scholarly journals Cell‐permeable CaaX‐peptides affect K‐Ras downstream signaling and promote cell death in cancer cells

FEBS Journal ◽  
2020 ◽  
Author(s):  
Annika Klimpel ◽  
Katharina Stillger ◽  
Janica L. Wiederstein ◽  
Marcus Krüger ◽  
Ines Neundorf
Keyword(s):  
Cell Death ◽  
Cancer Cells ◽  
Downstream Signaling ◽  
Promote Cell Death

scholarly journals Carboxylate Analogues of Aryl-Urea-Substituted Fatty Acids That Target the Mitochondria in MDA-MB-231 Breast Cancer Cells to Promote Cell Death

ChemMedChem ◽  
2018 ◽  
Vol 13 (10) ◽  
pp. 1036-1043 ◽  
Author(s):  
Nooshin Koolaji ◽  
Tristan Rawling ◽  
Kirsi Bourget ◽  
Michael Murray
Keyword(s):  
Breast Cancer ◽  
Fatty Acids ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Promote Cell Death

scholarly journals Future Therapeutic Directions for Smac-Mimetics

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 406 ◽  
Author(s):  
Emma Morrish ◽  
Gabriela Brumatti ◽  
John Silke
Keyword(s):  
Clinical Trials ◽  
Cell Death ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Inhibitor Of Apoptosis ◽  
Growth Strategies ◽  
Promote Tumor Growth ◽  
Cell Death Program ◽  
Smac Mimetics ◽  
Promote Cell Death

It is well accepted that the ability of cancer cells to circumvent the cell death program that untransformed cells are subject to helps promote tumor growth. Strategies designed to reinstate the cell death program in cancer cells have therefore been investigated for decades. Overexpression of members of the Inhibitor of APoptosis (IAP) protein family is one possible mechanism hindering the death of cancer cells. To promote cell death, drugs that mimic natural IAP antagonists, such as second mitochondria-derived activator of caspases (Smac/DIABLO) were developed. Smac-Mimetics (SMs) have entered clinical trials for hematological and solid cancers, unfortunately with variable and limited results so far. This review explores the use of SMs for the treatment of cancer, their potential to synergize with up-coming treatments and, finally, discusses the challenges and optimism facing this strategy.

scholarly journals Epigenetic Modifications in Thyroid Cancer Cells Restore NIS and Radio-Iodine Uptake and Promote Cell Death

2018 ◽  
Vol 7 (4) ◽  
pp. 61 ◽  
Author(s):  
Sabine Wächter ◽  
Alexander Damanakis ◽  
Moritz Elxnat ◽  
Silvia Roth ◽  
Annette Wunderlich ◽  
...  
Keyword(s):  
Cell Death ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Epigenetic Modifications ◽  
Iodine Uptake ◽  
Thyroid Cancer Cells ◽  
Promote Cell Death

scholarly journals Bromoethylindole (BEI-9) redirects NF-κB signaling induced by camptothecin and TNFα to promote cell death in colon cancer cells

APOPTOSIS ◽  
2017 ◽  
Vol 22 (12) ◽  
pp. 1553-1563 ◽  
Author(s):  
Rupak Chowdhury ◽  
Dominique Gales ◽  
Paloma Valenzuela ◽  
Sonni Miller ◽  
Teshome Yehualaeshet ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Promote Cell Death

Abstract 1672: Ganoderma lucidum (Reishi) induces autophagy in inflammatory breast cancer cells to promote cell death.

2013 ◽  
Author(s):  
Raysa Rosario-Acevedo ◽  
Tiffany Rios ◽  
Ivette Suarez-Arroyo ◽  
Luis A. Cubano ◽  
Michelle M. Martínez-Montemayor
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Inflammatory Breast Cancer ◽  
Ganoderma Lucidum ◽  
Breast Cancer Cells ◽  
Promote Cell Death

scholarly journals Lipid rafts as signaling hubs in cancer cell survival/death and invasion: implications in tumor progression and therapy

2020 ◽  
Vol 61 (5) ◽  
pp. 611-635 ◽  
Author(s):  
Faustino Mollinedo ◽  
Consuelo Gajate
Keyword(s):  
Signal Transduction ◽  
Cell Death ◽  
Tumor Progression ◽  
Cell Survival ◽  
Cancer Cells ◽  
Lipid Rafts ◽  
Critical Role ◽  
Death Receptors ◽  
Signaling Molecules ◽  
Downstream Signaling

Cholesterol/sphingolipid-rich membrane domains, known as lipid rafts or membrane rafts, play a critical role in the compartmentalization of signaling pathways. Physical segregation of proteins in lipid rafts may modulate the accessibility of proteins to regulatory or effector molecules. Thus, lipid rafts serve as sorting platforms and hubs for signal transduction proteins. Cancer cells contain higher levels of intracellular cholesterol and lipid rafts than their normal non-tumorigenic counterparts. Many signal transduction processes involved in cancer development (insulin-like growth factor system and phosphatidylinositol 3-kinase-AKT) and metastasis [cluster of differentiation (CD)44] are dependent on or modulated by lipid rafts. Additional proteins playing an important role in several malignant cancers (e.g., transmembrane glycoprotein mucin 1) are also being detected in association with lipid rafts, suggesting a major role of lipid rafts in tumor progression. Conversely, lipid rafts also serve as scaffolds for the recruitment and clustering of Fas/CD95 death receptors and downstream signaling molecules leading to cell death-promoting raft platforms. The partition of death receptors and downstream signaling molecules in aggregated lipid rafts has led to the formation of the so-called cluster of apoptotic signaling molecule-enriched rafts, or CASMER, which leads to apoptosis amplification and can be pharmacologically modulated. These death-promoting rafts can be viewed as a linchpin from which apoptotic signals are launched. In this review, we discuss the involvement of lipid rafts in major signaling processes in cancer cells, including cell survival, cell death, and metastasis, and we consider the potential of lipid raft modulation as a promising target in cancer therapy.

Activation of the intrinsic-apoptotic pathway in LNCaP prostate cancer cells by genistein- topotecan combination treatments

2013 ◽  
Vol 3 (3) ◽  
pp. 66 ◽  
Author(s):  
Vanessa Hörmann ◽  
Sivanesan Dhandayuthapani ◽  
James Kumi-Diaka ◽  
Appu Rathinavelu
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Treatment Options ◽  
Attractive Alternative ◽  
Intrinsic Apoptotic Pathway ◽  
Prostate Cancer Cells ◽  
Apoptotic Pathway ◽  
Combination Treatments

Background: Prostate cancer is the second most common cancer in American men. The development of alternative preventative and/or treatment options utilizing a combination of phytochemicals and chemotherapeutic drugs could be an attractive alternative compared to conventional carcinoma treatments. Genistein isoflavone is the primary dietary phytochemical found in soy and has demonstrated anti-tumor activities in LNCaP prostate cancer cells. Topotecan Hydrochloride (Hycamtin) is an FDA-approved chemotherapy for secondary treatment of lung, ovarian and cervical cancers. The purpose of this study was to detail the potential activation of the intrinsic apoptotic pathway in LNCaP prostate cancer cells through genistein-topotecan combination treatments. Methods: LNCaP cells were cultured in complete RPMI medium in a monolayer (70-80% confluency) at 37ºC and 5% CO2. Treatment consisted of single and combination groups of genistein and topotecan for 24 hours. The treated cells were assayed for i) growth inhibition through trypan blue exclusion assay and microphotography, ii) classification of cellular death through acridine/ ethidium bromide fluorescent staining, and iii) activation of the intrinsic apoptotic pathway through Jc-1: mitochondrial membrane potential assay, cytochrome c release and Bcl-2 protein expression.Results: The overall data indicated that genistein-topotecan combination was significantly more efficacious in reducing the prostate carcinoma’s viability compared to the single treatment options. In all treatment groups, cell death occurred primarily through the activation of the intrinsic apoptotic pathway.Conclusion: The combination of topotecan and genistein has the potential to lead to treatment options with equal therapeutic efficiency as traditional chemo- and radiation therapies, but lower cell cytotoxicity and fewer side effects in patients. Key words: topotecan; genistein; intrinsic apoptotic cell death

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