Upregulation of MIAT Regulates LOXL2 Expression by Competitively Binding MiR-29c in Clear Cell Renal Cell Carcinoma
Background/Aims: MIAT is a long noncoding RNA (lncRNA) involved in cell proliferation and the development of tumor. However, the exact effects and molecular mechanisms of MIAT in clear cell renal cell carcinoma (ccRCC) progression are still unknown. Methods: We screened the lncRNAs’ profile of ccRCC...
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| Format: | Article |
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Cell Physiol Biochem Press GmbH & Co KG
2018-07-01
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| Series: | Cellular Physiology and Biochemistry |
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| Online Access: | https://www.karger.com/Article/FullText/491974 |
| _version_ | 1819056609494564864 |
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| author | Yan Qu Haibing Xiao Wen Xiao Zhiyong Xiong Wenjun Hu Yaoying Gao Zeyuan Ru Cheng Wang Lin Bao Kesan Wang Hailong Ruan Zhengshuai Song Ke Chen Xiaoping Zhang Hongmei Yang |
| author_facet | Yan Qu Haibing Xiao Wen Xiao Zhiyong Xiong Wenjun Hu Yaoying Gao Zeyuan Ru Cheng Wang Lin Bao Kesan Wang Hailong Ruan Zhengshuai Song Ke Chen Xiaoping Zhang Hongmei Yang |
| author_sort | Yan Qu |
| collection | DOAJ |
| description | Background/Aims: MIAT is a long noncoding RNA (lncRNA) involved in cell proliferation and the development of tumor. However, the exact effects and molecular mechanisms of MIAT in clear cell renal cell carcinoma (ccRCC) progression are still unknown. Methods: We screened the lncRNAs’ profile of ccRCC in The Cancer Genome Atlas database, and then examined the expression levels of lncRNA MIAT in 45 paired ccRCC tissue specimens and in cell lines by q-RT-PCR. MTS, colony formation, EdU, and Transwell assays were performed to examine the effect of MIAT on proliferation and metastasis of ccRCC. Western blot and luciferase assays were performed to determine whether MIAT can regulate Loxl2 expression by competitively binding miR-29c in ccRCC. Results: MIAT was up-regulated in ccRCC tissues and cell lines. High MIAT expression correlated with worse clinicopathological features and shorter survival rate. Functional assays showed that knockdown of MIAT inhibited renal cancer cell proliferation and metastasis in vitro and in vivo. Luciferase and western blot assays further confirmed that miR-29c binds with MIAT. Additionally, the correlation of miR-29c with MIAT and Loxl2 was further verified in patients' samples. Conclusion: Our data indicated that MIAT might be an oncogenic lncRNA that promoted proliferation and metastasis of ccRCC, and could be a potential therapeutic target in human ccRCC. |
| first_indexed | 2024-12-21T13:26:08Z |
| format | Article |
| id | doaj.art-c7fa02b5e95a4381ab2c67a8b232c9c9 |
| institution | Directory Open Access Journal |
| issn | 1015-8987 1421-9778 |
| language | English |
| last_indexed | 2024-12-21T13:26:08Z |
| publishDate | 2018-07-01 |
| publisher | Cell Physiol Biochem Press GmbH & Co KG |
| record_format | Article |
| series | Cellular Physiology and Biochemistry |
| spelling | doaj.art-c7fa02b5e95a4381ab2c67a8b232c9c92022-12-21T19:02:28ZengCell Physiol Biochem Press GmbH & Co KGCellular Physiology and Biochemistry1015-89871421-97782018-07-014831075108710.1159/000491974491974Upregulation of MIAT Regulates LOXL2 Expression by Competitively Binding MiR-29c in Clear Cell Renal Cell CarcinomaYan QuHaibing XiaoWen XiaoZhiyong XiongWenjun HuYaoying GaoZeyuan RuCheng WangLin BaoKesan WangHailong RuanZhengshuai SongKe ChenXiaoping ZhangHongmei YangBackground/Aims: MIAT is a long noncoding RNA (lncRNA) involved in cell proliferation and the development of tumor. However, the exact effects and molecular mechanisms of MIAT in clear cell renal cell carcinoma (ccRCC) progression are still unknown. Methods: We screened the lncRNAs’ profile of ccRCC in The Cancer Genome Atlas database, and then examined the expression levels of lncRNA MIAT in 45 paired ccRCC tissue specimens and in cell lines by q-RT-PCR. MTS, colony formation, EdU, and Transwell assays were performed to examine the effect of MIAT on proliferation and metastasis of ccRCC. Western blot and luciferase assays were performed to determine whether MIAT can regulate Loxl2 expression by competitively binding miR-29c in ccRCC. Results: MIAT was up-regulated in ccRCC tissues and cell lines. High MIAT expression correlated with worse clinicopathological features and shorter survival rate. Functional assays showed that knockdown of MIAT inhibited renal cancer cell proliferation and metastasis in vitro and in vivo. Luciferase and western blot assays further confirmed that miR-29c binds with MIAT. Additionally, the correlation of miR-29c with MIAT and Loxl2 was further verified in patients' samples. Conclusion: Our data indicated that MIAT might be an oncogenic lncRNA that promoted proliferation and metastasis of ccRCC, and could be a potential therapeutic target in human ccRCC.https://www.karger.com/Article/FullText/491974ccRCCCeRNAMIATMiR-29cLoxl2 |
| spellingShingle | Yan Qu Haibing Xiao Wen Xiao Zhiyong Xiong Wenjun Hu Yaoying Gao Zeyuan Ru Cheng Wang Lin Bao Kesan Wang Hailong Ruan Zhengshuai Song Ke Chen Xiaoping Zhang Hongmei Yang Upregulation of MIAT Regulates LOXL2 Expression by Competitively Binding MiR-29c in Clear Cell Renal Cell Carcinoma Cellular Physiology and Biochemistry ccRCC CeRNA MIAT MiR-29c Loxl2 |
| title | Upregulation of MIAT Regulates LOXL2 Expression by Competitively Binding MiR-29c in Clear Cell Renal Cell Carcinoma |
| title_full | Upregulation of MIAT Regulates LOXL2 Expression by Competitively Binding MiR-29c in Clear Cell Renal Cell Carcinoma |
| title_fullStr | Upregulation of MIAT Regulates LOXL2 Expression by Competitively Binding MiR-29c in Clear Cell Renal Cell Carcinoma |
| title_full_unstemmed | Upregulation of MIAT Regulates LOXL2 Expression by Competitively Binding MiR-29c in Clear Cell Renal Cell Carcinoma |
| title_short | Upregulation of MIAT Regulates LOXL2 Expression by Competitively Binding MiR-29c in Clear Cell Renal Cell Carcinoma |
| title_sort | upregulation of miat regulates loxl2 expression by competitively binding mir 29c in clear cell renal cell carcinoma |
| topic | ccRCC CeRNA MIAT MiR-29c Loxl2 |
| url | https://www.karger.com/Article/FullText/491974 |
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