scholarly journals γ-Synuclein Promotes Cancer Cell Survival and Inhibits Stress- and Chemotherapy Drug-induced Apoptosis by Modulating MAPK Pathways

2002 ◽  
Vol 277 (38) ◽  
pp. 35050-35060 ◽  
Author(s):  
Zhong-Zong Pan ◽  
Wendy Bruening ◽  
Benoit I. Giasson ◽  
Virginia M.-Y. Lee ◽  
Andrew K. Godwin
Keyword(s):  
Cell Survival ◽  
Cancer Cell ◽  
Drug Induced ◽  
Chemotherapy Drug ◽  
Mapk Pathways ◽  
Cancer Cell Survival ◽  
Induced Apoptosis

scholarly journals CCR9 interactions support ovarian cancer cell survival and resistance to cisplatin-induced apoptosis in a PI3K-dependent and FAK-independent fashion

2010 ◽  
Vol 3 (1) ◽  
Author(s):  
Erica L Johnson ◽  
Rajesh Singh ◽  
Crystal M Johnson-Holiday ◽  
William E Grizzle ◽  
Edward E Partridge ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Survival ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Cancer Cell Survival ◽  
Induced Apoptosis

Targeting autophagy for the treatment of cancer

2018 ◽  
Vol 399 (7) ◽  
pp. 673-677 ◽  
Author(s):  
Simone Fulda
Keyword(s):  
Cell Death ◽  
Drug Treatment ◽  
Cell Survival ◽  
Cancer Cell ◽  
Anticancer Drug ◽  
Autophagic Cell Death ◽  
Eukaryotic Cells ◽  
Drug Induced ◽  
Cancer Cell Survival ◽  
Catabolic Process

Abstract Macroautophagy (herein termed autophagy) is evolutionarily highly conserved across eukaryotic cells and represents an intracellular catabolic process that targets damaged macromolecules and organelles for degradation. Autophagy is dysregulated in various human diseases including cancer. In addition, many drugs currently used for the treatment of cancer can engage autophagy, which typically promotes cancer cell survival by mitigating cellular stress. However, under certain circumstances activation of autophagy upon anticancer drug treatment can also trigger a lethal type of autophagy termed autophagic cell death (ACD). This may pave new avenues for exploiting the autophagic circuitry in oncology. This review presents the concept and some examples of anticancer drug-induced ACD.

scholarly journals Integrin Signaling in Cancer Cell Survival and Chemoresistance

2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
Fawzi Aoudjit ◽  
Kristiina Vuori
Keyword(s):  
Cell Survival ◽  
Cancer Cell ◽  
Antibody Therapy ◽  
Cancer Recurrence ◽  
Critical Factor ◽  
Cell Types ◽  
Integrin Signaling ◽  
Drug Induced ◽  
Major Pathway ◽  
Cancer Cell Survival

Resistance to apoptosis and chemotherapy is a hallmark of cancer cells, and it is a critical factor in cancer recurrence and patient relapse. Extracellular matrix (ECM) via its receptors, the integrins, has emerged as a major pathway contributing to cancer cell survival and resistance to chemotherapy. Several studies over the last decade have demonstrated that ECM/integrin signaling provides a survival advantage to various cancer cell types against numerous chemotherapeutic drugs and against antibody therapy. In this paper, we will discuss the major findings on how ECM/integrin signaling protects tumor cells from drug-induced apoptosis. We will also discuss the potential role of ECM in malignant T-cell survival and in cancer stem cell resistance. Understanding how integrins and their signaling partners promote tumor cell survival and chemoresistance will likely lead to the development of new therapeutic strategies and agents for cancer treatment.

scholarly journals Escin Chemosensitizes Human Pancreatic Cancer Cells and Inhibits the Nuclear Factor-kappaB Signaling Pathway

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
A. Rimmon ◽  
A. Vexler ◽  
L. Berkovich ◽  
G. Earon ◽  
I. Ron ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cyclin D ◽  
Pancreatic Cancer Cells ◽  
Cancer Cell Survival ◽  
Induced Apoptosis ◽  
Related Proteins

Background. There is an urgent need to develop new treatment strategies and drugs for pancreatic cancer that is highly resistant to radio-chemotherapy.Aesculus hippocastanum(the horse chestnut) known in Chinese medicine as a plant with anti-inflammatory, antiedema, antianalgesic, and antipyretic activities. The main active compound of this plant is Escin (C54H84O23).Objective. To evaluate the effect of Escin alone and combined with chemotherapy on pancreatic cancer cell survival and to unravel mechanism(s) of Escin anticancer activity.Methods. Cell survival was measured by XTT colorimetric assay. Synergistic effect of combined therapy was determined by CalcuSyn software. Cell cycle and induction of apoptosis were evaluated by FACS analysis. Expression of NF-κB-related proteins (p65, IκBα, and p-IκBα) and cyclin D was evaluated by western blot analysis.Results. Escin decreased the survival of pancreatic cancer cells with IC50= 10–20 M. Escin combined with gemcitabine showed only additive effect, while its combination with cisplatin resulted in a significant synergistic cytotoxic effect in Panc-1 cells. High concentrations of Escin induced apoptosis and decreased NF-κB-related proteins and cyclin D expression.Conclusions. Escin decreased pancreatic cancer cell survival, induced apoptosis, and downregulated NF-κB signaling pathway. Moreover, Escin sensitized pancreatic cancer cells to chemotherapy. Further translational research is required.

scholarly journals Macrophages are an abundant component of myeloma microenvironment and protect myeloma cells from chemotherapy drug–induced apoptosis

Blood ◽  
2009 ◽  
Vol 114 (17) ◽  
pp. 3625-3628 ◽  
Author(s):  
Yuhuan Zheng ◽  
Zhen Cai ◽  
Siqing Wang ◽  
Xiang Zhang ◽  
Jianfei Qian ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Survival ◽  
Stromal Cells ◽  
Myeloma Cell ◽  
Drug Induced ◽  
Myeloma Cells ◽  
Chemotherapy Drug ◽  
Response To Chemotherapy ◽  
Induced Apoptosis

Abstract Multiple myeloma remains an incurable disease. One of the major problems is that myeloma cells develop drug resistance on interaction with bone marrow stromal cells. In this study, we examined the effects of macrophages (Mφs), a type of stromal cells, on myeloma cell survival and response to chemotherapy. We showed that Mφ, in particular tumor-associated Mφ, is a protector of myeloma cells. The protective effect was dependent on direct contact between Mφs and myeloma cells. Mφs protected both myeloma cell lines and primary myeloma cells from spontaneous and chemotherapy drug-induced apoptosis by attenuating the activation and cleavage of caspase-dependent apoptotic signaling. These findings are clinically relevant because we found that CD68+ Mφs heavily infiltrate the bone marrow of patients with myeloma but not the bone marrow of control patients. Thus, our results indicate that Mφs may contribute to myeloma cell survival and resistance to chemotherapeutic treatment in vivo.

Co-targeting EGFR and Autophagy Impairs Ovarian Cancer Cell Survival during Detachment from the ECM

2015 ◽  
Vol 15 (3) ◽  
pp. 215-226 ◽  
Author(s):  
Zongyuan Yang ◽  
Yi Liu ◽  
Xiao Wei ◽  
Xiaoshui Zhou ◽  
Cheng Gong ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Survival ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Cancer Cell Survival

AMPA Receptor Antagonist CFM-2 Decreases Survivin Expression in Cancer Cells

2018 ◽  
Vol 18 (4) ◽  
pp. 591-596 ◽  
Author(s):  
Domingo Sanchez Ruiz ◽  
Hella Luksch ◽  
Marco Sifringer ◽  
Achim Temme ◽  
Christian Staufner ◽  
...  
Keyword(s):  
Cell Survival ◽  
Receptor Antagonist ◽  
Cancer Cells ◽  
Glutamate Receptors ◽  
Cancer Cell ◽  
Ampa Receptor ◽  
Ampa Receptors ◽  
Survivin Expression ◽  
Ampa Receptor Antagonist ◽  
Cancer Cell Survival

Background: Glutamate receptors are widely expressed in different types of cancer cells. α-Amino-3- hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors are ionotropic glutamate receptors which are coupled to intracellular signaling pathways that influence cancer cell survival, proliferation, and migration. Blockade of AMPA receptors by pharmacologic compounds may potentially constitute an effective tool in anticancer treatment strategies. Method: Here we investigated the impact of the AMPA receptor antagonist CFM-2 on the expression of the protein survivin, which is known to promote cancer cell survival and proliferation. We show that CFM-2 inhibits survivin expression at mRNA and protein levels and decreases the viability of cancer cells. Using a stably transfected cell line which overexpresses survivin, we demonstrate that over-expression of survivin enhances cancer cell viability and attenuates CFM-2–mediated inhibition of cancer cell growth. Result: These findings point towards suppression of survivin expression as a new mechanism contributing to anticancer effects of AMPA antagonists.

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