MiR-195 connects lncRNA RUNX1-IT1 and cyclin D1 to regulate the proliferation of glioblastoma cells

Wu, Zhongbao

doi:10.1080/00207454.2021.1881090

Cited by 7 publications

(6 citation statements)

References 15 publications

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“…miRNA was first transcribed into an initial transcript of 1000 nt by RNA polymerase II and then cleaved by Drosha enzyme to form a 70 nt miRNA precursor, and finally, a mature miRNA was formed by Dicer enzyme. miR-195 has been shown to suppress replication and speed up cell death in gastric cancer cells by aiming JAK2 [ 12 ]. Overexpression of miR-195-5p can inhibit the luciferase activity of JAK2-3′UTR-WT.…”

Section: Introductionmentioning

confidence: 99%

Effects of mir-195 Targeted Regulation of JAK2 on Proliferation, Invasion, and Apoptosis of Gastric Cancer Cells

Zhuang

Yuan

et al. 2022

Computational and Mathematical Methods in Medicine

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Background. Overexpression of miR-195 can make gastric cancer cells stay in G1/G2 phase. miR-195 has been shown to inhibit gastric cancer cell replication and accelerate cell death by targeting JAK2. However, the relationship between miR-195, JAK2, and gastric cancer is not clear. Objective. To observe the effect of mir-195 regulated by JAK2 on the growth, invasion, and death of gastric cancer cells. Methods. MGC803 and NCI gastric N87 cells were introduced into the negative control sequences of miR-195 and RNA, respectively. To detect the expression of miR-195 in cells, to detect the effect of miR-195 on mitosis and proliferation of tumor cells, to analyze the effect of miR-195 on cell invasion and metastasis, and to detect the regulation of miR-195 on JAK2 expression. Results. The level of miR-195 in miR-195-MIMICS group was significantly higher than that in miR-NC group. The cell survival rate of miR-195 mimic group was lower than that of miR-NC group ( P < 0.05 ). Compared with miR-NC group, the number of cells in G1 phase increased, the cells in G2 phase and S phase decreased, and the proportion of cells in G2 and S phase decreased in miR-195 mimic group. The scratch distance of miR-195 simulator group was larger than that of control group. The number of invasive cells in the miR-195 mimic group was significantly lower than that in the control group. The expression of JAK2 protein in miR-195 mimic group was lower than that in miR-NC group. There was a significant negative correlation between the expression level of miR-195 and JAK2 (rhabdomile 0.326 and record 0.00). There are continuous interaction fragments between JAK2 and miR-195. The luciferase activity of miR-195 mimic and wild type JAK2 sequence expression vector was significantly lower than that of wild type JAK2 sequence expression vector. Conclusion. miR-195 may inhibit the occurrence, metastasis, and invasion of gastric tumor by downregulating the expression of JAK2. miR-195/JAK2 may be a new molecular target for the treatment of gastrointestinal tumors.

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Section: Introductionmentioning

confidence: 99%

Effects of mir-195 Targeted Regulation of JAK2 on Proliferation, Invasion, and Apoptosis of Gastric Cancer Cells

Zhuang

Yuan

et al. 2022

Computational and Mathematical Methods in Medicine

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“…Our study characterized a novel SEMA3B-AS1/miR-195/cyclin D1 axis involved in GBM, while the upregulation of miR-195 by SEMA3B-AS1 still needs to be further investigated. A recent study reported that lncRNA RUNX1-IT1 can also sponge miR-195 to upregulate cyclin D1 in glioblastoma, thereby promoting cell proliferation [ 25 ]. Therefore, miR-195 in GBM may be sponged by multiple lncRNAs.…”

Section: Discussionmentioning

confidence: 99%

MicorRNA-195 links long non-coding RNA SEMA3B antisense RNA 1 (head to head) and cyclin D1 to regulate the proliferation of glioblastoma cells

et al. 2022

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Long non-coding RNA (lncRNA) SEMA3B antisense RNA 1 (head to head) (SEMA3B-AS1) is a recently identified tumor suppressor in gastric cancer. However, its role in glioblastoma (GBM) is unclear. This study was conducted to explore the role of SEMA3B-AS1 in GBM. In this study, the expression of SEMA3B-AS1, cyclin D1 and miR-195 were determined by RT-qPCR. Gene interactions were evaluated by dual-luciferase assay and overexpression experiments. BrdU assay was performed to monitor cell proliferation. We observed downregulation of SEMA3B-AS1 in GBM. The expression of SEMA3B-AS1 was inversely correlated with the expression of cyclin D1 but positively correlated with the expression of miR-195. In GBM cells, overexpression of SEMA3B-AS1 and miR-195 caused reduced expression levels of cyclin D1. MiR-195 inhibitor reduced the effects of overexpression of SEMA3B-AS1 on the expression of cyclin D1. Moreover, overexpression of SEMA3B-AS1 increased the expression levels of miR-195. Cell proliferation data showed that, SEMA3B-AS1 and miR-195 decreased cell proliferation, while overexpression of cyclin D1 increased GBM cell proliferation. In addition, miR-195 inhibitor inhibited the role of overexpression of SEMA3B-AS1 in cancer cell proliferation. Moreover, miR-195 interacted with cyclin D1, but not SEMA3B-AS1. Furthermore, SEMA3B-AS1 decreased the methylation of the promoter region of miR-195. Therefore, we concluded that miR-195 links lncRNA SEMA3B-AS1 and cyclin D1 to regulate the proliferation of GBM cells.

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“…LncRNA RUNX1-IT1 is a newly identified non-coding RNA with an important regulatory function, and can inhibit or promote cancer in different tumors; for example, it is lowly expressed in liver cancer, endometrial cancer, and colorectal cancer, but it is highly expressed in pancreatic cancer and glioma ( 11 , 13 , 14 , 20 , 21 ). The lncRNA RUNX1-IT1 expression level in liver cancer tissues is significantly reduced, and the overexpression of lncRNA RUNX1-IT1 can limit the growth of liver cancer cells and induce their apoptosis.…”

Section: Discussionmentioning

confidence: 99%

The molecular mechanism of long non-coding ribonucleic acid (lncRNA) RUNX1-IT1 promotes the proliferation and stemness of lung cancer cells

Miao¹,

Li²,

Liu³

et al. 2021

Transl Cancer Res TCR

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Background: This study sought to explore the role of long non-coding ribonucleic acid (lncRNA) RUNX1-IT1 in lung cancer proliferation and cell stemness and clarify its molecular mechanism.Methods: Quantitative reverse transcription polymerase chain reaction was used to detect the expression levels of lncRNA RUNX1-IT1 in lung cancer cell lines and tissues. Cell Counting Kit 8, a plate cloning experiment, a cell suspension sphere-forming assay and a Transwell assay were used to identify the effects of lncRNA RUNX1-IT1 overexpression or down-expression on clone formation, cell progression, cell stemness, and invasion. Western blot was used to detect the expression of associated proteins that regulate cell invasion and stemness.Results: Low expression levels of lncRNA RUNX1-IT1 were detected in the cancerous lung cells and tissues. The overexpression of lncRNA RUNX1-IT1 significantly restricted the ability of cells to proliferate, produce clones, form spheres, and invade lung cancer cells, while the knockdown of lncRNA RUNX1-IT1 had the opposite effect. The findings of the Western blot assessment showed that the overexpression or knockdown of lncRNA RUNX1-IT1 significantly affected the expression of cluster of differentiation 44, cluster of differentiation 133, sex-determining region Y-box 2, octamer-binding transcription factor 4, and Nanog, and regulated the sphere-forming ability of cells. Additionally, the overexpression or knockdown of lncRNA RUNX1-IT1 regulated the invasion ability of cells by affecting expressions of E-cadherin, N-cadherin, and Vimentin. Conclusions:The poor expression, overexpression, or knockdown of lncRNA RUNX1-IT1 affects the stemness and invasion ability of lung cancer cells.

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MiR-195 connects lncRNA RUNX1-IT1 and cyclin D1 to regulate the proliferation of glioblastoma cells

Cited by 7 publications

References 15 publications

Effects of mir-195 Targeted Regulation of JAK2 on Proliferation, Invasion, and Apoptosis of Gastric Cancer Cells

Effects of mir-195 Targeted Regulation of JAK2 on Proliferation, Invasion, and Apoptosis of Gastric Cancer Cells

MicorRNA-195 links long non-coding RNA SEMA3B antisense RNA 1 (head to head) and cyclin D1 to regulate the proliferation of glioblastoma cells

The molecular mechanism of long non-coding ribonucleic acid (lncRNA) RUNX1-IT1 promotes the proliferation and stemness of lung cancer cells

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