miR-124 downregulation leads to breast cancer progression via LncRNA-MALAT1 regulation and CDK4/E2F1 signal activation

Feng, Tianyu; Shao, Fang; Wu, Qiyong; Zhang, Xiaohang; Xu, Dong; Qian, Keqing; Xie, Yirui; Wang, Shizhong; Xu, Ning; Wang, Yong; Qi, Chunjian

doi:10.18632/oncotarget.7578

Cited by 102 publications

(95 citation statements)

References 39 publications

(50 reference statements)

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“…In the present study, our results indicated that MALAT1 expression was up-regulated in multiple breast cancer cell lines compared with normal breast cell line, as well as in ER-positive breast cancer tissues compared with adjacent normal breast cancer tissues. These data correlated with previous studies indicating that MALAT1 was overexpressed in primary breast cancer and promoted proliferation of breast cancer cells [27–29]. We identified for the first time that MALAT1 expression was correlated with ER and its target genes in breast cancer, providing a new perspective in MALAT1 function.…”

Section: Discussionsupporting

confidence: 90%

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Long non-coding RNA metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) interacts with estrogen receptor and predicted poor survival in breast cancer

et al. 2016

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Metastasis associated in lung adenocarcinoma transcript 1 (MALAT1), a lncRNA that was first recognized as a prognostic parameter for patient survival of stage I lung cancer, is up-regulated in multiple human malignancies, including breast cancer. However, the mechanism of its function remained elusive. In the current study, by examining MALAT1 expression on mRNA level, we demonstrated that compared with MCF10A, MALAT1 expression was up-regulated in the majority of breast cancer cell lines (9/12). In 26 pairs of estrogen receptor (ER)-positive breast cancer samples, MALAT1 expression was significantly up-regulated compared with adjacent normal tissues (P = 0.012). Furthermore, of 204 breast cancer patients, high MALAT1 expression was associated with positive ER (P = 0.023) and progesterone receptor (PR) (P = 0.024) status. Further analysis using TCGA database revealed that ER and its target genes PGR and CCND1, were overexpressed in MALAT1 altered group compared with unaltered group, both on the mRNA and protein level. Lastly, we verified MALAT1's prognostic value in breast cancer. At the cut-off value of 75%, MALAT1 was the only independent prognostic factor of recurrence-free survival (RFS) in ER-negative patients in a multivariate Cox regression model (hazard ratio [HR] = 2.83, 95% confidence interval [CI] 1.02–7.83). MALAT1 overexpression was also associated with poor RFS in tamoxifen treated ER-positive breast cancer patients, which might serve as a potential biomarker to predict endocrine treatment sensitivity.

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Section: Discussionsupporting

confidence: 90%

“…Bamodu et al identified MALAT1 as a mediator of KDM5B oncogenic potential in triple-negative breast cancer, and could be reversed by hsa-miR-448 [30]. Furthermore, MALAT1 reversed the inhibitory effect of miR-124 on breast cancer proliferation and was involved in the cyclin-dependent kinase 4 (CDK4) expression [29]. …”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) interacts with estrogen receptor and predicted poor survival in breast cancer

et al. 2016

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“…miRNAs can function as oncogenes or tumor suppressor genes in cancer, aiming at restoration of tumor suppressor genes and silence of oncogenes would be a novel anticancer therapy (23). The inhibitory effect of miR-124 in tumor growth and migration, as well as dysregulation of miR-124 has been reported in various tumor types (6)(7)(8)(9). In a previous (13) and the present study, miR-124 was downregulated in GC tissues and cell lines.…”

Section: Discussionsupporting

confidence: 57%

“…Recently, miR-124 has been found down-regulated in multiple tumor types, including cancer (6), prostate (7), lung (8) and colorectal cancer (9). It also been found that miR-124 could inhibit the proliferation of GC cells proliferation by targeting Rho-associated protein kinase 1, enhancer of zeste homolog 2 (EZH2) and sphingosine kinase 1 (SPHK1) (10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Lentivirus-mediated overexpression of miR-124 suppresses growth and invasion by targeting JAG1 and EZH2 in gastric cancer

Chen

et al. 2018

Oncol Lett

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Abstract. expression is downregulated and has a tumor suppressor role in various types of cancer. The present study revealed that genes encoding miR-124 were frequently methylated and the expression of miR-124 was downregulated in gastric cancer tissues. Stable expression of miR-124 using a lentiviral vector inhibited gastric cancer cell growth, migration and invasion in vitro. In addition, overexpression of miR-124 suppressed gastric cancer cell xenograft growth in nude mice. The expression of the Notch ligand Jagged1 (JAG1) and enhancer of zeste homolog 2 (EZH2) was downregulated upon miR-124 overexpression, and silencing of JAG1 or EZH2 by RNA interference also suppressed gastric cancer cell growth, migration and invasion. Furthermore, expression of fibronectin and vimentin, not able elements of the epithelial-mesenchymal transition, were suppressed by overexpression of miR-124 or inhibition of JAG1 or EZH2 expressions in GC. Together, these results indicated that miR-124 suppressed gastric cancer progression, partly through inhibiting JAG1 and EZH2. Thus, lentivirus-mediated overexpression of miR-124 may be a potential therapeutic strategy against gastric cancer.

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“…CDK4 is overexpression in several cancer comprising of breast cancer, pancreas cancer, clear cell renal cell carcinoma, and colorectal cancer [20–23]. Downregulation of MALAT1 (long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1) inhibits breast cancer cell proliferation and cell cycle progression in vitro and in vivo through miR-124 downregulation and CDK4 upregulation [20, 24]. Overexpression of cyclin D1/CDK4 is regulated by CEACAM6 and promotes cell proliferation in human pancreatic carcinoma [21].…”

Section: Discussionmentioning

confidence: 99%

Identification of the Key Genes and Pathways in Esophageal Carcinoma

Zhang

et al. 2016

Gastroenterology Research and Practice

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Objective. Esophageal carcinoma (EC) is a frequently common malignancy of gastrointestinal cancer in the world. This study aims to screen key genes and pathways in EC and elucidate the mechanism of it. Methods. 5 microarray datasets of EC were downloaded from Gene Expression Omnibus. Differentially expressed genes (DEGs) were screened by bioinformatics analysis. Gene Ontology (GO) enrichment, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and protein-protein interaction (PPI) network construction were performed to obtain the biological roles of DEGs in EC. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to verify the expression level of DEGs in EC. Results. A total of 1955 genes were filtered as DEGs in EC. The upregulated genes were significantly enriched in cell cycle and the downregulated genes significantly enriched in Endocytosis. PPI network displayed CDK4 and CCT3 were hub proteins in the network. The expression level of 8 dysregulated DEGs including CDK4, CCT3, THSD4, SIM2, MYBL2, CENPF, CDCA3, and CDKN3 was validated in EC compared to adjacent nontumor tissues and the results were matched with the microarray analysis. Conclusion. The significantly DEGs including CDK4, CCT3, THSD4, and SIM2 may play key roles in tumorigenesis and development of EC involved in cell cycle and Endocytosis.

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miR-124 downregulation leads to breast cancer progression via LncRNA-MALAT1 regulation and CDK4/E2F1 signal activation

Cited by 102 publications

References 39 publications

Long non-coding RNA metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) interacts with estrogen receptor and predicted poor survival in breast cancer

Long non-coding RNA metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) interacts with estrogen receptor and predicted poor survival in breast cancer

Lentivirus-mediated overexpression of miR-124 suppresses growth and invasion by targeting JAG1 and EZH2 in gastric cancer

Identification of the Key Genes and Pathways in Esophageal Carcinoma

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