MicroRNA‐342 inhibits tumor growth via targeting chemokine CXCL12 involved in macrophages recruitment/activation
| العنوان: | MicroRNA‐342 inhibits tumor growth via targeting chemokine CXCL12 involved in macrophages recruitment/activation |
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| المؤلفون: | Sayaka Matsui, Kenkichi Sugimoto, Qiong Wu, Yijun Tian, Maki Touma |
| المصدر: | Genes to Cells. 23:1009-1022 |
| بيانات النشر: | Wiley, 2018. |
| سنة النشر: | 2018 |
| مصطلحات موضوعية: | 0301 basic medicine, Chemokine, Population, Apoptosis, medicine.disease_cause, CXCR4, Mice, 03 medical and health sciences, Cell Line, Tumor, microRNA, Genetics, medicine, Animals, Macrophage, education, Cell Proliferation, education.field_of_study, Base Sequence, biology, Cell growth, Macrophages, Cell Cycle, Sarcoma, Cell Biology, Macrophage Activation, Chemokine CXCL12, MicroRNAs, 030104 developmental biology, Integrin alpha M, biology.protein, Cancer research, Carcinogenesis |
| الوصف: | MicroRNAs (miRNAs) play important roles in initiation, development, progression and metastasis of tumors. MiR-342 has been reported as a tumor suppressor or an onco-miRNA based on functions or expression changes in various types of cancers. However, the biological roles and underlying molecular mechanisms of miR-342 in tumorigenesis remain largely unknown. Here, we found that miR-342 was expressed significantly less in a murine MS-K tumor cell line that showed riched blood vessels. Over-expression of miR-342 in MS-K cells inhibited cell proliferation, colony formation, reduced frequency of S phase population in vitro and suppressed tumor growth in vivo. Moreover, increasing miR-342 impeded blood vessels formation and accumulation of macrophages (CD11b+ ) in tumors. By bioinformatic analysis and dual-luciferase reporter assays, chemokine CXCL12 was identified as a direct target of miR-342. Restored Cxcl12 expression in MS-K-miR-342 cells could rescue cell proliferation in vitro. In MS-K-miR-342 tumor-infiltrated macrophages, expression of proangiogenic genes (Vegf-A and Thbs1) and M2-subtype macrophage markers (Cd163, Dectin1 and Ym1) was significantly down-regulated compared with controls. Moreover, lower level of Cxcl12 and its receptor Cxcr4 was observed in the macrophages of MS-K-miR-342 tumors, and MS-K-miR-342 derived miR-342, but not endogenous miR-342, might contribute to Cxcl12 suppression in TAM. These results suggest that miR-342 is involved in MS-K tumor growth as a tumor suppressor by targeting chemokine CXCL12. |
| تدمد: | 1365-2443 1356-9597 |
| DOI: | 10.1111/gtc.12650 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0f2225b6bcc889882ed410480744be7f https://doi.org/10.1111/gtc.12650 |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....0f2225b6bcc889882ed410480744be7f |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 13652443 13569597 |
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| DOI: | 10.1111/gtc.12650 |