Curcumin's Biomedical ApplicationsCancer Cells and MetastasisMesenchymal stem cell research

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Curcumin Disrupts a Positive Feedback Loop between ADMSCs and Cancer Cells in the Breast Tumor Microenvironment via the CXCL12/CXCR4 Axis

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Jang, Bo-Young, Shin, Min, Han, Dong-Hee, Sung, Jung-Suk·2023·Pharmaceutics
DOI 10.3390/pharmaceutics15112627PMC PMC10675183
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Abstract

Adipose tissue has a significant impact on breast cancer initiation and progression owing to its substantial proportion in the breast. Adipose-derived mesenchymal stem cells (ADMSCs) are major players in the breast tumor microenvironment (TME) as they interact with cancer cells. The intricate interaction between ADMSCs and cancer cells not only drives the differentiation of ADMSCs into cancer-associated fibroblasts (CAFs) but also the metastasis of cancer cells, which is attributed to the CXCL12/CXCR4 axis. We investigated the effects of curcumin, a flavonoid known for CXCL12/CXCR4 axis inhibition, on breast TME by analyzing whether it can disrupt the ADMSC-cancer positive loop. Using MCF7 breast cancer cell-derived conditioned medium (MCF7-CM), we induced ADMSC transformation and verified that curcumin diminished the phenotypic change, inhibiting CAF marker expression. Additionally, curcumin suppressed the CXCL12/CXCR4 axis and its downstream signaling both in ADMSCs and MCF7 cells. The CM from ADMSCs, whose ADMSC-to-CAF transformation was repressed by the curcumin treatment, inhibited the positive feedback loop between ADMSCs and MCF7 as well as epithelial–mesenchymal transition in MCF7. Our study showed that curcumin is a potent anti-cancer agent that can remodel the breast TME, thereby restricting the ADMSC-cancer positive feedback loop associated with the CXCL12/CXCR4 axis.

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Figure 1 Curcumin inhibited the transformation of ADMSCs into CAFs. (A) Relative cell viability of curcumin and MCF7-CM on ADMSCs was measured using a WST-8 solution. ADMSCs were seeded, and various concentrations of curcumin were used to treat cells with or without 50% MCF-CM for 72 h. The gene expression of (B) vimentin, (C) α-SMA, and (D) FN1 was assessed by qRT-PCR. The protein levels of (E) vimentin, (F) α-SMA, and (G) fibronectin were measured via Western blotting analysis. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the control group; # p < 0.05, ## p < 0.01, and ### p < 0.001 compared to the group treated only with MCF7-CM.
Figure 1 Curcumin inhibited the transformation of ADMSCs into CAFs. (A) Relative cell viability of curcumin and MCF7-CM on ADMSCs was measured using a WST-8 solution. ADMSCs were seeded, and various concentrations of curcumin were used to treat cells with or without 50% MCF-CM for 72 h. The gene expression of (B) vimentin, (C) α-SMA, and (D) FN1 was assessed by qRT-PCR. The protein levels of (E) vimentin, (F) α-SMA, and (G) fibronectin were measured via Western blotting analysis. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the control group; # p < 0.05, ## p < 0.01, and ### p < 0.001 compared to the group treated only with MCF7-CM.CC BY · PubMed Central
Figure 2 Curcumin downregulated CXCL12 and CXCR4 expression in MCF7-CM-treated ADMSCs. (A–D) The relative mRNA and protein levels of CXCL12 and CXCR4 were determined. Curcumin inhibited both mRNA and protein levels of CXCR4 and CXCL12. (E,F) The relative fluorescence intensity of CXCR4 on the cell surface of ADMSCs was determined and quantified. * p < 0.05 and *** p < 0.001 compared to the control group; # p < 0.05, ## p < 0.01, and ### p < 0.001 compared to the group treated only with MCF7-CM; Con: control; CAF: MCF7-CM-treated group; AMD: MCF7-CM-treated group with 20 μM of AMD3100; Cur: MCF7-CM-treated group with 20 μM of curcumin; scale bar: 100 μm.
Figure 2 Curcumin downregulated CXCL12 and CXCR4 expression in MCF7-CM-treated ADMSCs. (A–D) The relative mRNA and protein levels of CXCL12 and CXCR4 were determined. Curcumin inhibited both mRNA and protein levels of CXCR4 and CXCL12. (E,F) The relative fluorescence intensity of CXCR4 on the cell surface of ADMSCs was determined and quantified. * p < 0.05 and *** p < 0.001 compared to the control group; # p < 0.05, ## p < 0.01, and ### p < 0.001 compared to the group treated only with MCF7-CM; Con: control; CAF: MCF7-CM-treated group; AMD: MCF7-CM-treated group with 20 μM of AMD3100; Cur: MCF7-CM-treated group with 20 μM of curcumin; scale bar: 100 μm.CC BY · PubMed Central
Figure 3 Curcumin inhibited the NF-κB signaling pathway and SHH expression, which are downstream of the CXCL12/CXCR4 axis in ADMSCs. (A,B) Relative pNF-κB translocation levels in nuclei of ADMSCs after treatment for 4 h were imaged via immunofluorescence staining and quantified. The protein levels of (C) pNF-κB, NF-κB, and (D) SHH were determined using Western blotting analysis. (E) The secretion level of SHH was quantified using ELISA kits. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the control group; # p < 0.05, ## p < 0.01, and ### p < 0.001 compared to the CAF group; Con: control; CAF: MCF7-CM-treated group; AMD: MCF7-CM-treated group with 20 μM of AMD3100; Cur: MCF7-CM-treated group with 20 μM of curcumin; scale bar: 100 μm.
Figure 3 Curcumin inhibited the NF-κB signaling pathway and SHH expression, which are downstream of the CXCL12/CXCR4 axis in ADMSCs. (A,B) Relative pNF-κB translocation levels in nuclei of ADMSCs after treatment for 4 h were imaged via immunofluorescence staining and quantified. The protein levels of (C) pNF-κB, NF-κB, and (D) SHH were determined using Western blotting analysis. (E) The secretion level of SHH was quantified using ELISA kits. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the control group; # p < 0.05, ## p < 0.01, and ### p < 0.001 compared to the CAF group; Con: control; CAF: MCF7-CM-treated group; AMD: MCF7-CM-treated group with 20 μM of AMD3100; Cur: MCF7-CM-treated group with 20 μM of curcumin; scale bar: 100 μm.CC BY · PubMed Central
Figure 4 Curcumin suppressed the CXCL12/CXCR4 axis and its downstream elements in MCF7 cells. (A–D) The mRNA and protein levels of CXCL12 and CXCR4 were assessed after curcumin treatment at various concentrations for 72 h. (E,F) Immunocytochemistry analysis was performed to visualize and quantify the relative translocation levels of pNF-κB into the nuclei of MCF7 cells. (G) Western blotting analysis was conducted to assess the protein levels of pNF-κB and NF-κB after treatment for 4 h. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the control group; Con: control; AMD: 20 μM of AMD3100-treated MCF7; Cur: 20 μM of curcumin-treated MCF7; scale bar: 100 μm.
Figure 4 Curcumin suppressed the CXCL12/CXCR4 axis and its downstream elements in MCF7 cells. (A–D) The mRNA and protein levels of CXCL12 and CXCR4 were assessed after curcumin treatment at various concentrations for 72 h. (E,F) Immunocytochemistry analysis was performed to visualize and quantify the relative translocation levels of pNF-κB into the nuclei of MCF7 cells. (G) Western blotting analysis was conducted to assess the protein levels of pNF-κB and NF-κB after treatment for 4 h. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the control group; Con: control; AMD: 20 μM of AMD3100-treated MCF7; Cur: 20 μM of curcumin-treated MCF7; scale bar: 100 μm.CC BY · PubMed Central
Figure 5 Curcumin-mediated inhibition of CAF transformation suppressed the positive interaction between CAFs and MCF7 cells mediated by the CXCL12/CXCR4 axis. The protein levels of (A) CXCL12 and (B) CXCR4 were evaluated following treatment with ADMSC-derived CM for 72 h. (C) Western blotting analysis was performed to examine the protein levels of pNF-κB and NF-κB following treatment with ADMSC-derived CM for 24 h. Immunofluorescence imaging was employed to visualize and quantitatively analyze (D,E) the relative translocation levels of pNF-κB in the nuclei and (F,G) SHH delivery levels on the cell surface of MCF7 cells following a 24 h treatment with ADMSC-derived CM. * p < 0.05 and *** p < 0.001 compared to the Con-CM-treated group; # p < 0.05, ## p < 0.01, and ### p < 0.001 compared to the CAF-CM-treated group; scale bar: 100 μm.
Figure 5 Curcumin-mediated inhibition of CAF transformation suppressed the positive interaction between CAFs and MCF7 cells mediated by the CXCL12/CXCR4 axis. The protein levels of (A) CXCL12 and (B) CXCR4 were evaluated following treatment with ADMSC-derived CM for 72 h. (C) Western blotting analysis was performed to examine the protein levels of pNF-κB and NF-κB following treatment with ADMSC-derived CM for 24 h. Immunofluorescence imaging was employed to visualize and quantitatively analyze (D,E) the relative translocation levels of pNF-κB in the nuclei and (F,G) SHH delivery levels on the cell surface of MCF7 cells following a 24 h treatment with ADMSC-derived CM. * p < 0.05 and *** p < 0.001 compared to the Con-CM-treated group; # p < 0.05, ## p < 0.01, and ### p < 0.001 compared to the CAF-CM-treated group; scale bar: 100 μm.CC BY · PubMed Central
Figure 6 Curcumin-mediated inhibition of CAF transformation promoted by the CXCL12/CXCR4 axis hindered the EMT in MCF7 cells. (A,B) Cell migration assays were performed after creating equal gaps between the experimental groups and quantified. (C) The permeability of cells through the basement membrane was quantified using a fluorescence reader. The protein levels of (D) E-cadherin, (E) N-cadherin, and (F) fibronectin were determined using immunoblot assays. ** p < 0.01; and *** p < 0.001 compared to the Con-CM-treated group; # p < 0.05 and ### p < 0.001 compared to the CAF-CM-treated group; scale bar: 200 μm.
Figure 6 Curcumin-mediated inhibition of CAF transformation promoted by the CXCL12/CXCR4 axis hindered the EMT in MCF7 cells. (A,B) Cell migration assays were performed after creating equal gaps between the experimental groups and quantified. (C) The permeability of cells through the basement membrane was quantified using a fluorescence reader. The protein levels of (D) E-cadherin, (E) N-cadherin, and (F) fibronectin were determined using immunoblot assays. ** p < 0.01; and *** p < 0.001 compared to the Con-CM-treated group; # p < 0.05 and ### p < 0.001 compared to the CAF-CM-treated group; scale bar: 200 μm.CC BY · PubMed Central

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Metadata

Authors
Jang, B.-Y., Shin, M., Han, D.-H., & Sung, J.-S.
Affiliations
Dongguk University (KR)
Corresponding author
Sung, Jung-Suk
ORCID
Venue
Pharmaceutics
Publisher
MDPI AG
Published
2023-11-15
Volume
15
Issue
11
Pages
2627
ISSN
1999-4923 (ISSN-L)
DOI
10.3390/pharmaceutics15112627
PMC
PMC10675183
OpenAlex
W4388723961
Cited by
19
References
0
Citations by year
2026: 5 · 2025: 6 · 2024: 7 · 2023: 1
FWCI
1.60
Type
journal article
Language
en
Open access
Licence
Locations
  • Pharmaceutics (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Research Foundation of Korea (NRF) (2022R1A6A1A03053343)
  • Ministry of Education (2022R1A6A1A03053343)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Medicine › Curcumin's Biomedical Applications
  • Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Mesenchymal stem cell research
Keywords
curcumin, adipose-derived stem cells, breast cancer, tumor microenvironment, CXCL12/CXCR4 axis, cancer-associated fibroblasts, epithelial-mesenchymal transition, MCF-7 cells, conditioned medium, metastasis, flavonoids

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