scholarly journals ERRα acts as a potential agonist of PPARγ to induce cell apoptosis and inhibit cell proliferation in endometrial cancer

Aging ◽  
2020 ◽  
Author(s):  
Meimei Huang ◽  
Lili Chen ◽  
Xiaodan Mao ◽  
Guifen Liu ◽  
Yuqin Gao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endometrial Cancer ◽  
Cell Apoptosis ◽  
Induce Cell Apoptosis ◽  
Inhibit Cell Proliferation

scholarly journals Metapristone (RU486 derivative) inhibits endometrial cancer cell progress through regulating miR-492/Klf5/Nrf1 axis

2020 ◽  
Author(s):  
Yue Chang ◽  
Min Hao ◽  
Ru Jia ◽  
Yihui Zhao ◽  
Yixuan Cai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endometrial Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Target Genes ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell ◽  
Downstream Target ◽  
Ishikawa Cells

Abstract Background: Endometrial cancer is one of the most common cancers affecting women's health. The pathogenesis of endometrial cancer involves many signaling pathways which are related with transcription factors or microRNAs. Recent studies have reported that endometrial cancer is also related with the sexual-mediated hormones. The purpose of this research is to treat the endometrial cancer with the hormone-related drugs, and find out the specific molecular mechanism. Methods: In this study, RL95-2 cells and Ishikawa cells were used as the endometrial cancer cell models. miR-492 was transfected into RL95-2 cells and Ishikawa cells. The miRNA expression was measured by qRT-PCR. The protein expression was measured by western blot. Cell proliferation was monitored using the MTT assay and cell colony formation assay. Cell apoptosis was monitored using EdU assay. Results: Firstly, the results indicated that metapristone as a kind of hormone-related drugs could significantly inhibit the endometrial cancer cell growth through regulating cell apoptosis-related gene expression. Meanwhile, miR-492 was detected to be highly expressed in the endometrial cancer cell lines. Overexpression of miR-492 could promote the cell proliferation and inhibit the cell apoptosis. Furthermore, the results demonstrated that the downstream target genes of miR-492 were Klf5 and Nrf1, which were inhibited by metapristone. At the animal level, metapristone also inhibited the endometrial cancer cell growth through down-regulating the expression of miR-492 and decreasing the protein level of Klf5 and Nrf1. Conclusion: Taken together, this study indicated that metapristone inhibited the endometrial cancer cell growth through regulating the cell apoptosis related signaling pathway and the expression of miR-492 and its downstream target genes (Klf5 and Nrf1), which provided the theoretical basis of endometrial cancer in clinical treatment.

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 Metapristone (RU486 derivative) inhibits endometrial cancer cell progress through regulating miR-492/Klf5/Nrf1 axis

2020 ◽  
Author(s):  
Yue Chang ◽  
Min Hao ◽  
Ru Jia ◽  
Yihui Zhao ◽  
Yixuan Cai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endometrial Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Target Genes ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell ◽  
Downstream Target ◽  
Ishikawa Cells

Abstract Background: Endometrial cancer is the prevalent invasive gynecological cancer in the world. The pathogenesis of endometrial cancer involves many signaling pathways which are related with transcription factors or microRNAs. Metapristone is a hormone related drug and widely used in endometrial cancer clinical therapeutics. However, the deep regulatory mechanism of metapristone is not clear. In this research, we aimed to figure out the specific molecular mechanism during the treatment of endometrial cancer with metapristone.Methods: In this study, RL95-2 cells and Ishikawa cells were used as the endometrial cancer cell models. miR-492 was transfected into RL95-2 cells and Ishikawa cells. The miRNA expression was measured by qRT-PCR. Moreover, the mice tumor model was used to confirm the function of metapristone and the regulating process by miR-492/Klf5/Nrf1 axis in vivo. The protein expression was measured by western blot. Cell proliferation and apoptosis was monitored using the MTT assay, cell colony formation assay and EdU assay.Results: Firstly, the results indicated that metapristone as a kind of hormone-related drugs could significantly inhibit the endometrial cancer cell growth through regulating cell apoptosis-related gene expression. Meanwhile, miR-492 was detected to be highly expressed in the endometrial cancer cell lines. Overexpression of miR-492 could promote the cell proliferation and inhibit the cell apoptosis. Furthermore, the results demonstrated that the downstream target genes of miR-492 were Klf5 and Nrf1, which were inhibited by metapristone. At the animal level, metapristone also inhibited the endometrial cancer cell growth through down-regulating the expression of miR-492 and decreasing the protein level of Klf5 and Nrf1. Conclusion: Taken together, this study indicated that metapristone inhibited the endometrial cancer cell growth through regulating the cell apoptosis related signaling pathway and the expression of miR-492 and its downstream target genes (Klf5 and Nrf1), which provided the theoretical basis of endometrial cancer in clinical treatment.

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

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 Metapristone(RU486 derivative) inhibits endometrial cancer cell progress through regulating miR-492/Klf5/Nrf1 axis

2020 ◽  
Author(s):  
Yun Liu ◽  
Yue Chang ◽  
Yixuan Cai
Keyword(s):  
Cell Proliferation ◽  
Endometrial Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Target Genes ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell ◽  
Downstream Target ◽  
Ishikawa Cells

Abstract Background: Endometrial cancer is one of the most common cancers affecting women's health. The pathogenesis of endometrial cancer involves many signaling pathways which are related with transcription factors or microRNAs. Recent studies have reported that endometrial cancer is also related with the sexual-mediated hormones. The purpose of this research is to treat the endometrial cancer with the hormone-related drugs, and find out the specific molecular mechanism. Methods: In this study, RL95-2 cells and Ishikawa cells were used as the endometrial cancer cell models. miR-492 was transfected into RL95-2 cells and Ishikawa cells. The miRNA expression was measured by qRT-PCR. The protein expression was measured by western blot. Cell proliferation was monitored using the MTT assay and cell colony formation assay. Cell apoptosis was monitored using EdU assay. Results: Firstly, the results indicated that metapristone as a kind of hormone-related drugs could significantly inhibit the endometrial cancer cell growth through regulating cell apoptosis-related gene expression. Meanwhile, miR-492 was detected to be highly expressed in the endometrial cancer cell lines. Overexpression of miR-492 could promote the cell proliferation and inhibit the cell apoptosis. Furthermore, the results demonstrated that the downstream target genes of miR-492 were Klf5 and Nrf1, which were inhibited by metapristone. At the animal level, metapristone also inhibited the endometrial cancer cell growth through down-regulating the expression of miR-492 and decreasing the protein level of Klf5 and Nrf1. Conclusion: Taken together, this study indicated that metapristone inhibited the endometrial cancer cell growth through regulating the cell apoptosis related signaling pathway and the expression of miR-492 and its downstream target genes (Klf5 and Nrf1), which provided the theoretical basis of endometrial cancer in clinical treatment.

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