Up-regulated miR-548k promotes esophageal squamous cell carcinoma progression via targeting long noncoding RNA-LET

Chen, Zhiyao; Lin, Jianqing; Wu, Shuhua; Xu, Changlu; Chen, Feng; Huang, Zhijun

doi:10.1016/j.yexcr.2017.11.006

Cited by 26 publications

(37 citation statements)

References 38 publications

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“…Over the past few years, previous studies have reported that non-coding RNAs, including miRNAs and long non-coding RNAs, serve important roles in cancer ( 23 – 25 ). For example, miR-543 was observed to promote ESCC cell migration, invasion and EMT via targeting phospholipase A2 Group IVA ( 26 ).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑590 inhibits migration, invasion and epithelial‑to‑mesenchymal transition of esophageal squamous cell carcinoma by targeting low‑density lipoprotein receptor‑related protein 6

Guan

Liu

et al. 2020

Oncol Rep

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MicroRNA-590 (miR-590) has been revealed as a tumor suppressor, while low-density lipoprotein receptor-related protein 6 (LRP6) is considered to act as a tumor promoter. However, their roles and underlying molecular regulatory mechanisms in esophageal squamous cell carcinoma (ESCC) have yet to be fully elucidated. Therefore, the present study aimed to investigate these mechanisms. The expression levels of miR-590 and LRP6 in human ESCC samples and cell lines were determined using reverse transcription-quantitative PCR. Bioinformatics analysis was used to predict the relationship between miR-590 and LRP6, and luciferase assay was performed to validate the relationship between these factors. Transwell assays were used to determine cell migration and invasion, while western blotting assays were used to detect the protein expression levels of LRP6, E-cadherin, N-cadherin and Vimentin. The present study demonstrated that miR-590 was downregulated and LRP6 was upregulated in ESCC tissues and cell lines. Furthermore, it was found that miR-590 overexpression and LRP6 knockdown inhibited cell migration, invasion and epithelial-to-mesenchymal transition (EMT) in ESCC cell lines. Additional mechanistic studies identified that LRP6 was a target of, and was inhibited by, miR-590. Collectively, the present findings suggested that miR-590 inhibited the invasion, migration and EMT of ESCC cells by mediating LRP6.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑590 inhibits migration, invasion and epithelial‑to‑mesenchymal transition of esophageal squamous cell carcinoma by targeting low‑density lipoprotein receptor‑related protein 6

Guan

Liu

et al. 2020

Oncol Rep

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“…For example, miR-146a, miR-133b, miR-106b-3p, miR-219-5p, miR-206, miR-384, miR-455-5p, miR-128, miR-145-3p/5p, miR-10b-3p, miR-874-3p, miR-10a, miR-365, miR-301a, miR-6775-3p, miR-139-5p, miR-516b, miR-449a-5p, miR-125b, miR-433-3p, miR-370, miR-133b, miR-30a-3p/5p, miR-34a, miR-196a, and miR-125b-5p have been shown to act as tumor suppressors by inhibiting ESCC cell proliferation, promoting apoptosis by directly targeting oncogenes, or antagonizing pro-cancer signaling pathways [29,33,35,[40][41][42][43][44][45][46][47][48][49][50][51][52][54][55][56][57][58][60][61][62][63]110,133]. In contrast, pro-oncogenes such as miR-141, miR-21, miR-10b-3p, miR-424, miR-675-3p, miR-543, miR-135, miR-23b-3p, miR-502, miR-21-5p, and miR-548k have been reported to play contrasting roles in promoting cell proliferation or suppressing apoptosis in ESCC [47,[64][65][66][67][68][69][70][71][72][73]. Overall, the roles of miRNAs in cell proliferation and apoptosis can be crucial in ESCC pathogenesis.…”

Section: Non-coding Rnas Regulate Cell Proliferation and Apoptosis Dumentioning

confidence: 99%

Emerging Role of Non-Coding RNAs in Esophageal Squamous Cell Carcinoma

Feng

Zhang

Yao

et al. 2019

IJMS

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Esophageal squamous cell carcinoma (ESCC) is a highly prevalent tumor and is associated with ethnicity, genetics, and dietary intake. Non-coding RNAs (ncRNAs), specifically microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs) have been reported as functional regulatory molecules involved in the development of many human cancers, including ESCC. Recently, several ncRNAs have been detected as oncogenes or tumor suppressors in ESCC progression. These ncRNAs influence the expression of specific genes or their associated signaling pathways. Moreover, interactions of ncRNAs are evident in ESCC, as miRNAs regulate the expression of lncRNAs, and further, lncRNAs and circRNAs function as miRNA sponges to compete with the endogenous RNAs. Here, we discuss and summarize the findings of recent investigations into the role of ncRNAs (miRNAs, lncRNAs, and circRNAs) in the development and progression of ESCC and how their interactions regulate ESCC development.

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“…For example, lncRNA is involved in DNA methylation, chromatin remodeling, and genetic mechanisms of miRNAs, which can affect the development of tumors by disrupting the stability of the genome and affecting the function of the corresponding proteins . LncRNA LET is downregulated in cervical cancer, gastric cancer, and esophageal cancer, and its high expression predicts a good prognosis. In addition, lncRNA LET can inhibit the proliferation and EMT of lung adenocarcinoma cells .…”

Section: Introductionmentioning

confidence: 99%

LncRNA GMDS‐AS1 inhibits lung adenocarcinoma development by regulating miR‐96‐5p/CYLD signaling

Zhao

Zhang

et al. 2019

Cancer Medicine

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According to the global cancer statistic, lung cancer is one of the most dangerous tumors, which poses a serious threat to human health. Exploration the mechanism of lung cancer and new targeted therapeutic measures is always the hot topic. Long noncoding RNA (lncRNA) is an important factor affecting the development of tumors. However, the research on the mechanism of lncRNA in the progress of lung cancer needs to be further expanded. In this study, we found that the expression of lncRNA GMDS‐AS1 was significantly reduced in lung adenocarcinoma (LUAD) tissues and cells. Upregulated GMDS‐AS1 can significantly inhibit the proliferation of LUAD cells and promote cell apoptosis in vitro and in vivo. The results indicate that GMDS‐AS1 acts as a tumor suppressor gene to affect the development of LUAD. Further studies revealed that GMDS‐AS1 is a target gene of miR‐96‐5p, and GMDS‐AS1 regulates proliferation and apoptosis of LUAD cells in association with miR‐96‐5p. In addition, we also confirmed that CYLD lysine 63 deubiquitinase (CYLD) is also a target gene of miR‐96‐5p. Through various validations, we confirmed that GMDS‐AS1 can act as a ceRNA to upregulate the expression of CYLD by sponging miR‐96‐5p. Moreover, the intervention of GMDS‐AS1/miR‐96‐5p/CYLD network can regulate the proliferation and apoptosis of LUAD cells. In this study, we revealed that the GMDS‐AS1/miR‐96‐5p/CYLD network based on ceRNA mechanism plays an important role in the development of LUAD and provides a new direction and theoretical basis for targeted therapy of LUAD.

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Up-regulated miR-548k promotes esophageal squamous cell carcinoma progression via targeting long noncoding RNA-LET

Cited by 26 publications

References 38 publications

MicroRNA‑590 inhibits migration, invasion and epithelial‑to‑mesenchymal transition of esophageal squamous cell carcinoma by targeting low‑density lipoprotein receptor‑related protein 6

MicroRNA‑590 inhibits migration, invasion and epithelial‑to‑mesenchymal transition of esophageal squamous cell carcinoma by targeting low‑density lipoprotein receptor‑related protein 6

Emerging Role of Non-Coding RNAs in Esophageal Squamous Cell Carcinoma

LncRNA GMDS‐AS1 inhibits lung adenocarcinoma development by regulating miR‐96‐5p/CYLD signaling

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