microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway
Abstract Objectives Nasopharyngeal carcinoma (NPC) is a type of nasopharyngeal disease with high metastasis and invasion properties. Tumor-associated alternative activated (M2) macrophages are evidenced to connect with NPC. Based on this, this study purposes to explore the mechanism and participatio...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
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SpringerOpen
2020-10-01
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| Series: | Nanoscale Research Letters |
| Subjects: | |
| Online Access: | http://link.springer.com/article/10.1186/s11671-020-03416-8 |
| _version_ | 1797761762676703232 |
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| author | Ya Peng Xiangsheng Li Huowang Liu Xiaowen Deng Chang She Chenxi Liu Xinxing Wang An Liu |
| author_facet | Ya Peng Xiangsheng Li Huowang Liu Xiaowen Deng Chang She Chenxi Liu Xinxing Wang An Liu |
| author_sort | Ya Peng |
| collection | DOAJ |
| description | Abstract Objectives Nasopharyngeal carcinoma (NPC) is a type of nasopharyngeal disease with high metastasis and invasion properties. Tumor-associated alternative activated (M2) macrophages are evidenced to connect with NPC. Based on this, this study purposes to explore the mechanism and participation of microRNA-18a (miR-18a) from M2 macrophages in NPC. Methods Peripheral blood mononuclear cells were differentiated to macrophages and macrophages were polarized to M2 type by interleukin-4. SUNE-1 and CNE2 cells were transfected with restored or depleted miR-18a or transforming growth factor-beta III receptor (TGFBR3) to explore their roles in NPC progression with the involvement of the TGF-β signaling pathway. Next, SUNE-1 and CNE2 cells were co-cultured with M2 macrophages that had been treated with restored or depleted miR-18a or TGFBR3 to comprehend their combined roles in NPC with the involvement of the TGF-β signaling pathway. Results MiR-18a was highly expressed and TGFBR3 was lowly expressed in NPC cells. MiR-18a restoration, TGFBR3 knockdown or co-culture with miR-18a mimics, or si-TGFBR3-transfected M2 macrophages promoted SUNE-1 cell progression, tumor growth in mice, decreased p-Smad1/t-Smad1, and elevated p-Smad3/t-Smad3. miR-18a downregulation, TGFBR3 overexpression, or co-culture with miR-18a inhibitors or OE-TGFBR3-transfected M2 macrophages depressed CNE2 cell progression, tumor growth in mice, increased p-Smad1/t-Smad1, and decreased p-Smad3/t-Smad3. Conclusion Our study elucidates that miR-18a from M2 macrophages results in promoted NPC cell progression and tumor growth in nude mice via TGFBR3 repression, along with the Smad1 inactivation and Smad3 activation. |
| first_indexed | 2024-03-12T19:18:34Z |
| format | Article |
| id | doaj.art-2e264318d3c44facacf77f5bc38bb4b1 |
| institution | Directory Open Access Journal |
| issn | 1556-276X |
| language | English |
| last_indexed | 2024-03-12T19:18:34Z |
| publishDate | 2020-10-01 |
| publisher | SpringerOpen |
| record_format | Article |
| series | Nanoscale Research Letters |
| spelling | doaj.art-2e264318d3c44facacf77f5bc38bb4b12023-08-02T05:22:07ZengSpringerOpenNanoscale Research Letters1556-276X2020-10-0115111710.1186/s11671-020-03416-8microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling PathwayYa Peng0Xiangsheng Li1Huowang Liu2Xiaowen Deng3Chang She4Chenxi Liu5Xinxing Wang6An Liu7Department of Otolaryngology Head and Neck Surgery, Affiliated Changsha Hospital of Hunan Normal University, The Fourth Hospital of ChangshaDepartment of Otolaryngology Head and Neck Surgery, Affiliated Changsha Hospital of Hunan Normal University, The Fourth Hospital of ChangshaDepartment of Otolaryngology Head and Neck Surgery, Third Xiangya Hospital, Central South UniversityDepartment of Otolaryngology Head and Neck Surgery, Affiliated Changsha Hospital of Hunan Normal University, The Fourth Hospital of Changsha5th Department of Cardiology, Hunan Provincial People’s Hospital, The First Affiliated Hospital of Hunan Normal UniversityThird Xiangya Hospital, Central South UniversityThird Xiangya Hospital, Central South UniversityDepartment of Otolaryngology Head and Neck Surgery, Third Xiangya Hospital, Central South UniversityAbstract Objectives Nasopharyngeal carcinoma (NPC) is a type of nasopharyngeal disease with high metastasis and invasion properties. Tumor-associated alternative activated (M2) macrophages are evidenced to connect with NPC. Based on this, this study purposes to explore the mechanism and participation of microRNA-18a (miR-18a) from M2 macrophages in NPC. Methods Peripheral blood mononuclear cells were differentiated to macrophages and macrophages were polarized to M2 type by interleukin-4. SUNE-1 and CNE2 cells were transfected with restored or depleted miR-18a or transforming growth factor-beta III receptor (TGFBR3) to explore their roles in NPC progression with the involvement of the TGF-β signaling pathway. Next, SUNE-1 and CNE2 cells were co-cultured with M2 macrophages that had been treated with restored or depleted miR-18a or TGFBR3 to comprehend their combined roles in NPC with the involvement of the TGF-β signaling pathway. Results MiR-18a was highly expressed and TGFBR3 was lowly expressed in NPC cells. MiR-18a restoration, TGFBR3 knockdown or co-culture with miR-18a mimics, or si-TGFBR3-transfected M2 macrophages promoted SUNE-1 cell progression, tumor growth in mice, decreased p-Smad1/t-Smad1, and elevated p-Smad3/t-Smad3. miR-18a downregulation, TGFBR3 overexpression, or co-culture with miR-18a inhibitors or OE-TGFBR3-transfected M2 macrophages depressed CNE2 cell progression, tumor growth in mice, increased p-Smad1/t-Smad1, and decreased p-Smad3/t-Smad3. Conclusion Our study elucidates that miR-18a from M2 macrophages results in promoted NPC cell progression and tumor growth in nude mice via TGFBR3 repression, along with the Smad1 inactivation and Smad3 activation.http://link.springer.com/article/10.1186/s11671-020-03416-8Nasopharyngeal carcinomaM2 macrophagesMicroRNA-18aTransforming growth factor-beta III receptorTransforming growth factor signaling pathwayViability |
| spellingShingle | Ya Peng Xiangsheng Li Huowang Liu Xiaowen Deng Chang She Chenxi Liu Xinxing Wang An Liu microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway Nanoscale Research Letters Nasopharyngeal carcinoma M2 macrophages MicroRNA-18a Transforming growth factor-beta III receptor Transforming growth factor signaling pathway Viability |
| title | microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway |
| title_full | microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway |
| title_fullStr | microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway |
| title_full_unstemmed | microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway |
| title_short | microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway |
| title_sort | microrna 18a from m2 macrophages inhibits tgfbr3 to promote nasopharyngeal carcinoma progression and tumor growth via tgf β signaling pathway |
| topic | Nasopharyngeal carcinoma M2 macrophages MicroRNA-18a Transforming growth factor-beta III receptor Transforming growth factor signaling pathway Viability |
| url | http://link.springer.com/article/10.1186/s11671-020-03416-8 |
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