miR‐150 might inhibit cell proliferation and promote cell apoptosis by targeting LMO4 in Burkitt lymphoma

2018 ◽  
Vol 234 (6) ◽  
pp. 9652-9662 ◽  
Author(s):  
Dandan Zhang ◽  
Yanshuan Wei ◽  
Jun Zhou ◽  
Guannan Wang ◽  
Lin Xiao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Burkitt Lymphoma ◽  
Cell Apoptosis ◽  
Inhibit Cell Proliferation

scholarly journals MEG3 inhibits proliferation and promote apoptosis in osteoarthritis chondrocytes by miR-361-5p/wnt/β-catenin axis

2019 ◽  
Author(s):  
Anying Wang ◽  
Naixia Hu ◽  
Yefeng Zhang ◽  
Yuanzhen Chen ◽  
Changhui Su ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Rat Model ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Control Group ◽  
Oa Chondrocytes ◽  
Inhibit Cell Proliferation

Abstract Background: This study aimed to investigate the role of long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were involved in OA group and control group, respectively. Cartilage tissues of all patients were isolated and cultured. Based on different transfection, MEG3 cells were grouped into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics group. The cells transfected with pcDNA3.1-NC and pcDNA3.1-MEG3, and then cultured with XAV939 was named as pcDNA3.1-NC +XAV939 group and pcDNA3.1-MEG3 + XAV939 group respectively. The RT-qPCR was used to detect the expression of MEG3 and miR-361-5p. Moreover, Western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis in cartilage cells. Finally, the histological analysis and immunostaining were performed on OA rat model. Results: The expression of lncRNA MEG3 and miR-361-5p in OA was significantly decreased and increased respectively than that in normal. Meanwhile, MEG3 was competitive binding with miR-361-5p in OA chondrocytes. Moreover, the Western blot and CCK-8 assay showed that MEG3 might inhibit cell proliferation and promote cell apoptosis via Wnt/β-catenin pathway. Finally, rat model analysis showed that MEG3 contributed to the cartilage matrix degradation. Conclusion: MEG3 and miR-361-5p might down-regulated and up-regulated respectively in the chondrocytes of OA patients. Furthermore, MEG3 might inhibit cell proliferation and promote cell apoptosis via miR-361-5p/Wnt/β-catenin axis in OA chondrocytes.

miR-198 targets SHMT1 to inhibit cell proliferation and enhance cell apoptosis in lung adenocarcinoma

Tumor Biology ◽  
2015 ◽  
Vol 37 (4) ◽  
pp. 5193-5202 ◽  
Author(s):  
Shujun Wu ◽  
Guojun Zhang ◽  
Ping Li ◽  
Shanshan Chen ◽  
Furui Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Cell Apoptosis ◽  
Inhibit Cell Proliferation

Lenti-shRNA-mediated FAM54A knockdown suppresses the proliferation and induces apoptosis of human Burkitt lymphoma cells

2020 ◽  
Author(s):  
Guang Yang ◽  
Hua Xiao Wang ◽  
Bin Yan ◽  
Yan Chun Xu ◽  
Yi Ru Zheng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Line ◽  
Burkitt Lymphoma ◽  
Cell Apoptosis ◽  
Annexin V ◽  
Negative Control ◽  
Namalwa Cell ◽  
Control Shrna ◽  
Burkitt Lymphoma Cell Line

Abstract Background Burkitt lymphoma is a kind of non-Hodgkin B-cell-derived malignancy, derived from germinal center B cells. FAM54A has been proved to be involved in various physiological and pathological processes of cancers, but the biological function of FAM54A in Burkitt lymphoma remains unclear. Thus, the aim of our research was to elucidate the roles of FAM54A in proliferation, apoptosis and cell cycle of Burkitt lymphoma.Methods Burkitt lymphoma cell line (Namalwa) was chosen to perform the following experiments. FAM54A-shRNA and negative control-shRNA lentivirus that were synthesized, respectively by Qiagen were used to transfect targeted cells in order to knockdown FAM54A or as negative control. Then, cell proliferation, cell cycle and cell apoptosis were detected by using MTS assay, propidium iodide staining and Annexin V-APC staining, respectively.Results Our results showed that high expression of FAM54A protein was found in Namalwa cell line. Furthermore, MTS analysis exhibited that knockdown of FAM54A obviously inhibited cell proliferation in Namalwa cells. What’s more, cell cycle analysis showed that knockdown of FAM54A induced Namalwa cell apoptosis and arrested cell cycle in G2/M phase.Conclusions These findings suggest that FAM54A is essential for Namalwa cell proliferation and may be a potential therapeutic target for the treatment of Burkitt lymphoma.

Novel function of scutellarin in inhibiting cell proliferation and inducing cell apoptosis of human Burkitt lymphoma Namalwa cells

2012 ◽  
Vol 53 (12) ◽  
pp. 2456-2464 ◽  
Author(s):  
Yizhong Feng ◽  
Shasha Zhang ◽  
Jian Tu ◽  
Zhifei Cao ◽  
Yanyan Pan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Burkitt Lymphoma ◽  
Cell Apoptosis

scholarly journals MEG3 inhibits proliferation and promote apoptosis in osteoarthritis chondrocytes by miR-361-5p/wnt/β-catenin axis

2019 ◽  
Author(s):  
Anying Wang ◽  
Naixia Hu ◽  
Yefeng Zhang ◽  
Yuanzhen Chen ◽  
Changhui Su ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Rat Model ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Control Group ◽  
Oa Chondrocytes ◽  
Inhibit Cell Proliferation

Abstract Background: This study aimed to investigate the role of long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were involved in OA group and control group, respectively. Cartilage tissues of all patients were isolated and cultured. Based on different transfection, MEG3 cells were grouped into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics group. The cells transfected with pcDNA3.1-NC and pcDNA3.1-MEG3, and then cultured with XAV939 was named as pcDNA3.1-NC +XAV939 group and pcDNA3.1-MEG3 + XAV939 group respectively. The RT-qPCR was used to detect the expression of MEG3 and miR-361-5p . Moreover, Western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis in cartilage cells. Finally, the histological analysis and immunostaining were performed on OA rat model. Results: The expression of lncRNA MEG3 and miR-361-5p in OA was significantly decreased and increased respectively than that in normal. Meanwhile, MEG3 was competitive binding with miR-361-5p in OA chondrocytes. Moreover, the Western blot and CCK-8 assay showed that MEG3 might inhibit cell proliferation and promote cell apoptosis via Wnt/β-catenin pathway. Finally, rat model analysis showed that MEG3 contributed to the cartilage matrix degradation. Conclusion: MEG3 and miR-361-5p might down-regulated and up-regulated respectively in the chondrocytes of OA patients. Furthermore, MEG3 might inhibit cell proliferation and promote cell apoptosis via miR-361-5p/Wnt/β-catenin axis in OA chondrocytes.

scholarly journals miR-100 inhibits cell proliferation in mantle cell lymphoma by targeting mTOR

2020 ◽  
Vol 9 (1) ◽  
Author(s):  
Luhui Lin ◽  
Yiqun Huang ◽  
Wei Zhuang ◽  
Ping Lin ◽  
Xudong Ma
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Mantle Cell Lymphoma ◽  
Cell Lines ◽  
Cell Apoptosis ◽  
Cell Lymphoma ◽  
G1 Phase ◽  
Mantle Cell ◽  
Mtor Protein ◽  
Inhibit Cell Proliferation

Abstract Background miR-100 is reported to be associated with cell proliferation and apoptosis. However, the function of miR-100 in mantle cell lymphoma (MCL) is unknown. The purpose of this study is to analyze the abnormal expression of miR-100 and mTOR in MCL together with their potential biological function and pathogenesis. Method Eighteen MCL tissue samples and 3 cell lines (Jeko-1, Mino, Granta-519) were investigated in this research study, while eighteen samples of proliferative lymphadenitis from patients and peripheral lymphocyte cells from healthy volunteers served as controls. The expression and alteration of miR-100 and mTOR mRNA were detected by RT-PCR. The expression and alteration of mTOR protein were explored by Western blot. LV-miR-100-up and LV-mTOR-RNAi were constructed and transfected by lentivirus transfection. Cell proliferation, cell apoptosis and the cell cycle were detected using CCK-8 and flow cytometry. Bioinformatics prediction software was used to predict the miR-100 target gene of mTOR. A double luciferase experiment was used to verify miR-100 targeting at the mTOR-3′-UTR. The interaction between miR-100 and mTOR was further studied using recovery experiments. GraphPad Prism 7 software (version 7.2) was used for statistical analysis, and a P value < 0.05 was considered statistically significant. Results We found that the expression of miR-100 mRNA in MCL tissues and cell lines was lower, while that of the mTOR protein was higher. There was a negative correlation between miR-100 and mTOR in both MCL tissues and cell lines. Promoting miR-100 and inhibiting mTOR could inhibit cell proliferation, induce cell apoptosis and block the cell cycle in the G1 phase. A double luciferase reporter assay showed that mTOR was one of the target genes of miR-100. The recovery experiment demonstrated that PV-mTOR-up partially set off the effect of LV-miR-100-up on decreasing mTOR expression, inhibiting proliferation, inducing apoptosis and blocking the cell cycle in G1 phase in both Jeko-1 and Mino cells. Conclusions Abnormal expression of miR-100 and mTOR was found in MCL, which included downregulation of miR-100 and upregulation of mTOR. The expression of mTOR is negatively correlated with miR-100. It may play an important role in MCL pathogenesis. miR-100 up-regulation can inhibit cell proliferation, promote cell apoptosis, and inhibit cell cycle in G1 phase by targeting the mTOR gene. miR-100 may potentially be an anti-mantle cell lymphoma gene.

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