Investigation of Epothilone B-Induced Cell Death Mechanisms in Human Epithelial Cancer Cells –in Consideration of Combined Treatment With Ionizing Radiation

2015 ◽  
Vol 33 (6) ◽  
pp. 213-224 ◽  
Author(s):  
Tonja Baumgart ◽  
Stephan Kriesen ◽  
Oliver Neels ◽  
Guido Hildebrandt ◽  
Katrin Manda
Keyword(s):  
Cell Death ◽  
Ionizing Radiation ◽  
Cancer Cells ◽  
Combined Treatment ◽  
Epithelial Cancer ◽  
Epothilone B ◽  
Cell Death Mechanisms

scholarly journals The Application of Embelin for Cancer Prevention and Therapy

Molecules ◽  
2018 ◽  
Vol 23 (3) ◽  
pp. 621 ◽  
Author(s):  
Jeong-Hyeon Ko ◽  
Seok-Geun Lee ◽  
Woong Yang ◽  
Jae-Young Um ◽  
Gautam Sethi ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Prevention ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Human Cancer ◽  
Biological Properties ◽  
Multiple Cancer ◽  
Stat3 Signaling ◽  
Oncogenic Pathways ◽  
Cell Death Mechanisms

Embelin is a naturally-occurring benzoquinone compound that has been shown to possess many biological properties relevant to human cancer prevention and treatment, and increasing evidence indicates that embelin may modulate various characteristic hallmarks of tumor cells. This review summarizes the information related to the various oncogenic pathways that mediate embelin-induced cell death in multiple cancer cells. The mechanisms of the action of embelin are numerous, and most of them induce apoptotic cell death that may be intrinsic or extrinsic, and modulate the NF-κB, p53, PI3K/AKT, and STAT3 signaling pathways. Embelin also induces autophagy in cancer cells; however, these autophagic cell-death mechanisms of embelin have been less reported than the apoptotic ones. Recently, several autophagy-inducing agents have been used in the treatment of different human cancers, although they require further exploration before being transferred from the bench to the clinic. Therefore, embelin could be used as a potential agent for cancer therapy.

Methotrexate induced cell death mechanisms in MCF-7 adenocarcinoma breast cancer cells: Enhanced cytotoxicity following dff45-siRNA pre-treatment

Synergy ◽  
2018 ◽  
Vol 7 ◽  
pp. 10-16
Author(s):  
Fatemeh Kiani ◽  
Negin Rasouli ◽  
Tahereh Kashkoolinejad ◽  
Shahrokh Safarian ◽  
Seyed Jalal Zargar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Pre Treatment ◽  
Cell Death Mechanisms ◽  
Mcf 7

scholarly journals The Akt-inhibitor Erufosine induces apoptotic cell death in prostate cancer cells and increases the short term effects of ionizing radiation

2010 ◽  
Vol 5 (1) ◽  
pp. 108 ◽  
Author(s):  
Justine Rudner ◽  
Carola-Ellen Ruiner ◽  
René Handrick ◽  
Hans-Jörg Eibl ◽  
Claus Belka ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Ionizing Radiation ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Prostate Cancer Cells ◽  
Akt Inhibitor ◽  
Short Term ◽  
Short Term Effects

scholarly journals Inhibition of Autophagy by Deguelin Sensitizes Pancreatic Cancer Cells to Doxorubicin

2016 ◽  
Author(s):  
Xiao-Dong Xu ◽  
Yan Zhao ◽  
Min Zhang ◽  
Rui-Zhi He ◽  
Xiu-Hui Shi ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Combined Treatment ◽  
Protective Role ◽  
Pancreatic Cancer Cells ◽  
Effective Therapeutic Strategy ◽  
Cancer Experience

Pancreatic cancer is the fourth most common cause of cancer mortality worldwide. Furthermore, patients with pancreatic cancer experience limited benefit from current chemotherapeutic approaches because of drug resistance. Therefore, an effective therapeutic strategy for patients with pancreatic cancer is urgently required. Deguelin is a natural chemopreventive drug that exerts potent antiproliferative activity in solid tumors by inducing cell death. However, the molecular mechanisms underlying this activity have not been fully elucidated. Here we show that deguelin blocks autophagy and induces apoptosis in pancreatic cancer cells in vitro. Autophagy induced by doxorubicin plays a protective role in pancreatic cancer cells, and suppressing autophagy by chloroquine or silencing autophagy protein 5 enhanced doxorubicin-induced cell death. Similarly, inhibition of autophagy by deguelin also chemosensitized pancreatic cancer cell lines to doxorubicin. These findings suggest that deguelin has potent anticancer effects against pancreatic cancer and potentiates the anti-cancer effects of doxorubicin. These findings provide evidence that combined treatment with deguelin and doxorubicin represents an effective strategy for treating pancreatic cancer.

scholarly journals Graphene-Induced Hyperthermia (GIHT) Combined With Radiotherapy Fosters Immunogenic Cell Death

2021 ◽  
Vol 11 ◽  
Author(s):  
Malgorzata J. Podolska ◽  
Xiaomei Shan ◽  
Christina Janko ◽  
Rabah Boukherroub ◽  
Udo S. Gaipl ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Combined Treatment ◽  
Infrared Light ◽  
Immunogenic Cell Death ◽  
Tumor Cell Death ◽  
Induced Hyperthermia ◽  
B16f10 Cells ◽  
Melanoma B16f10

Radiotherapy and chemotherapy are the standard interventions for cancer patients, although cancer cells often develop radio- and/or chemoresistance. Hyperthermia reduces tumor resistance and induces immune responses resulting in a better prognosis. We have previously described a method to induce tumor cell death by local hyperthermia employing pegylated reduced graphene oxide nanosheets and near infrared light (graphene-induced hyperthermia, GIHT). The spatiotemporal exposure/release of heat shock proteins (HSP), high group mobility box 1 protein (HMGB1), and adenosine triphosphate (ATP) are reported key inducers of immunogenic cell death (ICD). We hypothesize that GIHT decisively contributes to induce ICD in irradiated melanoma B16F10 cells, especially in combination with radiotherapy. Therefore, we investigated the immunogenicity of GIHT alone or in combination with radiotherapy in melanoma B16F10 cells. Tumor cell death in vitro revealed features of apoptosis that is progressing fast into secondary necrosis. Both HSP70 and HMGB1/DNA complexes were detected 18 hours post GIHT treatment, whereas the simultaneous release of ATP and HMGB1/DNA was observed only 24 hours post combined treatment. We further confirmed the adjuvant potential of these released DAMPs by immunization/challenge experiments. The inoculation of supernatants of cells exposed to sole GIHT resulted in tumor growth at the site of inoculation. The immunization with cells exposed to sole radiotherapy rather fostered the growth of secondary tumors in vivo. Contrarily, a discreet reduction of secondary tumor volumes was observed in mice immunized with a single dose of cells and supernatants treated with the combination of GIHT and irradiation. We propose the simultaneous release of several DAMPs as a potential mechanism fostering anti-tumor immunity against previously irradiated cancer cells.

scholarly journals A Potential Antineoplastic Peptide of Human Prostate Cancer Cells Derived from the Lesser Spotted Dogfish (Scyliorhinus canicula L.)

Marine Drugs ◽  
2019 ◽  
Vol 17 (10) ◽  
pp. 585 ◽  
Author(s):  
Adrien Bosseboeuf ◽  
Amandine Baron ◽  
Elise Duval ◽  
Aude Gautier ◽  
Pascal Sourdaine ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cell Death ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Prostate Cancer Cells ◽  
Cell Death Mechanisms ◽  
Autophagy Inhibition

The purpose of the present paper is to investigate the mechanism of action of a pyroglutamate-modified peptide (pE-K092D) on in vitro growth inhibition of MDA-Pca-2b prostate cancer cells. This peptide was derived from a peptide previously isolated from the testis of the lesser spotted dogfish and identified as QLTPEALADEEEMNALAAR (K092D). The effect of the peptide on cell proliferation and cell death mechanisms was studied by flow cytometry. Cellular morphology and cytoskeleton integrity of peptide-treated cells were observed by immunofluorescence microscopy. Results showed the onset of peptide induced early cytoskeleton perturbation, inhibition of autophagy, inhibition of cell proliferation and, at the end, non-apoptotic cell death mechanisms (membrane destabilization and necrosis). All those mechanisms seem to contribute to MDA-Pca-2b growth inhibition by a main cytostatic fate.

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