Targeting crosstalk of STAT3 between tumor-associated M2 macrophages and Tregs in colorectal cancer
A comprehensive analysis of the molecular mechanism underlying colorectal tumor evaluated the development of colorectal cancer (CRC) and proposed targeting small molecular inhibitors. Nonetheless, the adoptive resistance of these therapies remains a challenge with respect to achieving an effective c...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Taylor & Francis Group
2023-12-01
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| Series: | Cancer Biology & Therapy |
| Subjects: | |
| Online Access: | http://dx.doi.org/10.1080/15384047.2023.2226418 |
| _version_ | 1797404078482915328 |
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| author | Lili Huang Yu Zhao Mengying Shan Sitong Wang Jianhua Chen Zhuqing Liu Qing Xu |
| author_facet | Lili Huang Yu Zhao Mengying Shan Sitong Wang Jianhua Chen Zhuqing Liu Qing Xu |
| author_sort | Lili Huang |
| collection | DOAJ |
| description | A comprehensive analysis of the molecular mechanism underlying colorectal tumor evaluated the development of colorectal cancer (CRC) and proposed targeting small molecular inhibitors. Nonetheless, the adoptive resistance of these therapies remains a challenge with respect to achieving an effective clinical response. Thus, identifying the molecular mechanisms guiding CRC growth is essential. The results of The Cancer Genome Atlas (TCGA) dataset analysis demonstrated a critical role of signal transducer and activator of transcription 3 (STAT3) pathway in tumor immune suppression via modulation of the recruitment of Treg cells and M2 type tumor-associated macrophages. The in vivo experiments elucidate that targeting STAT3 pathways markedly reduce the proportions of TAMs and Tregs by inhibiting tumor progression. These findings revealed crosstalk between Treg cells and M2 macrophages, proving a potential therapeutic strategy for CRC therapy. Combinatorial treatment with STAT3 inhibitor and programmed death 1 (PD-1) antibody therapy effectively prevents CRC tumor growth in a mouse model with high anti-tumor immunity. In summary, targeting STAT3 disrupts the interaction between Treg cells and M2 macrophages and improves the anti-tumor response in CRC, thereby offering a promising strategy to treat patients with CRC. |
| first_indexed | 2024-03-09T02:47:47Z |
| format | Article |
| id | doaj.art-d58254adc57c4f3e951698bb48159354 |
| institution | Directory Open Access Journal |
| issn | 1538-4047 1555-8576 |
| language | English |
| last_indexed | 2024-03-09T02:47:47Z |
| publishDate | 2023-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Cancer Biology & Therapy |
| spelling | doaj.art-d58254adc57c4f3e951698bb481593542023-12-05T15:58:14ZengTaylor & Francis GroupCancer Biology & Therapy1538-40471555-85762023-12-0124110.1080/15384047.2023.22264182226418Targeting crosstalk of STAT3 between tumor-associated M2 macrophages and Tregs in colorectal cancerLili Huang0Yu Zhao1Mengying Shan2Sitong Wang3Jianhua Chen4Zhuqing Liu5Qing Xu6Tongji University School of MedicineTongji University School of MedicineTongji University School of MedicineTongji University School of MedicineTongji University School of MedicineTongji University School of MedicineTongji University School of MedicineA comprehensive analysis of the molecular mechanism underlying colorectal tumor evaluated the development of colorectal cancer (CRC) and proposed targeting small molecular inhibitors. Nonetheless, the adoptive resistance of these therapies remains a challenge with respect to achieving an effective clinical response. Thus, identifying the molecular mechanisms guiding CRC growth is essential. The results of The Cancer Genome Atlas (TCGA) dataset analysis demonstrated a critical role of signal transducer and activator of transcription 3 (STAT3) pathway in tumor immune suppression via modulation of the recruitment of Treg cells and M2 type tumor-associated macrophages. The in vivo experiments elucidate that targeting STAT3 pathways markedly reduce the proportions of TAMs and Tregs by inhibiting tumor progression. These findings revealed crosstalk between Treg cells and M2 macrophages, proving a potential therapeutic strategy for CRC therapy. Combinatorial treatment with STAT3 inhibitor and programmed death 1 (PD-1) antibody therapy effectively prevents CRC tumor growth in a mouse model with high anti-tumor immunity. In summary, targeting STAT3 disrupts the interaction between Treg cells and M2 macrophages and improves the anti-tumor response in CRC, thereby offering a promising strategy to treat patients with CRC.http://dx.doi.org/10.1080/15384047.2023.2226418tregsm2 macrophagescrosstalkstat3crc |
| spellingShingle | Lili Huang Yu Zhao Mengying Shan Sitong Wang Jianhua Chen Zhuqing Liu Qing Xu Targeting crosstalk of STAT3 between tumor-associated M2 macrophages and Tregs in colorectal cancer Cancer Biology & Therapy tregs m2 macrophages crosstalk stat3 crc |
| title | Targeting crosstalk of STAT3 between tumor-associated M2 macrophages and Tregs in colorectal cancer |
| title_full | Targeting crosstalk of STAT3 between tumor-associated M2 macrophages and Tregs in colorectal cancer |
| title_fullStr | Targeting crosstalk of STAT3 between tumor-associated M2 macrophages and Tregs in colorectal cancer |
| title_full_unstemmed | Targeting crosstalk of STAT3 between tumor-associated M2 macrophages and Tregs in colorectal cancer |
| title_short | Targeting crosstalk of STAT3 between tumor-associated M2 macrophages and Tregs in colorectal cancer |
| title_sort | targeting crosstalk of stat3 between tumor associated m2 macrophages and tregs in colorectal cancer |
| topic | tregs m2 macrophages crosstalk stat3 crc |
| url | http://dx.doi.org/10.1080/15384047.2023.2226418 |
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