scholarly journals The TAM family as a therapeutic target in combination with radiation therapy

2017 ◽  
Vol 1 (5) ◽  
pp. 493-500 ◽  
Author(s):  
Garth W. Tormoen ◽  
Marka R. Crittenden ◽  
Michael J. Gough
Keyword(s):  
Cell Death ◽  
Radiation Therapy ◽  
Immune Responses ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Tyrosine Kinases ◽  
Cancer Cell Death ◽  
Radiation Induced Cancer ◽  
Tumor Environment ◽  
Radiation Induced

Radiation therapy is primarily a modality to kill cancer cells in the treatment field. It is becoming increasingly clear that radiation therapy can also be used to direct immune responses that have the potential to clear residual local or distant disease outside the treatment field. We believe that cancer cell death is the critical link between these processes. Understanding the handling of dying cancer cells by immune cells in the tumor environment is crucial to facilitate immune responses following radiation therapy. We review the role of the TAM (Tyro3 Axl Mertk) group of receptor tyrosine kinases and their role following radiation-induced cancer cell death in the tumor environment.

Magneto Mitochondrial Dysfunction Mediated Cancer Cell Death Using Intracellular Magnetic Nano-Transducers

2021 ◽  
Author(s):  
Wooram Park ◽  
Seok-Jo Kim ◽  
Paul Cheresh ◽  
Jeanho Yun ◽  
Byeongdu Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Therapy ◽  
Mitochondrial Dysfunction ◽  
Cancer Cells ◽  
Cancer Cell ◽  
High Sensitivity ◽  
Intrinsic Pathway ◽  
Cancer Cell Death

Mitochondria are crucial regulators of the intrinsic pathway of cancer cell death. The high sensitivity of cancer cells to mitochondrial dysfunction offers opportunities for emerging targets in cancer therapy. Herein,...

scholarly journals Selective imaging and cancer cell death via pH switchable near-infrared fluorescence and photothermal effects

2016 ◽  
Vol 7 (9) ◽  
pp. 5995-6005 ◽  
Author(s):  
Jingye Zhang ◽  
Zining Liu ◽  
Peng Lian ◽  
Jun Qian ◽  
Xinwei Li ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Near Infrared ◽  
Near Infrared Fluorescence ◽  
Ph Changes ◽  
Cancer Cell Death ◽  
Photothermal Effects

A theranostic probe is designed that specifically illuminates and photoablates cancer cells by sensing pH changes in the lysosomes and mitochondria.

scholarly journals Mitochondrial Complex I Inhibitors and Forced Oxidative Phosphorylation Synergize in Inducing Cancer Cell Death

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Roberta Palorini ◽  
Tiziana Simonetto ◽  
Claudia Cirulli ◽  
Ferdinando Chiaradonna
Keyword(s):  
Cell Death ◽  
Oxidative Phosphorylation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Complex I ◽  
Mitochondrial Complex I ◽  
Low Doses ◽  
Mitochondrial Complex ◽  
Cancer Cell Death ◽  
Glucose Depletion

Cancer cells generally rely mostly on glycolysis rather than oxidative phosphorylation (OXPHOS) for ATP production. In fact, they are particularly sensitive to glycolysis inhibition and glucose depletion. On the other hand mitochondrial dysfunctions, involved in the onset of the Warburg effect, are sometimes also associated with the resistance to apoptosis that characterizes cancer cells. Therefore, combined treatments targeting both glycolysis and mitochondria function, exploiting peculiar tumor features, might be lethal for cancer cells. In this study, we show that glucose deprivation and mitochondrial Complex I inhibitors synergize in inducing cancer cell death. In particular, our results reveal that low doses of Complex I inhibitors, ineffective on immortalized cells and in high glucose growth, become specifically cytotoxic on cancer cells deprived of glucose. Importantly, the cytotoxic effect of the inhibitors on cancer cells is strongly enhanced by forskolin, a PKA pathway activator, that we have previously shown to stimulate OXPHOS. Taken together, we demonstrate that induction in cancer cells of a switch from a glycolytic to a more respirative metabolism, obtained by glucose depletion or mitochondrial activity stimulation, strongly increases their sensitivity to low doses of mitochondrial Complex I inhibitors. Our findings might be a valuable approach to eradicate cancer cells.

Fluorinated thiazolidinols cause cell death in A549 lung cancer cells via PI3K/AKT/mTOR and MAPK/ERK signalling pathways

MedChemComm ◽  
2016 ◽  
Vol 7 (6) ◽  
pp. 1197-1203 ◽  
Author(s):  
Ravindra M. Kumbhare ◽  
Tulshiram L. Dadmal ◽  
Dinesh Kumar ◽  
M. Janaki Ramaiah ◽  
Anudeep Kota ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Lung Cancer Cells ◽  
Signalling Pathways ◽  
Lung Cancer Cell ◽  
Cancer Cell Death ◽  
A549 Lung Cancer Cell ◽  
A549 Lung

Fluorinated thiazolidinols cause A549 lung cancer cell death by acting via PI3K/Akt/mTOR and MEK/ERK pathways.

New Fe(iii) and Co(ii) salen complexes with pendant distamycins: selective targeting of cancer cells by DNA damage and mitochondrial pathways

2016 ◽  
Vol 45 (22) ◽  
pp. 9345-9353 ◽  
Author(s):  
Asfa Ali ◽  
Mohini Kamra ◽  
Arunoday Bhan ◽  
Subhrangsu S. Mandal ◽  
Santanu Bhattacharya
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Metal Complexes ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Cell Death ◽  
Salen Complexes ◽  
Selective Targeting

Distamycin like moieties conjugated with core Fe(iii) and Co(ii) based salens were synthesized and studied. The metal complexes showed better and differential activity toward cancer cell death.

Tripeptide consisting of benzyl protected di-cysteine and phenylalanine forms spherical assembly and induces cytotoxicity in cancer cells via apoptosis

RSC Advances ◽  
2016 ◽  
Vol 6 (113) ◽  
pp. 112667-112676 ◽  
Author(s):  
Biswadip Banerji ◽  
Moumita Chatterjee ◽  
Chandraday Prodhan ◽  
Keya Chaudhuri
Keyword(s):  
Cell Death ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Growth Medium ◽  
Cancer Cell Death

Tripeptide self assemblies in cell growth medium induce apoptosis and promoting cancer cell death at submicromolar concentration.

scholarly journals GPR55 Receptor Activation by the N-Acyl Dopamine Family Lipids Induces Apoptosis in Cancer Cells via the Nitric Oxide Synthase (nNOS) Over-Stimulation

2021 ◽  
Vol 22 (2) ◽  
pp. 622
Author(s):  
Mikhail G. Akimov ◽  
Alina M. Gamisonia ◽  
Polina V. Dudina ◽  
Natalia M. Gretskaya ◽  
Anastasia A. Gaydaryova ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Nitric Oxide Synthase ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Receptor Activation ◽  
Gene Expression Measurement ◽  
Fatty Acid Amides ◽  
Cancer Cell Death ◽  
Oxide Synthase

GPR55 is a GPCR of the non-CB1/CB2 cannabinoid receptor family, which is activated by lysophosphatidylinositol (LPI) and stimulates the proliferation of cancer cells. Anandamide, a bioactive lipid endocannabinoid, acts as a biased agonist of GPR55 and induces cancer cell death, but is unstable and psychoactive. We hypothesized that other endocannabinoids and structurally similar compounds, which are more hydrolytically stable, could also induce cancer cell death via GPR55 activation. We chemically synthesized and tested a set of fatty acid amides and esters for cell death induction via GPR55 activation. The most active compounds appeared to be N-acyl dopamines, especially N-docosahexaenoyl dopamine (DHA-DA). Using a panel of cancer cell lines and a set of receptor and intracellular signal transduction machinery inhibitors together with cell viability, Ca2+, NO, ROS (reactive oxygen species) and gene expression measurement, we showed for the first time that for these compounds, the mechanism of cell death induction differed from that published for anandamide and included neuronal nitric oxide synthase (nNOS) overstimulation with concomitant oxidative stress induction. The combination of DHA-DA with LPI, which normally stimulates cancer proliferation and is increased in cancer setting, had an increased cytotoxicity for the cancer cells indicating a therapeutic potential.

scholarly journals Nanoscale coordination polymers induce immunogenic cell death by amplifying radiation therapy mediated oxidative stress

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Zhusheng Huang ◽  
Yuxiang Wang ◽  
Dan Yao ◽  
Jinhui Wu ◽  
Yiqiao Hu ◽  
...  
Keyword(s):  
Cell Death ◽  
Radiation Therapy ◽  
Immune Responses ◽  
Coordination Polymers ◽  
Glutathione Depletion ◽  
Immunogenic Cell Death ◽  
Adaptive Immune ◽  
Cancer Models ◽  
Radiation Induced ◽  
Nanoscale Coordination Polymers

AbstractRadiation therapy can potentially induce immunogenic cell death, thereby priming anti-tumor adaptive immune responses. However, radiation-induced systemic immune responses are very rare and insufficient to meet clinical needs. Here, we demonstrate a synergetic strategy for boosting radiation-induced immunogenic cell death by constructing gadolinium-hemin based nanoscale coordination polymers to simultaneously perform X-ray deposition and glutathione depletion. Subsequently, immunogenic cell death is induced by sensitized radiation to potentiate checkpoint blockade immunotherapies against primary and metastatic tumors. In conclusion, nanoscale coordination polymers-sensitized radiation therapy exhibits biocompatibility and therapeutic efficacy in preclinical cancer models, and has the potential for further application in cancer radio-immunotherapy.

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