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 Antidepressant Drug Enhanced Trail Receptor-2 Expression and Sensitized Lung Cancer Cells to Trail-Induced Apoptosis via Inhibition of Autophagic Flux

2020 ◽  
Author(s):  
K.M.A. Zinnah ◽  
Jae-Won Seol ◽  
Sang-Youel Park
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Antidepressant Drug ◽  
Lung Cancer Cells ◽  
Autophagic Flux ◽  
Trail Receptor ◽  
Treatment Needs ◽  
Induced Apoptosis ◽  
Autophagy Inhibition

Autophagy, an alternative cell death mechanism, is also termed programmed cell death type II. Autophagy in cancer treatment needs to be regulated. In our study, autophagy inhibition by desipramine or the autophagy inhibitor chloroquine (CQ) enhanced tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor-2 [death receptor (DR5)] expression and subsequently TRAIL-induced apoptosis in TRAIL-resistant A549 lung cancer cells. Genetic inhibition of DR5 substantially reduced desipramine-enhanced TRAIL-mediated apoptosis, proving that DR5 was required to increase TRAIL sensitivity in TRAIL-resistant cancer cells. Desipramine treatment upregulated p62 expression and promoted conversion of light chain 3 (LC3)-I to its lipid-conjugated form, LC3-II, indicating that autophagy inhibition occurred at the final stages of autophagic flux. Transmission electron microscopy analysis showed the presence of condensed autophagosomes, which resulted from the late stages of autophagy inhibition by desipramine. TRAIL, in combination with desipramine or CQ, augmented the expression of apoptosis-related proteins cleaved caspase-8 and cleaved caspase-3. Our results contributed to the understanding of the mechanism underlying the synergistic anti-cancer effect of desipramine and TRAIL and presented a novel mechanism of DR5 upregulation. These findings demonstrated that autophagic flux inhibition by desipramine potentiated TRAIL-induced apoptosis, suggesting that appropriate regulation of autophagy is required for sensitizing TRAIL-resistant cancer cells to TRAIL-mediated 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 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

GDC-0980-induced apoptosis is enhanced by autophagy inhibition in human pancreatic cancer cells

2014 ◽  
Vol 453 (3) ◽  
pp. 533-538 ◽  
Author(s):  
Jian-ying Tang ◽  
Tu Dai ◽  
Hui Zhang ◽  
Wu-jun Xiong ◽  
Ming-zheng Xu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells ◽  
Induced Apoptosis ◽  
Autophagy Inhibition

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.

The anti-malarial chloroquine suppresses proliferation and overcomes cisplatin resistance of endometrial cancer cells via autophagy inhibition

2015 ◽  
Vol 137 (3) ◽  
pp. 538-545 ◽  
Author(s):  
Tomohiko Fukuda ◽  
Katsutoshi Oda ◽  
Osamu Wada-Hiraike ◽  
Kenbun Sone ◽  
Kanako Inaba ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Autophagy Inhibition

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 Promotes Bevacizumab-induced Apoptosis and Proliferation Inhibition in Colorectal Cancer Cells

2018 ◽  
Vol 9 (18) ◽  
pp. 3407-3416 ◽  
Author(s):  
Zhi Zhao ◽  
Guanggai Xia ◽  
Ni Li ◽  
Ruping Su ◽  
Xiao Chen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Proliferation Inhibition ◽  
Colorectal Cancer Cells ◽  
Induced Apoptosis ◽  
Autophagy Inhibition
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