Long non-coding RNA CCAT1 is overexpressed in endometrial cancer and regulates growth and transcriptome of endometrial adenocarcinoma cells

2020 ◽  
Author(s):  
S Schüler-Toprak ◽  
M Skrzypczak ◽  
F Weber ◽  
O Ortmann ◽  
O Treeck
Keyword(s):  
Endometrial Cancer ◽  
Endometrial Adenocarcinoma ◽  
Non Coding Rna ◽  
Adenocarcinoma Cells ◽  
Long Non Coding Rna

scholarly journals PD-L1 lncRNA splice isoform promotes lung adenocarcinoma progression via enhancing c-Myc activity

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Shuang Qu ◽  
Zichen Jiao ◽  
Geng Lu ◽  
Bing Yao ◽  
Ting Wang ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Lung Adenocarcinoma ◽  
Solid Tumors ◽  
Immune Checkpoint ◽  
Checkpoint Inhibition ◽  
Immune Checkpoint Inhibition ◽  
Non Coding Rna ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
Long Non Coding Rna

Abstract Background Although using a blockade of programmed death-ligand 1 (PD-L1) to enhance T cell immune responses shows great promise in tumor immunotherapy, the immune-checkpoint inhibition strategy is limited for patients with solid tumors. The mechanism and efficacy of such immune-checkpoint inhibition strategies in solid tumors remains unclear. Results Employing qRT-PCR, Sanger sequencing, and RNA BaseScope analysis, we show that human lung adenocarcinoma (LUAD) all produce a long non-coding RNA isoform of PD-L1 (PD-L1-lnc) by alternative splicing, regardless if the tumor is positive or negative for the protein PD-L1. Similar to PD-L1 mRNA, PD-L1-lnc in various lung adenocarcinoma cells is significantly upregulated by IFNγ. Both in vitro and in vivo studies demonstrate that PD-L1-lnc increases proliferation and invasion but decreases apoptosis of lung adenocarcinoma cells. Mechanistically, PD-L1-lnc promotes lung adenocarcinoma progression through directly binding to c-Myc and enhancing c-Myc transcriptional activity. Conclusions In summary, the PD-L1 gene can generate a long non-coding RNA through alternative splicing to promote lung adenocarcinoma progression by enhancing c-Myc activity. Our results argue in favor of investigating PD-L1-lnc depletion in combination with PD-L1 blockade in lung cancer therapy.

scholarly journals Long non-coding RNA TUG1 promotes endometrial cancer development via inhibiting miR-299 and miR-34a-5p

Oncotarget ◽  
2017 ◽  
Vol 8 (19) ◽  
pp. 31386-31394 ◽  
Author(s):  
Lifen Liu ◽  
Xin Chen ◽  
Ying Zhang ◽  
Yanrong Hu ◽  
Xiaoqing Shen ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cancer Development ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Metformin Treatment Exerts Antiinvasive and Antimetastatic Effects in Human Endometrial Carcinoma Cells

2011 ◽  
Vol 96 (3) ◽  
pp. 808-816 ◽  
Author(s):  
Bee K. Tan ◽  
Raghu Adya ◽  
Jing Chen ◽  
Hendrik Lehnert ◽  
Louis J. Sant Cassia ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Endometrial Adenocarcinoma ◽  
Gelatin Zymography ◽  
Luciferase Reporter ◽  
Metformin Treatment ◽  
Invasion And Metastasis ◽  
In Vitro Invasion ◽  
Adenocarcinoma Cells ◽  
Increased Risk

Context: Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women associated with an increased risk of endometrial hyperplasia. We sought to study the effects of metformin treatment (widely used in the management of PCOS women) on human endometrial adenocarcinoma cells. Objectives: To study the effects of metformin treatment on in vitro invasion and metastasis in human endometrial adenocarcinoma cells. Also, given the link between inflammation with endometrial cancer invasion and metastasis, we explored the roles of nuclear factor-κB (NF-κB), matrix metalloproteinases (MMPs) as well as v-akt murine thymoma viral oncogene homolog 1 (Akt) and extracellular signal-regulated kinases (Erk1/2) signaling pathways. Design: Sera were obtained from PCOS and control subjects. In vitro invasion were assessed in human endometrial cells (ECC-1 cells) by wound-healing motility and migration assays. NF-κB was studied by stably transfecting ECC-1 cells with a cis-reporter plasmid containing luciferase reporter gene linked to five repeats of NF-κB binding sites. The gelatinolytic activities of secreted MMP-2/9 in conditioned media were measured by gelatin zymography. Akt and Erk1/2 phosphorylation were assessed by Western blotting. Results: In vitro invasion in ECC-1 cells was significantly attenuated by sera from PCOS women after 6 months of metformin treatment (850 mg twice daily) compared to matched controls (P < 0.01). These effects appear to be associated with NF-κB, MMP-2/9, as well as Akt and Erk1/2 pathways that are known to be important regulators of inflammation, tumor invasion and metastasis. Conclusions: Metformin, potentially, may serve as adjuvant treatment in the management of patients with endometrial cancer.

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