LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cells
Abstract Background The long non-coding RNAs (lncRNAs) have participated in the promotion of hepatocellular carcinoma (HCC) initiation and progression. Nevertheless, the biological role and underlying mechanism of LINC01287 in HCC has never been reported. Methods The TGCA database was used to explor...
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| Format: | Article |
| Language: | English |
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BMC
2018-07-01
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| Series: | Journal of Experimental & Clinical Cancer Research |
| Subjects: | |
| Online Access: | http://link.springer.com/article/10.1186/s13046-018-0831-2 |
| _version_ | 1811282843067744256 |
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| author | Yichao Mo Longguang He Zeru Lai Zhiheng Wan Qinshou Chen Sibo Pan Liangfu Li Dasheng Li Junwei Huang Fan Xue Siyao Che |
| author_facet | Yichao Mo Longguang He Zeru Lai Zhiheng Wan Qinshou Chen Sibo Pan Liangfu Li Dasheng Li Junwei Huang Fan Xue Siyao Che |
| author_sort | Yichao Mo |
| collection | DOAJ |
| description | Abstract Background The long non-coding RNAs (lncRNAs) have participated in the promotion of hepatocellular carcinoma (HCC) initiation and progression. Nevertheless, the biological role and underlying mechanism of LINC01287 in HCC has never been reported. Methods The TGCA database was used to explore the abnormal expression of lncRNAs in HCC. Real-time PCR and in situ hybridization assays were used to examine the expression of LINC01287 in HCC tissues. The clinicopathological characteristics of HCC patients in relation to LINC01287 expression were then analyzed. Infection of cells with the si-LINC01287 lentiviral vector was performed to down-regulate LINC01287 expression in HCC cells. MTT and colony formation assays were performed to examine cell growth ability, and FACS analysis was performed to examine the cell cycle and apoptosis. A Boyden assay was used to examine HCC cell invasion ability, and RNA immunoprecipitation tested the interaction between LINC01287 and miR-298. A luciferase reporter assay was used to examine whether STAT3 was a direct target of miR-298, and chromatin immunoprecipitation (ChIP) was used to examine the potential binding of c-jun to the miR-298 promoter. Results We revealed that the expression of LINC01287 was increased in HCC cell lines, as well as tissues. Knockdown of LINC01287 decreased HCC cell growth and invasion both in vitro and in vivo. LINC01287 can negatively regulate miR-298 expression by acting as a ceRNA. miR-298 directly targeted STAT3 and inhibited its expression. LINC01287 exerted its function via the miR-298/STAT3 axis in HCC. Interestingly, STAT3 elevated LINC01287 expression via c-jun, which bound to the LINC01287 promoter. A feedback loop was also discovered between LINC01287 and the miR-298/STAT3 axis. Conclusions Our data indicated that LINC01287 played an oncogenic role in HCC growth and metastasis and that this lncRNA might serve as a novel molecular target for the treatment of HCC. |
| first_indexed | 2024-04-13T01:59:49Z |
| format | Article |
| id | doaj.art-cacdec81bbb6485f8a741634a17f8a5a |
| institution | Directory Open Access Journal |
| issn | 1756-9966 |
| language | English |
| last_indexed | 2024-04-13T01:59:49Z |
| publishDate | 2018-07-01 |
| publisher | BMC |
| record_format | Article |
| series | Journal of Experimental & Clinical Cancer Research |
| spelling | doaj.art-cacdec81bbb6485f8a741634a17f8a5a2022-12-22T03:07:40ZengBMCJournal of Experimental & Clinical Cancer Research1756-99662018-07-0137111210.1186/s13046-018-0831-2LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cellsYichao Mo0Longguang He1Zeru Lai2Zhiheng Wan3Qinshou Chen4Sibo Pan5Liangfu Li6Dasheng Li7Junwei Huang8Fan Xue9Siyao Che10Department of Hepatobiliary Surgery, Gaozhou People’s HospitalDepartment of Hepatobiliary Surgery, Gaozhou People’s HospitalDepartment of Hepatobiliary Surgery, Gaozhou People’s HospitalDepartment of General Surgery, The First Affiliated Hospital of BaoTou Medical UniversityDepartment of Hepatobiliary Surgery, Gaozhou People’s HospitalDepartment of Hepatobiliary Surgery, Gaozhou People’s HospitalDepartment of Hepatobiliary Surgery, Gaozhou People’s HospitalDepartment of Hepatobiliary Surgery, Gaozhou People’s HospitalDepartment of Hepatobiliary Surgery, Gaozhou People’s HospitalDepartment of Hepatobiliary Surgery, Gaozhou People’s HospitalDepartment of Hepatobiliary Surgery, Gaozhou People’s HospitalAbstract Background The long non-coding RNAs (lncRNAs) have participated in the promotion of hepatocellular carcinoma (HCC) initiation and progression. Nevertheless, the biological role and underlying mechanism of LINC01287 in HCC has never been reported. Methods The TGCA database was used to explore the abnormal expression of lncRNAs in HCC. Real-time PCR and in situ hybridization assays were used to examine the expression of LINC01287 in HCC tissues. The clinicopathological characteristics of HCC patients in relation to LINC01287 expression were then analyzed. Infection of cells with the si-LINC01287 lentiviral vector was performed to down-regulate LINC01287 expression in HCC cells. MTT and colony formation assays were performed to examine cell growth ability, and FACS analysis was performed to examine the cell cycle and apoptosis. A Boyden assay was used to examine HCC cell invasion ability, and RNA immunoprecipitation tested the interaction between LINC01287 and miR-298. A luciferase reporter assay was used to examine whether STAT3 was a direct target of miR-298, and chromatin immunoprecipitation (ChIP) was used to examine the potential binding of c-jun to the miR-298 promoter. Results We revealed that the expression of LINC01287 was increased in HCC cell lines, as well as tissues. Knockdown of LINC01287 decreased HCC cell growth and invasion both in vitro and in vivo. LINC01287 can negatively regulate miR-298 expression by acting as a ceRNA. miR-298 directly targeted STAT3 and inhibited its expression. LINC01287 exerted its function via the miR-298/STAT3 axis in HCC. Interestingly, STAT3 elevated LINC01287 expression via c-jun, which bound to the LINC01287 promoter. A feedback loop was also discovered between LINC01287 and the miR-298/STAT3 axis. Conclusions Our data indicated that LINC01287 played an oncogenic role in HCC growth and metastasis and that this lncRNA might serve as a novel molecular target for the treatment of HCC.http://link.springer.com/article/10.1186/s13046-018-0831-2LINC01287miR-298STAT3Hepatocellular carcinoma |
| spellingShingle | Yichao Mo Longguang He Zeru Lai Zhiheng Wan Qinshou Chen Sibo Pan Liangfu Li Dasheng Li Junwei Huang Fan Xue Siyao Che LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cells Journal of Experimental & Clinical Cancer Research LINC01287 miR-298 STAT3 Hepatocellular carcinoma |
| title | LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cells |
| title_full | LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cells |
| title_fullStr | LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cells |
| title_full_unstemmed | LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cells |
| title_short | LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cells |
| title_sort | linc01287 mir 298 stat3 feedback loop regulates growth and the epithelial to mesenchymal transition phenotype in hepatocellular carcinoma cells |
| topic | LINC01287 miR-298 STAT3 Hepatocellular carcinoma |
| url | http://link.springer.com/article/10.1186/s13046-018-0831-2 |
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