scholarly journals PARP inhibition sensitizes endometrial cancer cells to paclitaxel-induced apoptosis

2017 ◽  
Vol 13 (4) ◽  
pp. 2847-2851 ◽  
Author(s):  
Christine Dinkic ◽  
Friederike Jahn ◽  
Marek Zygmunt ◽  
Florian Schuetz ◽  
Joachim Rom ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cells ◽  
Parp Inhibition ◽  
Induced Apoptosis

Abstract 3810: Leptomycin B sensitizes ovarian and endometrial cancer cells to TRAIL-induced apoptosis

2015 ◽  
Author(s):  
François Fabi ◽  
France-Hélène Joncas ◽  
Sophie Parent ◽  
Valérie Leblanc ◽  
Eric Asselin
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cells ◽  
Leptomycin B ◽  
Induced Apoptosis

scholarly journals Effect of microRNA-29b on proliferation, migration, and invasion of endometrial cancer cells

2019 ◽  
Vol 47 (8) ◽  
pp. 3803-3817
Author(s):  
Jian Kong ◽  
Xiuting He ◽  
Yan Wang ◽  
Jie Li
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cells ◽  
Water Soluble ◽  
Migration And Invasion ◽  
Chemotherapy Response ◽  
Aberrant Expression ◽  
Altered Expression ◽  
Matrigel Invasion ◽  
Tensin Homolog ◽  
Induced Apoptosis

Objective Aberrant expression of microRNAs is a key regulator of tumorigenesis and progression in endometrial cancer. We assessed the effect of microRNA-29b (miR-29b) on proliferation, chemosensitivity, migration, and invasion of endometrial cancer cells. Methods The proliferation of endometrial cancer cells was examined by water-soluble tetrazolium (WST)-1 assay. The effects of miR-29b on migration and invasion were evaluated by transwell migration and Matrigel invasion assays. Western blotting was used to assess protein expression levels after altered expression of miR-29b. The effect of miR-29b on cisplatin-induced apoptosis was examined by Caspase-Glo 3/7 assay. Results miR-29b inhibited proliferation and decreased migration and invasion of endometrial cancer cells. It also enhanced the sensitivity of endometrial cancer cells to cisplatin and increased cisplatin-induced apoptosis by regulating expression of BAX and Bcl-2. Moreover, miR-29b changed the expression level of phosphatase and tensin homolog (PTEN) and p-AKT by directly binding to the 3′ untranslated region of PTEN. Conclusion miR-29b played important roles in proliferation and progression in endometrial cancer cells by direct regulation of PTEN. It might be used as a biomarker to predict chemotherapy response and prognosis in endometrial cancer.

scholarly journals Induction of apoptosis in RL95-2 human endometrial cancer cells by combination treatment with docosahexaenoic acid and triacsin C

2021 ◽  
Author(s):  
Soo‐Ho Chung ◽  
Hea-Hyeog Lee ◽  
Yeon-Suk Kim ◽  
Kisung Song ◽  
Tae-Hee Kim
Keyword(s):  
Endometrial Cancer ◽  
Docosahexaenoic Acid ◽  
Endometrial Carcinoma ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Combined Treatment ◽  
Carcinoma Cells ◽  
Tumour Development ◽  
Triacsin C ◽  
Induced Apoptosis

IntroductionDocosahexaenoic acid (DHA) supplementation has been reported to negatively correlate with cancer cell proliferation and tumour development in many cancer types. Although cumulative evidence has demonstrated the apoptotic effect and cytotoxicity of DHA against tumour development in many cell types, the precise cellular and biochemical mechanisms of DHA-induced apoptosis in human endometrial cancer cells have not been investigated.Material and methodsMTT assay was performed to confirm the degree of apoptosis by combining treatment with DHA and triacsin C in endometrial cancer cell line. The synergistic effects of triacsin C and DHA were identified by performing flowcytometry and immunoblotting analysis.ResultsCombined treatment with DHA and triacsin C significantly induced apoptosis in RL95-2 endometrial carcinoma cells. Combined treatment with 125 μM DHA and 5 μM triacsin C significantly increased the sub-G1 population and apoptotic fragments in endometrial carcinoma cells. It was also demonstrated that DHA and triacsin C induced apoptosis through mitochondrial pathways via caspases-9, -3, and -7 as well as through the extrinsic pathway by activation of caspase-8/BID.ConclusionsFurther elucidation of the apoptotic mechanisms involving DHA treatment with ACS ablation could shed light on possible new treatment strategies for endometrial cancer. In addition, further research into the mechanisms of DHA and triacsin C-induced apoptotic mechanisms may lead to the development of therapeutic strategies for endometrial cancer.

scholarly journals Autophagy inhibition augments resveratrol-induced apoptosis in Ishikawa endometrial cancer cells

2016 ◽  
Vol 12 (4) ◽  
pp. 2560-2566 ◽  
Author(s):  
Tomohiko Fukuda ◽  
Katsutoshi Oda ◽  
Osamu Wada-Hiraike ◽  
Kenbun Sone ◽  
Kanako Inaba ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cells ◽  
Induced Apoptosis ◽  
Autophagy Inhibition

scholarly journals PARP inhibition sensitizes p53-deficient breast cancer cells to doxorubicin-induced apoptosis

2005 ◽  
Vol 386 (1) ◽  
pp. 119-125 ◽  
Author(s):  
José Antonio MUÑOZ-GÁMEZ ◽  
David MARTÍN-OLIVA ◽  
Rocío AGUILAR-QUESADA ◽  
Ana CAÑUELO ◽  
M. Isabel NUÑEZ ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cytotoxic Effect ◽  
Parp Inhibition ◽  
Breast Cancer Cell Lines ◽  
Dependent Manner ◽  
Mitochondrial Potential ◽  
Induced Apoptosis

p53 deficiency confers resistance to doxo (doxorubicin), a clinically active and widely used antitumour anthracycline antibiotic. The purpose of the present study was to investigate the reversal mechanism of doxo resistance by the potent PARP [poly(ADP-ribose) polymerase] inhibitor ANI (4-amino-1,8-naphthalimide) in the p53-deficient breast cancer cell lines EVSA-T and MDA-MB-231. The effects of ANI, in comparison with doxo alone, on doxo-induced apoptosis, were investigated in matched pairs of EVSA-T or MDA-MB-231 with or without ANI co-treatment. Doxo elicited PARP activation as determined by Western blotting and immunofluorescence of poly(ADP-ribose), and ANI enhanced the cytotoxic activity of doxo 2.3 times and in a caspase-dependent manner. The long-term cytotoxic effect was studied by a colony-forming assay. Using this assay, ANI also significantly potentiates the long-term cytotoxic effect with respect to treatment with doxo alone. Decrease in mitochondrial potential together with an increase in cytochrome c release, association of Bax with the mitochondria and caspase 3 activation were also observed in the presence of ANI. Therefore PARP inhibition may represent a novel way of selectively targeting p53-deficient breast cancer cells. The underlying mechanism is probably a potentiation of unrepaired DNA damage, shifting from DNA repair to apoptosis due to the effective inhibition of PARP activity.

scholarly journals The GLP-1R Agonist Exendin-4 Attenuates Hyperglycemia-Induced Chemoresistance in Human Endometrial Cancer Cells Through ROS-Mediated Mitochondrial Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Yu Zhang ◽  
Juan Cheng ◽  
Jing Li ◽  
Junxian He ◽  
Xiaomao Li ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cells ◽  
Topoisomerase Ii ◽  
Prolonged Exposure ◽  
Endometrial Adenocarcinoma ◽  
Mitochondrial Pathway ◽  
Cell Counting ◽  
Normal Glucose ◽  
Topo Ii ◽  
Induced Apoptosis

This study aimed to assess the effects of the antidiabetic drug Exendin-4 (Exe-4), a GLP-1 receptor agonist, on the response of human endometrial cancer cells to chemotherapy under high glucose (HG) conditions. Cell viability was detected using a cell counting kit (CCK)-8. Cell apoptosis and reactive oxygen species (ROS) levels were measured by flow cytometry. Gene expression was evaluated by real-time PCR and immunoblotting. The chemotherapeutic drug cisplatin (DDP) dose-dependently inhibited both human endometrial adenocarcinoma Ishikawa and HEC1B cells, a response reversed by HG. Meanwhile, Exe-4 attenuated hyperglycemia’s effect by elevating intracellular lactate dehydrogenase (LDH) and ROS production. Similarly, DDP-induced elevation of intracellular rhodamine123 was attenuated by HG, and Exe-4 reversed HG’s impact. The chemoresistance genes multidrug resistance-associated protein 1 (MRP1) and P-glycoprotein (Pgp) were upregulated. At the same time, topoisomerase II (TOPO II) was downregulated under HG conditions, suggesting HG-induced chemoresistance. Exe-4 did not significantly influence the above genes. DDP downregulated Bcl-2 and Bcl-XL and upregulated Bax, cytosolic cytochrome c, and PARP under normal glucose (NG) versus HG conditions, and Exe-4 attenuated these effects. Upstream of Bax/Bcl, acetylated P53 was upregulated by DDP and downregulated by HG, whose effect was reversed by Exe-4. DPP treatment significantly induced apoptosis and cell cycle arrest in the S phase under NG, and HG reduced these effects. Prolonged exposure to HG induces DDP chemoresistance in human endometrial cancer cells but is alleviated by Exe-4.

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