MiR-155 promotes anaplastic thyroid cancer progression by directly targeting SOCS1
Abstract Background Anaplastic thyroid cancer (ATC) is considered to be a rare type of thyroid cancer but takes up the most important proportion of thyroid cancer-related deaths. Therefore, the development of molecular targeted therapy is an exciting strategy in the management of ATC. Methods miR-15...
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| Format: | Article |
| Language: | English |
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BMC
2019-11-01
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| Series: | BMC Cancer |
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| Online Access: | http://link.springer.com/article/10.1186/s12885-019-6319-4 |
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| author | Wei Zhang Wenyue Ji Xudong Zhao |
| author_facet | Wei Zhang Wenyue Ji Xudong Zhao |
| author_sort | Wei Zhang |
| collection | DOAJ |
| description | Abstract Background Anaplastic thyroid cancer (ATC) is considered to be a rare type of thyroid cancer but takes up the most important proportion of thyroid cancer-related deaths. Therefore, the development of molecular targeted therapy is an exciting strategy in the management of ATC. Methods miR-155 and SOCS1 expression were measured by qRT-PCR as well as western blot analysis. 8305c and FRO cells were transfected and cultured for apoptosis assays, transwell, MTT on miR-155 or SOCS1 suppression and overexpression. Dual-luciferase reporter assays and SOCS1 restoration experimentswas implemented for define the relation between SOCS1 and miR-155. In addition, the correlation between miR-155 expression and patients’ clinicopathological features were also explored. Results Aberrant miR-155 and SOCS1 expression and inverse correlation were found in ATC samples. In addition, it indicated that miR-155 expression correlated with cervical metastasis as well as extrathyroidal invasion. Moreover, we demonstrated that miR-155 inhibited 8305c and FRO cells apoptosis, promoted proliferation, invasion and migration. Furthermore, miR-155 inhibition was associated with a significant overexpression of SOCS1. Additionally, luciferase reporter assays presented that miR-155 could bind to SOCS1 3′-UTR, influencing its stability negatively and finally lowering SOCS1 levels. Moreover, it was illustrated that the impacts of miR-155 suppression were reversed by the inhibition of SOCS1 on cell proliferation, apoptosis as well as invasion. Conclusions Aberrant miR-155/SOCS1 expression has been included in ATC progression: miR-155 overexpression leads to SOCS1 suppression and develops ATC progression. Thus, miR-155 has been considered to be an underlying therapeutic target for ATC. |
| first_indexed | 2024-12-12T09:05:13Z |
| format | Article |
| id | doaj.art-1bbb7a16daa44e2bbcd874a28749d399 |
| institution | Directory Open Access Journal |
| issn | 1471-2407 |
| language | English |
| last_indexed | 2024-12-12T09:05:13Z |
| publishDate | 2019-11-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Cancer |
| spelling | doaj.art-1bbb7a16daa44e2bbcd874a28749d3992022-12-22T00:29:41ZengBMCBMC Cancer1471-24072019-11-0119111110.1186/s12885-019-6319-4MiR-155 promotes anaplastic thyroid cancer progression by directly targeting SOCS1Wei Zhang0Wenyue Ji1Xudong Zhao2Department of Endocrinology, Shengjing Hospital, China Medical UniversityDepartment of Otorhinolaryngology Shengjing Hospital, China Medical UniversityDepartment of Otorhinolaryngology Shengjing Hospital, China Medical UniversityAbstract Background Anaplastic thyroid cancer (ATC) is considered to be a rare type of thyroid cancer but takes up the most important proportion of thyroid cancer-related deaths. Therefore, the development of molecular targeted therapy is an exciting strategy in the management of ATC. Methods miR-155 and SOCS1 expression were measured by qRT-PCR as well as western blot analysis. 8305c and FRO cells were transfected and cultured for apoptosis assays, transwell, MTT on miR-155 or SOCS1 suppression and overexpression. Dual-luciferase reporter assays and SOCS1 restoration experimentswas implemented for define the relation between SOCS1 and miR-155. In addition, the correlation between miR-155 expression and patients’ clinicopathological features were also explored. Results Aberrant miR-155 and SOCS1 expression and inverse correlation were found in ATC samples. In addition, it indicated that miR-155 expression correlated with cervical metastasis as well as extrathyroidal invasion. Moreover, we demonstrated that miR-155 inhibited 8305c and FRO cells apoptosis, promoted proliferation, invasion and migration. Furthermore, miR-155 inhibition was associated with a significant overexpression of SOCS1. Additionally, luciferase reporter assays presented that miR-155 could bind to SOCS1 3′-UTR, influencing its stability negatively and finally lowering SOCS1 levels. Moreover, it was illustrated that the impacts of miR-155 suppression were reversed by the inhibition of SOCS1 on cell proliferation, apoptosis as well as invasion. Conclusions Aberrant miR-155/SOCS1 expression has been included in ATC progression: miR-155 overexpression leads to SOCS1 suppression and develops ATC progression. Thus, miR-155 has been considered to be an underlying therapeutic target for ATC.http://link.springer.com/article/10.1186/s12885-019-6319-4miR-155SOCS1Anaplastic thyroid cancerATC |
| spellingShingle | Wei Zhang Wenyue Ji Xudong Zhao MiR-155 promotes anaplastic thyroid cancer progression by directly targeting SOCS1 BMC Cancer miR-155 SOCS1 Anaplastic thyroid cancer ATC |
| title | MiR-155 promotes anaplastic thyroid cancer progression by directly targeting SOCS1 |
| title_full | MiR-155 promotes anaplastic thyroid cancer progression by directly targeting SOCS1 |
| title_fullStr | MiR-155 promotes anaplastic thyroid cancer progression by directly targeting SOCS1 |
| title_full_unstemmed | MiR-155 promotes anaplastic thyroid cancer progression by directly targeting SOCS1 |
| title_short | MiR-155 promotes anaplastic thyroid cancer progression by directly targeting SOCS1 |
| title_sort | mir 155 promotes anaplastic thyroid cancer progression by directly targeting socs1 |
| topic | miR-155 SOCS1 Anaplastic thyroid cancer ATC |
| url | http://link.springer.com/article/10.1186/s12885-019-6319-4 |
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