scholarly journals Long non-coding RNA RP5-833A20.1 inhibits proliferation, metastasis and cell cycle progression by suppressing the expression of NFIA in U251 cells

2016 ◽  
Vol 14 (6) ◽  
pp. 5288-5296 ◽  
Author(s):  
Chun-Min Kang ◽  
Yan-Wei Hu ◽  
Ying Nie ◽  
Jia-Yi Zhao ◽  
Shu-Fen Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
U251 Cells

scholarly journals The long non-coding RNA LINC00152 is essential for cell cycle progression through mitosis in HeLa cells

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Linda Nötzold ◽  
Lukas Frank ◽  
Minakshi Gandhi ◽  
Maria Polycarpou-Schwarz ◽  
Matthias Groß ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Hela Cells ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA CDKN2B-AS1 regulates high glucose-induced human mesangial cell injury via regulating the miR-15b-5p/WNT2B axis

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Jing Chang ◽  
Yanming Yu ◽  
Zhan Fang ◽  
Haiyan He ◽  
Dan Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
High Glucose ◽  
Cell Cycle Progression ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cycle Progression ◽  
Inflammation Response ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Background Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) has been reported to be related to diabetic nephropathy (DN) progression. However, the regulatory mechanisms of CDKN2B-AS1 in DN are unclear. Methods High glucose (HG) was used to induce human mesangial cells (HMCs) for establishing the DN model. Expression levels of CDKN2B-AS1, microRNA (miR)-15b-5p, wingless-Type family member 2B (WNT2B) mRNA in serum and HMCs were detected through quantitative real-time polymerase chain reaction (qRT-PCR). The viability and cell cycle progression of HMCs were determined with Cell Counting Kit-8 (CCK-8) or flow cytometry assays. The levels of several proteins and inflammatory factors in HMCs were analyzed by western blotting or enzyme-linked immunosorbent assay (ELISA). The relationship between CDKN2B-AS1 or WNT2B and miR-15b-5p was verified with dual-luciferase reporter assay. Results CDKN2B-AS1 and WNT2B were upregulated while miR-15b-5p was downregulated in serum of DN patients and HG-treated HMCs. CDKN2B-AS1 inhibition reduced HG-induced viability, cell cycle progression, ECM accumulation, and inflammation response in HMCs. CDKN2B-AS1 regulated WNT2B expression via competitively binding to miR-15b-5p. MiR-15b-5p inhibitor reversed CDKN2B-AS1 knockdown-mediated influence on viability, cell cycle progression, ECM accumulation, and inflammation response of HG-treated HMCs. The repressive effect of miR-15b-5p mimic on viability, cell cycle progression, ECM accumulation, and inflammation response of HG-treated HMCs was abolished by WNT2B overexpression. Conclusion CDKN2B-AS1 regulated HG-induced HMC viability, cell cycle progression, ECM accumulation, and inflammation response via regulating the miR-15b-5p/WNT2B axis, provided a new mechanism for understanding the development of DN.

scholarly journals Upregulation of long non-coding RNA PRNCR1 in colorectal cancer promotes cell proliferation and cell cycle progression

2015 ◽  
Vol 35 (1) ◽  
pp. 318-324 ◽  
Author(s):  
LIU YANG ◽  
MANTANG QIU ◽  
YOUTAO XU ◽  
JIE WANG ◽  
YANYAN ZHENG ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA LINC00630 facilitates hepatocellular carcinoma progression through recruiting transcription factor E2F1 to up-regulate cyclin-dependent kinase 2 expression

2021 ◽  
pp. 096032712110387
Author(s):  
Jian Kang ◽  
Xu Huang ◽  
Weiguo Dong ◽  
Xueying Zhu ◽  
Ming Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Promoter Region ◽  
Cell Cycle Progression ◽  
Cyclin Dependent Kinase ◽  
Chain Reaction ◽  
Cycle Progression ◽  
Non Coding Rna ◽  
Polymerase Chain ◽  
Long Non Coding Rna

This study is aimed to investigate the role of long non-coding RNA 630 (LINC00630) in hepatocellular carcinoma (HCC). Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to examine LINC00630 expression in HCC cell lines and tissues. After LINC00630 was overexpressed or depleted in HCC cell lines, cell counting kit-8 (CCK-8) assay, BrdU assay, and flow cytometry were conducted for detecting HCC cell multiplication, apoptosis, and cell cycle progression. The catRAPID database was adopted to predict the binding relationship between LINC00630 and E2F transcription factor 1 (E2F1), and RNA pull-down and RNA immunoprecipitation (RIP) assays were carried out to verify this binding relationship. The binding of E2F1 to the cyclin-dependent kinase 2 (CDK2) promoter region was verified by dual-luciferase reporter gene assay and chromatin immunoprecipitation-quantitative polymerase chain reaction (ChIP-qPCR) assay. Western blotting was conducted to detect the protein expression of E2F1 and CDK2 in HCC cells. We report that LINC00630 expression was up-regulated in HCC and was significantly correlated with TNM stage and lymph node metastasis. LINC00630 overexpression facilitated HCC cell proliferation and cell cycle progression and inhibited the cell apoptosis, while LINC00630 knockdown had the opposite effects. LINC00630 directly bounds with E2F1. LINC00630 overexpression enhanced the binding of E2F1 to the CDK2 promoter region, thereby promoting CDK2 transcription, whereas knocking down LINC00630 inhibited CDK2 transcription. Collectively, LINC00630 promoted CDK2 transcription by recruiting E2F1 to the promoter region of CDK2, thereby promoting the malignant progression of HCC. Our data suggest that LINC00630 is a promising molecular target for HCC.

scholarly journals Long non-coding RNA NNT-AS1 sponges miR-424/E2F1 to promote the tumorigenesis and cell cycle progression of gastric cancer

2018 ◽  
Vol 22 (10) ◽  
pp. 4751-4759 ◽  
Author(s):  
Beibei Chen ◽  
Qingfang Zhao ◽  
Lulu Guan ◽  
Huifang Lv ◽  
Liangyu Bie ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals The Human RNA Surveillance Factor UPF1 Modulates Gastric Cancer Progression by Targeting Long Non-Coding RNA MALAT1

2017 ◽  
Vol 42 (6) ◽  
pp. 2194-2206 ◽  
Author(s):  
Li Li ◽  
Yingying Geng ◽  
Ru Feng ◽  
Qinqin Zhu ◽  
Bei Miao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Progression ◽  
Cell Cycle Progression ◽  
Promoter Hypermethylation ◽  
Migration And Invasion ◽  
Cycle Progression ◽  
Non Coding Rna ◽  
Tumor Tissues ◽  
Long Non Coding Rna

Background/Aims: The long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is overexpressed in numerous cancers. However, whether MALAT1 is regulated and the related mechanisms in gastric cancer remain unclear. Methods: Immunohistochemistry and qRT-PCR analyses were used to detect the expression levels of UPF1 and MALAT1 in gastric cancer and adjacent normal tissues. MTT, cell cycle, apoptosis and transwell assays were performed to examine the effects of UPF1 on cell cycle progression, cell proliferation, apoptosis, migration and invasion. Additionally, sodium bisulfate sequencing was used to test the promoter hypermethylation on UPF1 in gastric tumor tissues. Finally, RNA immunoprecipitation and luciferase reporter analyses demonstrated that UPF1 directly bound with MALAT1. Results: The expression of UPF1 was significantly downregulated in gastric cancer and negatively correlated with MALAT1 expression. Patients with lower expression of UPF1 had poorer prognosis than those with higher expression. Overexpression of UPF1 inhibited cell proliferation, cell cycle progression, cell migration and invasion, and promoted cell apoptosis in gastric cancer cells. Moreover, the UPF1-mediated inhibition of gastric cancer progression was reversed by overexpression of MALAT1. A profound downregulation of UPF1 in gastric tumor tissues was due to promoter hypermethylation. Overexpression of UPF1 increased nonsense-mediated mRNA decay (NMD) efficiency and thus led to downregulation of MALAT1. Conclusion: Our results demonstrate that UPF1 is a potential modulator of MALAT1 and that UPF1/MALAT1 pathway could be a therapeutic target for gastric cancer.

Sign in / Sign up

Export Citation Format

Share Document