LINC00844 promotes proliferation and migration of hepatocellular carcinoma by regulating NDRG1 expression
Background Aberrant expression of long noncoding RNAs are implicated in the pathogenesis of human malignancies. LINC00844 expression is dramatically downregulated in prostate cancer, and functional studies have revealed the association between the aberrant expression of LINC00844 and prostate cancer...
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PeerJ Inc.
2020-01-01
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| author | Wei Zhou Kang Huang Qiuyan Zhang Shaojun Ye Zibiao Zhong Cheng Zeng Guizhu Peng Ling Li Qifa Ye |
| author_facet | Wei Zhou Kang Huang Qiuyan Zhang Shaojun Ye Zibiao Zhong Cheng Zeng Guizhu Peng Ling Li Qifa Ye |
| author_sort | Wei Zhou |
| collection | DOAJ |
| description | Background Aberrant expression of long noncoding RNAs are implicated in the pathogenesis of human malignancies. LINC00844 expression is dramatically downregulated in prostate cancer, and functional studies have revealed the association between the aberrant expression of LINC00844 and prostate cancer cell invasion and metastasis. However, the function and mechanism of action of LINC00844 in the pathogenesis of hepatocellular carcinoma (HCC) are poorly understood. Methods LINC00844 and N-Myc downstream-regulated 1 (NDRG1) expression in HCC tissues and cell lines was detected with real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. Correlations between LINC00844 expression level and clinicopathological features were investigated using the original data from The Cancer Genome Atlas (TCGA) database. HepG2 and HCCLM9 cell lines were transfected with Lv-LIN00844 virus to obtain LINC00844-overexpressing cell lines. Cell proliferation and cell invasion and migration were examined with the cell counting kit-8 (CCK-8) and transwell assay, respectively. Furthermore, the correlation between LINC00844 and NDRG1 expression was analysed using Pearson’s correlation analysis. Results LINC00844 expression was significantly downregulatedin HCC tissues and cell lines, and a statistical correlation was detected between low LINC00844 expression and sex (Female), advanced American Joint Committee on Cancer (AJCC) stage (III + IV), histological grade (G3 + G4), and vascular invasion (Micro and Macro). In vitro experiments showed that LINC00844 overexpression significantly repressed the proliferation, migration, and invasion of HCC cells. NDRG1 expression was higher in HCC tissues and LINC00844 could partly inhibit the expression of NDRG1. |
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| last_indexed | 2024-03-09T08:01:51Z |
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| spelling | doaj.art-ac27ebc937b64822b2b6977759fbc3ef2023-12-03T00:41:31ZengPeerJ Inc.PeerJ2167-83592020-01-018e839410.7717/peerj.8394LINC00844 promotes proliferation and migration of hepatocellular carcinoma by regulating NDRG1 expressionWei Zhou0Kang Huang1Qiuyan Zhang2Shaojun Ye3Zibiao Zhong4Cheng Zeng5Guizhu Peng6Ling Li7Qifa Ye8Zhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, ChinaZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, ChinaZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, ChinaZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, ChinaZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, ChinaZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, ChinaZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, ChinaZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, ChinaZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, ChinaBackground Aberrant expression of long noncoding RNAs are implicated in the pathogenesis of human malignancies. LINC00844 expression is dramatically downregulated in prostate cancer, and functional studies have revealed the association between the aberrant expression of LINC00844 and prostate cancer cell invasion and metastasis. However, the function and mechanism of action of LINC00844 in the pathogenesis of hepatocellular carcinoma (HCC) are poorly understood. Methods LINC00844 and N-Myc downstream-regulated 1 (NDRG1) expression in HCC tissues and cell lines was detected with real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. Correlations between LINC00844 expression level and clinicopathological features were investigated using the original data from The Cancer Genome Atlas (TCGA) database. HepG2 and HCCLM9 cell lines were transfected with Lv-LIN00844 virus to obtain LINC00844-overexpressing cell lines. Cell proliferation and cell invasion and migration were examined with the cell counting kit-8 (CCK-8) and transwell assay, respectively. Furthermore, the correlation between LINC00844 and NDRG1 expression was analysed using Pearson’s correlation analysis. Results LINC00844 expression was significantly downregulatedin HCC tissues and cell lines, and a statistical correlation was detected between low LINC00844 expression and sex (Female), advanced American Joint Committee on Cancer (AJCC) stage (III + IV), histological grade (G3 + G4), and vascular invasion (Micro and Macro). In vitro experiments showed that LINC00844 overexpression significantly repressed the proliferation, migration, and invasion of HCC cells. NDRG1 expression was higher in HCC tissues and LINC00844 could partly inhibit the expression of NDRG1.https://peerj.com/articles/8394.pdfHepatocellular carcinomaLINC00844NDRG1ProliferationMigrationInvasion |
| spellingShingle | Wei Zhou Kang Huang Qiuyan Zhang Shaojun Ye Zibiao Zhong Cheng Zeng Guizhu Peng Ling Li Qifa Ye LINC00844 promotes proliferation and migration of hepatocellular carcinoma by regulating NDRG1 expression PeerJ Hepatocellular carcinoma LINC00844 NDRG1 Proliferation Migration Invasion |
| title | LINC00844 promotes proliferation and migration of hepatocellular carcinoma by regulating NDRG1 expression |
| title_full | LINC00844 promotes proliferation and migration of hepatocellular carcinoma by regulating NDRG1 expression |
| title_fullStr | LINC00844 promotes proliferation and migration of hepatocellular carcinoma by regulating NDRG1 expression |
| title_full_unstemmed | LINC00844 promotes proliferation and migration of hepatocellular carcinoma by regulating NDRG1 expression |
| title_short | LINC00844 promotes proliferation and migration of hepatocellular carcinoma by regulating NDRG1 expression |
| title_sort | linc00844 promotes proliferation and migration of hepatocellular carcinoma by regulating ndrg1 expression |
| topic | Hepatocellular carcinoma LINC00844 NDRG1 Proliferation Migration Invasion |
| url | https://peerj.com/articles/8394.pdf |
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