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

Wu, Aihua; Xu, Fei; Chen, Chao; Jiang, Lei; Jin, Rong

doi:10.3892/ol.2018.8194

Cited by 8 publications

(8 citation statements)

References 30 publications

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“…To enhance our capacity in enhancing miRNA expression, delivery methods including viral vectors have been used. A recent experiment uses lentivirus for delivery of miRNA-124 to down-regulate EZH2 expression and successfully inhibit to gastric cancer progression [ 169 ].…”

Section: Non-coding Rnas and Ezh2 Signalingmentioning

confidence: 99%

The long and short non-coding RNAs modulating EZH2 signaling in cancer

et al. 2022

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Non-coding RNAs (ncRNAs) are a large family of RNA molecules with no capability in encoding proteins. However, they participate in developmental and biological processes and their abnormal expression affects cancer progression. These RNA molecules can function as upstream mediators of different signaling pathways and enhancer of zeste homolog 2 (EZH2) is among them. Briefly, EZH2 belongs to PRCs family and can exert functional roles in cells due to its methyltransferase activity. EZH2 affects gene expression via inducing H3K27me3. In the present review, our aim is to provide a mechanistic discussion of ncRNAs role in regulating EZH2 expression in different cancers. MiRNAs can dually induce/inhibit EZH2 in cancer cells to affect downstream targets such as Wnt, STAT3 and EMT. Furthermore, miRNAs can regulate therapy response of cancer cells via affecting EZH2 signaling. It is noteworthy that EZH2 can reduce miRNA expression by binding to promoter and exerting its methyltransferase activity. Small-interfering RNA (siRNA) and short-hairpin RNA (shRNA) are synthetic, short ncRNAs capable of reducing EZH2 expression and suppressing cancer progression. LncRNAs mainly regulate EZH2 expression via targeting miRNAs. Furthermore, lncRNAs induce EZH2 by modulating miRNA expression. Circular RNAs (CircRNAs), like lncRNAs, affect EZH2 expression via targeting miRNAs. These areas are discussed in the present review with a focus on molecular pathways leading to clinical translation.

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Section: Non-coding Rnas and Ezh2 Signalingmentioning

confidence: 99%

The long and short non-coding RNAs modulating EZH2 signaling in cancer

et al. 2022

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“…After transfection, although proliferation curves of all three groups showed an upward trend, cell proliferation rate in miR-124 group was significantly lower than that in NC group and control group, indicating inhibited cell proliferation after miR-124 transfection. Pan et al (20) found that lentiviral vectors that stably express miR124 can inhibit the growth, migration, and invasion of gastric cancer cells. Li et al (21) found that miR-124 can inhibit cell invasion and epithelial mesenchymal transformation by inhibiting Snail2 expression.…”

Section: Discussionmentioning

confidence: 99%

Expression of miR-124 in gastric adenocarcinoma and the effect on proliferation and invasion of gastric adenocarcinoma SCG-7901 cells

Wang

et al. 2019

Oncol Lett

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Expression of miR-124 in gastric adenocarcinoma cell line SGC-7901 and its effect on biological functions was investigated. Expression of miR-124 in cancer tissues and paracancerous tissues of gastric adenocarcinoma patients was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). RT-qPCR was used to detect the expression of miR-124 in human normal gastric epithelial cells GES-1 and gastric adenocarcinoma SGC-7901 cells. Cells in miR-124 group were transfected with miR-124 agomir, cells in NC group were transfected with agomir-negative control sequence and cells in the control group were not transfected. MTT assay was used to detect cell proliferation, and Transwell invasion assay to detect cell invasion ability, and the effect of transfected miR-124 agonist on the proliferation and invasive ability of gastric adenocarcinoma cells was evaluated. RT-qPCR results showed that miR-124 expression was significantly downregulated in gastric adenocarcinoma tumor tissues compared with paracancerous tissues. Compared with cells of normal human gastric epithelial cell line GES-1, the expression of miR-124 human gastric adenocarcinoma SGC-7901 cells was significantly downregulated. At 12 h, there was no significant difference in OD at 490 nm in the three groups (P>0.05). OD (490) in the three groups showed a gradual upward trend. After transfection, proliferation curves of the three groups showed an upward trend, proliferation rate of miR-124 group was significantly lower than that of NC and control groups (P<0.05). The number of invading cells in miR-124 group was significantly lower than that in NC group and control group, but there was no significant difference in the number of cell invasion between the NC and control groups. miR-124 can inhibit the proliferation and invasion of gastric adenocarcinoma cells. Downregulation of miR-124 expression in gastric adenocarcinoma may be closely related to the development of gastric adenocarcinoma.

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“…It is known that miR-124 is also downregulated in gastric cancer cell lines, and the expression of miR-124 has been reported to inhibit growth, decrease colony-forming ability, induce apoptosis, and suppress metastasis and invasion [84][85][86][87][88] (Table 5). In gastric cancer cells, the transfection of miR-124 can reportedly enhance the anticancer effect of 5-fluorouracil [88].…”

Section: Stat3mentioning

confidence: 99%

“…Another frequently reported target gene of miR-124 is the enhancer of zeste homolog 2 (EZH2), which has been found in lung adenocarcinoma [67], hepatocellular carcinoma cancer [87,88], cholangiocarcinoma [107], laryngeal squamous cell carcinoma [114], multiple myeloma [115], and ovarian cancer [23]. EZH2 is reportedly essential for the proliferation of cancer cell lines and for regulating the expression of genes related to EMT [116,117].…”

Section: Target Genes Responsible For the Tumor Suppressor Effect Of Mir-124 Stat3 And Ezh2mentioning

confidence: 99%

“…EZH2 is reportedly essential for the proliferation of cancer cell lines and for regulating the expression of genes related to EMT [116,117]. Therefore, it is responsible for miR-124-induced tumor suppression in cell growth inhibition [50,67,87] and EMT inhibition [23,67,79,88]. In cholangiocarcinoma, miR-124 targets both EZH2 and STAT3, and more interestingly, knockdown of EZH2 is associated with a decreased expression of STAT3.…”

Section: Target Genes Responsible For the Tumor Suppressor Effect Of Mir-124 Stat3 And Ezh2mentioning

confidence: 99%

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Tumor Suppressive Effects of miR-124 and Its Function in Neuronal Development

Sanuki

Yamamura

2021

IJMS

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MicroRNA-124 (miR-124) is strongly expressed in neurons, and its expression increases as neurons mature. Through DNA methylation in the miR-124 promoter region and adsorption of miR-124 by non-coding RNAs, miR-124 expression is known to be reduced in many cancer cells, especially with high malignancy. Recently, numerous studies have focused on miR-124 due to its promising tumor-suppressive effects; however, the overview of their results is unclear. We surveyed the tumor-suppressive effect of miR-124 in glial cell lineage cancers, which are the most frequently reported cancer types involving miR-124, and in lung, colon, liver, stomach, and breast cancers, which are the top five causes of cancer death. Reportedly, miR-124 not only inhibits proliferation and accelerates apoptosis, but also comprehensively suppresses tumor malignant transformation. Moreover, we found that miR-124 exerts its anti-tumor effects by regulating a wide range of target genes, most notably STAT3 and EZH2. In addition, when compared to the original role of miR-124 in neuronal development, we found that the miR-124 target genes that contribute to neuronal maturation share similarities with genes that cause cancer cell metastasis and epithelial-mesenchymal transition. We believe that the two apparently unrelated fields, cancer and neuronal development, can bring new discoveries to each other through the study of miR-124.

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

Cited by 8 publications

References 30 publications

The long and short non-coding RNAs modulating EZH2 signaling in cancer

The long and short non-coding RNAs modulating EZH2 signaling in cancer

Expression of miR-124 in gastric adenocarcinoma and the effect on proliferation and invasion of gastric adenocarcinoma SCG-7901 cells

Tumor Suppressive Effects of miR-124 and Its Function in Neuronal Development

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