Sirtuin 1 promotes autophagy and proliferation of endometrial cancer cells by reducing acetylation level of LC3

2021 ◽  
Author(s):  
Shuai Huang ◽  
Ye Li ◽  
Guihua Sheng ◽  
Qingwei Meng ◽  
Qian Hu ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cells ◽  
Sirtuin 1 ◽  
Acetylation Level

Emodin Enhances the Chemosensitivity of Endometrial Cancer by Inhibiting ROS-Mediated Cisplatin-resistance

2018 ◽  
Vol 18 (7) ◽  
pp. 1054-1063 ◽  
Author(s):  
Ning Ding ◽  
Hong Zhang ◽  
Shan Su ◽  
Yumei Ding ◽  
Xiaohui Yu ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Endometrial Cancer ◽  
Cancer Cells ◽  
Chemotherapeutic Agent ◽  
Annexin V ◽  
Chemotherapeutic Agents ◽  
Endometrial Cancer Cell ◽  
Animal Survival ◽  
Apoptosis Level

Background: Endometrial cancer is a common cause of death in gynecological malignancies. Cisplatin is a clinically chemotherapeutic agent. However, drug-resistance is the primary cause of treatment failure. Objective: Emodin is commonly used clinically to increase the sensitivity of chemotherapeutic agents, yet whether Emodin promotes the role of Cisplatin in the treatment of endometrial cancer has not been studied. Method: CCK-8 kit was utilized to determine the growth of two endometrial cancer cell lines, Ishikawa and HEC-IB. The apoptosis level of Ishikawa and HEC-IB cells was detected by Annexin V / propidium iodide double-staining assay. ROS level was detected by DCFH-DA and NADPH oxidase expression. Expressions of drug-resistant genes were examined by real-time PCR and Western blotting. Results: Emodin combined with Cisplatin reduced cell growth and increased the apoptosis of endometrial cancer cells. Co-treatment of Emodin and Cisplatin increased chemosensitivity by inhibiting the expression of drugresistant genes through reducing the ROS levels in endometrial cancer cells. In an endometrial cancer xenograft murine model, the tumor size was reduced and animal survival time was increased by co-treatment of Emodin and Cisplatin. Conclusion: This study demonstrates that Emodin enhances the chemosensitivity of Cisplatin on endometrial cancer by inhibiting ROS-mediated expression of drug-resistance genes.

scholarly journals Akt regulates progesterone receptor B-dependent transcription and angiogenesis in endometrial cancer cells

Oncogene ◽  
2016 ◽  
Vol 35 (39) ◽  
pp. 5191-5201 ◽  
Author(s):  
I I Lee ◽  
K Maniar ◽  
J P Lydon ◽  
J J Kim
Keyword(s):  
Endometrial Cancer ◽  
Progesterone Receptor ◽  
Cancer Cells ◽  
Progesterone Receptor B

Progesterone induces apoptosis by activation of caspase-8 and calcitriol via activation of caspase-9 pathways in ovarian and endometrial cancer cells in vitro

APOPTOSIS ◽  
2021 ◽  
Author(s):  
Latoya McGlorthan ◽  
Ana Paucarmayta ◽  
Yovanni Casablanca ◽  
G. Larry Maxwell ◽  
Viqar Syed
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cells ◽  
Caspase 8 ◽  
Caspase 9

scholarly journals Metformin Dysregulates the Unfolded Protein Response and the WNT/β-Catenin Pathway in Endometrial Cancer Cells through an AMPK-Independent Mechanism

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1067
Author(s):  
Domenico Conza ◽  
Paola Mirra ◽  
Gaetano Calì ◽  
Luigi Insabato ◽  
Francesca Fiory ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Unfolded Protein Response ◽  
Cancer Cells ◽  
Independent Manner ◽  
Growth And Survival ◽  
Unfolded Protein ◽  
Compound C ◽  
Survival Pathways ◽  
The Unfolded Protein Response ◽  
Protein Response

Multiple lines of evidence suggest that metformin, an antidiabetic drug, exerts anti-tumorigenic effects in different types of cancer. Metformin has been reported to affect cancer cells’ metabolism and proliferation mainly through the activation of AMP-activated protein kinase (AMPK). Here, we show that metformin inhibits, indeed, endometrial cancer cells’ growth and induces apoptosis. More importantly, we report that metformin affects two important pro-survival pathways, such as the Unfolded Protein Response (UPR), following endoplasmic reticulum stress, and the WNT/β-catenin pathway. GRP78, a key protein in the pro-survival arm of the UPR, was indeed downregulated, while GADD153/CHOP, a transcription factor that mediates the pro-apoptotic response of the UPR, was upregulated at both the mRNA and protein level. Furthermore, metformin dramatically inhibited β-catenin mRNA and protein expression. This was paralleled by a reduction in β-catenin transcriptional activity, since metformin inhibited the activity of a TCF/LEF-luciferase promoter. Intriguingly, compound C, a well-known inhibitor of AMPK, was unable to prevent all these effects, suggesting that metformin might inhibit endometrial cancer cells’ growth and survival through the modulation of specific branches of the UPR and the inhibition of the Wnt/β-catenin pathway in an AMPK-independent manner. Our findings may provide new insights on the mechanisms of action of metformin and refine the use of this drug in the treatment of endometrial cancer.

Inhibition of sirtuin 1 deacetylase by miR-211-5p provides a mechanism for the induction of cell death in breast cancer cells

Gene ◽  
2019 ◽  
Vol 711 ◽  
pp. 143939 ◽  
Author(s):  
Sahar Yarahmadi ◽  
Zohreh Abdolvahabi ◽  
Zahra Hesari ◽  
Masoumeh Tavakoli-Yaraki ◽  
Zeynab Yousefi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Sirtuin 1

scholarly journals Pterostilbene suppresses human endometrial cancer cells in vitro by down-regulating miR-663b

2017 ◽  
Vol 38 (10) ◽  
pp. 1394-1400 ◽  
Author(s):  
Ya-ling Wang ◽  
Yuan Shen ◽  
Jian-ping Xu ◽  
Kun Han ◽  
Yan Zhou ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cells

Estrogen receptor-mediated effects of tamoxifen on human endometrial cancer cells

2002 ◽  
Vol 192 (1-2) ◽  
pp. 93-104 ◽  
Author(s):  
Takako Sakamoto ◽  
Hidetaka Eguchi ◽  
Yoko Omoto ◽  
Takuya Ayabe ◽  
Hiroyuki Mori ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Endometrial Cancer ◽  
Cancer Cells ◽  
Mediated Effects

scholarly journals Protein kinase C-independent stimulation of activator protein-1 and c-Jun N-terminal kinase activity in human endometrial cancer cells by the LHRH agonist triptorelin

2001 ◽  
pp. 651-658 ◽  
Author(s):  
C Grundker ◽  
L Schlotawa ◽  
V Viereck ◽  
G Emons
Keyword(s):  
Cell Proliferation ◽  
Endometrial Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Fold Increase ◽  
Lhrh Agonist ◽  
Activator Protein 1 ◽  
Kinase C ◽  
Lhrh Receptor

OBJECTIVE: The expression of luteinizing hormone-releasing hormone (LHRH) and its receptor as a part of an autocrine regulatory system of cell proliferation has been demonstrated in a number of human malignant tumours, including cancers of the endometrium. The signalling pathway through which LHRH acts in endometrial cancer is distinct from that in pituitary gonadotrophs. The LHRH receptor interacts with the mitogenic signal transduction of growth factor receptors via activation of a phosphotyrosine phosphatase, resulting in down-regulation of cancer cell proliferation. In addition, LHRH activates nucleus factor kappaB (NFkappaB) and protects the cancer cells from apoptosis. This study was conducted to investigate additional signalling mechanisms of the LHRH receptor cooperating with NFkappaB in endometrial cancer cells. DESIGN: The LHRH agonist triptorelin-induced activator protein-1 (AP-1) activation was analysed using a pAP-1-SEAP reporter gene assay. Expression of c-jun mRNA was quantified using quantitative reverse transcription (RT)-PCR. c-Jun N-terminal kinase (JNK) activity was measured by quantification of phosphorylated c-Jun protein. RESULTS: Treatment of Ishikawa and Hec-1A human endometrial cancer cells with 100 nM triptorelin resulted in a 3.1-fold and 3.5-fold activation of AP-1 respectively (P<0.05). If the cells had been made quiescent, treatment with triptorelin (100 nM) resulted in a 41.7-fold and 48.6-fold increase of AP-1 activation respectively (P<0.001). This effect was completely blocked by simultaneous treatment with pertussis toxin (PTX). A 17.6-fold and 17.3-fold increase of c-jun mRNA expression respectively (P<0.001) was obtained after 20 min of stimulation with triptorelin (100 nM). Treatment with 1 nM triptorelin resulted in a 12.5-fold or an 11.9-fold increase, and treatment with 10 pM triptorelin resulted in a 6.5-fold or a 5.2-fold increase of maximal c-jun mRNA expression respectively (P<0.001). Maximal c-Jun phosphorylation (68.5-fold and 60.2-fold, respectively, P<0.001) was obtained after 90 min incubation with triptorelin (100 nM). CONCLUSIONS: These results suggest that the LHRH agonist triptorelin stimulates the activity of AP-1 in human endometrial cancer cells mediated through PTX-sensitive G-protein alphai. In addition, triptorelin activates JNK, known to activate AP-1. In earlier investigations we have shown that triptorelin does not activate phospholipase and protein kinase C (PKC) in endometrial cancer cells. In addition, it has been demonstrated that triptorelin inhibits growth factor-induced mitogen activated protein kinase (MAPK, ERK) activity. Thus triptorelin-induced activation of the JNK/AP-1 pathway in endometrial cancer cells is independent of the known AP-1 activators, PKC or MAPK (ERK).

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