Rosmarinic acid represses colitis-associated colon cancer: A pivotal involvement of the TLR4-mediated NF-κB-STAT3 axis
Previously, we found that rosmarinic acid (RA) exerted anti-inflammatory activities in a dextran sulfate sodium (DSS)-induced colitis model. Here, we investigated the anti-tumor effects of RA on colitis-associated colon cancer (CAC) and the underlying molecular mechanisms. We established an azoxymet...
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| Published in: | Neoplasia (New York, N.Y.) Vol. 23; no. 6; pp. 561 - 573 |
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| Main Authors: | , , , , , , |
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Elsevier Inc
01.06.2021
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| ISSN: | 1476-5586, 1522-8002, 1476-5586 |
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| Abstract | Previously, we found that rosmarinic acid (RA) exerted anti-inflammatory activities in a dextran sulfate sodium (DSS)-induced colitis model. Here, we investigated the anti-tumor effects of RA on colitis-associated colon cancer (CAC) and the underlying molecular mechanisms. We established an azoxymethane (AOM)/DSS-induced CAC murine model for in vivo studies and used a conditioned media (CM) culture system in vitro. H&E staining, immunohistochemistry, western blot assay, enzyme-linked immunosorbent assay, molecular docking, co-immunoprecipitation, and immunofluorescence assay were utilized to investigate how RA prevented colorectal cancer. In the AOM/DSS-induced CAC murine model, RA significantly reduced colitis severity, inflammation-related protein expression, tumor incidence, and colorectal adenoma development. It significantly modulated toll-like receptor-4 (TLR4)-mediated nuclear factor-kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) activation, thus attenuating the expression of anti-apoptotic factors, which mediate transcription factor-dependent tumor growth. In vitro, RA inhibited CM-induced TLR4 overexpression and competitively inhibited TLR4-myeloid differentiation factor 2 complex in an inflammatory microenvironment. Thus, RA suppressed NF-κB and STAT3 activation in colon cancer cells in an inflammatory microenvironment. Therefore, RA suppressed colitis-associated tumorigenesis in the AOM/DSS-induced CAC murine model and abrogated human colon cancer progression in an inflammatory microenvironment by propitiating TLR4-mediated NF-κB and STAT3 activation, pleiotropically. |
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| AbstractList | Previously, we found that rosmarinic acid (RA) exerted anti-inflammatory activities in a dextran sulfate sodium (DSS)-induced colitis model. Here, we investigated the anti-tumor effects of RA on colitis-associated colon cancer (CAC) and the underlying molecular mechanisms. We established an azoxymethane (AOM)/DSS-induced CAC murine model for in vivo studies and used a conditioned media (CM) culture system in vitro. H&E staining, immunohistochemistry, western blot assay, enzyme-linked immunosorbent assay, molecular docking, co-immunoprecipitation, and immunofluorescence assay were utilized to investigate how RA prevented colorectal cancer. In the AOM/DSS-induced CAC murine model, RA significantly reduced colitis severity, inflammation-related protein expression, tumor incidence, and colorectal adenoma development. It significantly modulated toll-like receptor-4 (TLR4)-mediated nuclear factor-kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) activation, thus attenuating the expression of anti-apoptotic factors, which mediate transcription factor-dependent tumor growth. In vitro, RA inhibited CM-induced TLR4 overexpression and competitively inhibited TLR4-myeloid differentiation factor 2 complex in an inflammatory microenvironment. Thus, RA suppressed NF-κB and STAT3 activation in colon cancer cells in an inflammatory microenvironment. Therefore, RA suppressed colitis-associated tumorigenesis in the AOM/DSS-induced CAC murine model and abrogated human colon cancer progression in an inflammatory microenvironment by propitiating TLR4-mediated NF-κB and STAT3 activation, pleiotropically. Previously, we found that rosmarinic acid (RA) exerted anti-inflammatory activities in a dextran sulfate sodium (DSS)-induced colitis model. Here, we investigated the anti-tumor effects of RA on colitis-associated colon cancer (CAC) and the underlying molecular mechanisms. We established an azoxymethane (AOM)/DSS-induced CAC murine model for in vivo studies and used a conditioned media (CM) culture system in vitro. H&E staining, immunohistochemistry, western blot assay, enzyme-linked immunosorbent assay, molecular docking, co-immunoprecipitation, and immunofluorescence assay were utilized to investigate how RA prevented colorectal cancer. In the AOM/DSS-induced CAC murine model, RA significantly reduced colitis severity, inflammation-related protein expression, tumor incidence, and colorectal adenoma development. It significantly modulated toll-like receptor-4 (TLR4)-mediated nuclear factor-kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) activation, thus attenuating the expression of anti-apoptotic factors, which mediate transcription factor-dependent tumor growth. In vitro, RA inhibited CM-induced TLR4 overexpression and competitively inhibited TLR4-myeloid differentiation factor 2 complex in an inflammatory microenvironment. Thus, RA suppressed NF-κB and STAT3 activation in colon cancer cells in an inflammatory microenvironment. Therefore, RA suppressed colitis-associated tumorigenesis in the AOM/DSS-induced CAC murine model and abrogated human colon cancer progression in an inflammatory microenvironment by propitiating TLR4-mediated NF-κB and STAT3 activation, pleiotropically.Previously, we found that rosmarinic acid (RA) exerted anti-inflammatory activities in a dextran sulfate sodium (DSS)-induced colitis model. Here, we investigated the anti-tumor effects of RA on colitis-associated colon cancer (CAC) and the underlying molecular mechanisms. We established an azoxymethane (AOM)/DSS-induced CAC murine model for in vivo studies and used a conditioned media (CM) culture system in vitro. H&E staining, immunohistochemistry, western blot assay, enzyme-linked immunosorbent assay, molecular docking, co-immunoprecipitation, and immunofluorescence assay were utilized to investigate how RA prevented colorectal cancer. In the AOM/DSS-induced CAC murine model, RA significantly reduced colitis severity, inflammation-related protein expression, tumor incidence, and colorectal adenoma development. It significantly modulated toll-like receptor-4 (TLR4)-mediated nuclear factor-kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) activation, thus attenuating the expression of anti-apoptotic factors, which mediate transcription factor-dependent tumor growth. In vitro, RA inhibited CM-induced TLR4 overexpression and competitively inhibited TLR4-myeloid differentiation factor 2 complex in an inflammatory microenvironment. Thus, RA suppressed NF-κB and STAT3 activation in colon cancer cells in an inflammatory microenvironment. Therefore, RA suppressed colitis-associated tumorigenesis in the AOM/DSS-induced CAC murine model and abrogated human colon cancer progression in an inflammatory microenvironment by propitiating TLR4-mediated NF-κB and STAT3 activation, pleiotropically. |
| Author | Hwang, Soonjae Lee, Minho Chung, Kyung-Sook Hwang, Sam Noh An, Hyo-Jin Jin, Bo-Ram Rhee, Ki-Jong |
| Author_xml | – sequence: 1 givenname: Bo-Ram surname: Jin fullname: Jin, Bo-Ram organization: Department of Pharmacology, College of Korean Medicine, Sangji University, Wonju-si, Gangwon-do, Korea – sequence: 2 givenname: Kyung-Sook surname: Chung fullname: Chung, Kyung-Sook organization: Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung Hee University, Seoul, Republic of Korea – sequence: 3 givenname: Soonjae surname: Hwang fullname: Hwang, Soonjae organization: Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University at Wonju, Wonju-si, Gangwon-do, Republic of Korea – sequence: 4 givenname: Sam Noh surname: Hwang fullname: Hwang, Sam Noh organization: Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University at Wonju, Wonju-si, Gangwon-do, Republic of Korea – sequence: 5 givenname: Ki-Jong surname: Rhee fullname: Rhee, Ki-Jong organization: Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University at Wonju, Wonju-si, Gangwon-do, Republic of Korea – sequence: 6 givenname: Minho orcidid: 0000-0002-0168-9546 surname: Lee fullname: Lee, Minho email: MinhoLee@dgu.edu organization: Department of Life Science, Dongguk University-Seoul, Goyang-si, Gyeonggi-do, Republic of Korea – sequence: 7 givenname: Hyo-Jin orcidid: 0000-0002-2937-874X surname: An fullname: An, Hyo-Jin email: sangjipharm@gmail.com organization: Department of Pharmacology, College of Korean Medicine, Sangji University, Wonju-si, Gangwon-do, Korea |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34077834$$D View this record in MEDLINE/PubMed |
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| Keywords | CAC Rosmarinic acid (RA) DSS IHC CPT STAT3 Myeloid differentiation factor 2 (MD-2) IBD Toll-like receptor-4 (TLR4) UC Colitis-associated colon cancer (CAC) RA Signal transducer and activator of transcription 3 (STAT3) NF-κB CRC Nuclear factor-kappa B (NF-κB) TLR4 AOM |
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| SubjectTerms | Animals Biomarkers Cell Line, Tumor Cinnamates - chemistry Cinnamates - pharmacology Colitis-associated colon cancer (CAC) Colitis-Associated Neoplasms - drug therapy Colitis-Associated Neoplasms - etiology Colitis-Associated Neoplasms - metabolism Colitis-Associated Neoplasms - pathology Colonic Neoplasms - drug therapy Colonic Neoplasms - etiology Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Depsides - chemistry Depsides - pharmacology Disease Models, Animal Humans Immunohistochemistry Male Mice Models, Molecular Myeloid differentiation factor 2 (MD-2) NF-kappa B - metabolism Nuclear factor-kappa B (NF-κB) Original Research Rosmarinic Acid Rosmarinic acid (RA) Signal transducer and activator of transcription 3 (STAT3) Signal Transduction - drug effects STAT3 Transcription Factor - metabolism Structure-Activity Relationship Toll-Like Receptor 4 - metabolism Toll-like receptor-4 (TLR4) Xenograft Model Antitumor Assays |
| Title | Rosmarinic acid represses colitis-associated colon cancer: A pivotal involvement of the TLR4-mediated NF-κB-STAT3 axis |
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