Evaluation of Apoptotic Signals in Human Cancer Malignant Melanoma Me45 and Ovarian Carcinoma SKOV3 Cell Death after Chemotherapeutic Reaction with Cisplatin

In this paper, the plasmon resonance effects of gold nanorods was used to achieve rapid photothermal therapy for malignant melanoma cells (A375 cells). After incubation with A375 cells for 24 h, gold nanorods were taken up by the cells and gold nanorod clusters were formed naturally in the organelles of A375 cells. After analyzing the angle and space between the nanorods in clusters, a series of numerical simulations were performed and the results show that the plasmon resonance coupling between the gold nanorods can lead to a field enhancement of up to 60 times. Such high energy localization causes the temperature around the nanorods to rise rapidly and induce cell death. In this treatment, a laser as low as 9.3 mW was used to irradiate a single cell for 20 s and the cell died two h later. The cell death time can also be controlled by changing the power of laser which is focused on the cells. The advantage of this therapy is low laser treatment power, short treatment time, and small treatment range. As a result, the damage of the normal tissue by the photothermal effect can be greatly avoided.

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Mitochondrial Markers for Cancer: Relevance to Diagnosis, Therapy, and Prognosis and General Understanding of Malignant Disease Mechanisms

ISRN Pathology ◽

10.5402/2012/217162 ◽

2012 ◽

Vol 2012 ◽

pp. 1-15 ◽

Cited By ~ 4

Author(s):

Boel De Paepe

Keyword(s):

Cell Death ◽

Cancer Cells ◽

Energy Production ◽

Malignant Disease ◽

Human Cancer ◽

Biosynthetic Pathways ◽

Mitochondrial Markers ◽

Pathologic Evaluation ◽

Disease Mechanisms ◽

Diagnosis Therapy

Cancer cells display changes that aid them to escape from cell death, sustain their proliferative powers, and shift their metabolism toward glycolytic energy production. Mitochondria are key organelles in many metabolic and biosynthetic pathways, and the adaptation of mitochondrial function has been recognized as crucial to the changes that occur in cancer cells. This paper zooms in on the pathologic evaluation of mitochondrial markers for diagnosing and staging of human cancer and determining the patients’ prognoses.

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The Application of Embelin for Cancer Prevention and Therapy

Molecules ◽

10.3390/molecules23030621 ◽

2018 ◽

Vol 23 (3) ◽

pp. 621 ◽

Cited By ~ 12

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.

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Molecular interactions of autophagy with the immune system and cancer

10.20944/preprints201706.0121.v1 ◽

2017 ◽

Author(s):

Yonggeun Hong ◽

Yunho Jin ◽

Yunkyung Hong ◽

Chanyoung Park

Keyword(s):

Cell Death ◽

Cancer Cell ◽

Human Cancer ◽

Therapeutic Option ◽

Cancer Cell Line ◽

Tissue Type ◽

Alternative Source ◽

Cancer Cell Death ◽

Cell Tissue ◽

Cellular Components

Autophagy is a highly conserved catabolic mechanism that mediates the degradation of damaged cellular components by inducing their fusion with lysosomes. This process provides cells with an alternative source of energy for the synthesis of new proteins and the maintenance of metabolic homeostasis in stressful environments. Numerous studies have demonstrated beneficial roles for the induction as well as the suppression of autophagy in cancer cells. Autophagy may induce either survival or death depending on the cell/tissue type. Radiation therapy is widely used therapeutic option to treat cancer, and it induces autophagy in human cancer cell line. Also, melatonin seems to affect cancer cell death via regulation of programmed cell death. In this review, we summarize the current understanding of autophagy and its regulation in cancer.

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Effect of Calomelanone, a Dihydrochalcone Analogue, on Human Cancer Apoptosis/Regulated Cell Death in an In Vitro Model

BioMed Research International ◽

10.1155/2020/4926821 ◽

2020 ◽

Vol 2020 ◽

pp. 1-16

Author(s):

Wasitta Rachakhom ◽

Ratana Banjerdpongchai

Keyword(s):

Cell Death ◽

Cancer Cells ◽

Hepg2 Cells ◽

Cytotoxic Effect ◽

Human Cancer ◽

Autophagic Flux ◽

Dependent Manner ◽

Anticancer Activities ◽

Human Cancer Cells ◽

Regulated Cell Death

Calomelanone, 2 ′ ,6 ′ -dihydroxy-4,4 ′ -dimethoxydihydrochalcone, possesses anticancer activities. This study was conducted to investigate the cytotoxic effect of calomelanone, a dihydrochalcone analogue, on human cancer cells and its associated mechanisms. The cytotoxic effect of calomelanone was measured by MTT assay. Annexin V-FITC/propidium iodide and DiOC6 staining that employed flow cytometry were used to determine the mode of cell death and reduction of mitochondrial transmembrane potential (MTP), respectively. Caspase activities were measured using specific substrates and colorimetric analysis. The expression levels of Bcl-2 family proteins were determined by immunoblotting. Reactive oxygen species were also measured using 2 ′ ,7 ′ -dihydrodichlorofluorescein diacetate and dihydroethidium (fluorescence dyes). Calomelanone was found to be toxic towards various human cancer cells, including acute promyelocytic HL-60 and monocytic leukemic U937 cells, in a dose-dependent manner at 24 h and human hepatocellular HepG2 cells at 48 h. However, the proliferation of HepG2 cells increased at 24 h. Calomelanone was found to induce apoptosis in HL-60 and U937 at 24 h and HepG2 apoptosis at 48 h via the intrinsic pathway by inducing MTP disruption. This compound also induced caspase-3, caspase-8, and caspase-9 activities. Calomelanone upregulated proapoptotic Bax and Bak and downregulated antiapoptotic Bcl-xL proteins in HepG2 cells. Moreover, signaling was also associated with oxidative stress in HepG2 cells. Calomelanone induced autophagy at 24 h of treatment, which was evidenced by staining with monodansylcadaverine (MDC) to represent autophagic flux. This was associated with a decrease of Akt (survival pathway) and an upregulation of Atg5 (the marker of autophagy). Thus, calomelanone induced apoptosis/regulated cell death in HL-60, U937, and HepG2 cells. However, it also induced autophagy in HepG2 depending on duration, dose, and type of cells. Thus, calomelanone could be used as a potential anticancer agent for cancer treatment. Nevertheless, acute and chronic toxicity should be further investigated in animals before conducting investigations in human patients.

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Suppression of Extracellular Signal-related Kinase and Activation of p38 MAPK Are Two Critical Events Leading to Caspase-8- and Mitochondria-mediated Cell Death in Phytosphingosine-treated Human Cancer Cells

Journal of Biological Chemistry ◽

10.1074/jbc.m309011200 ◽

2003 ◽

Vol 278 (50) ◽

pp. 50624-50634 ◽

Cited By ~ 91

Author(s):

Moon-Taek Park ◽

Jung-A Choi ◽

Min-Jeong Kim ◽

Hong-Duck Um ◽

Sangwoo Bae ◽

...

Keyword(s):

Cell Death ◽

Cancer Cells ◽

P38 Mapk ◽

Human Cancer ◽

Caspase 8 ◽

Critical Events ◽

Human Cancer Cells ◽

Extracellular Signal

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Comparison of Cellular Death Pathways after mTHPC-mediated Photodynamic Therapy (PDT) in Five Human Cancer Cell Lines

Cancers ◽

10.3390/cancers11050702 ◽

2019 ◽

Vol 11 (5) ◽

pp. 702 ◽

Cited By ~ 9

Author(s):

Carsten Lange ◽

Christiane Lehmann ◽

Martin Mahler ◽

Patrick J. Bednarski

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Photodynamic Therapy ◽

Cell Lines ◽

Cancer Cell ◽

Human Cancer ◽

Human Cancer Cell ◽

Human Cancer Cell Lines ◽

Cell Death Mechanisms

One of the most promising photosensitizers (PS) used in photodynamic therapy (PDT) is the porphyrin derivative 5,10,15,20-tetra(m-hydroxyphenyl)chlorin (mTHPC, temoporfin), marketed in Europe under the trade name Foscan®. A set of five human cancer cell lines from head and neck and other PDT-relevant tissues was used to investigate oxidative stress and underlying cell death mechanisms of mTHPC-mediated PDT in vitro. Cells were treated with mTHPC in equitoxic concentrations and illuminated with light doses of 1.8–7.0 J/cm2 and harvested immediately, 6, 24, or 48 h post illumination for analyses. Our results confirm the induction of oxidative stress after mTHPC-based PDT by detecting a total loss of mitochondrial membrane potential (Δψm) and increased formation of ROS. However, lipid peroxidation (LPO) and loss of cell membrane integrity play only a minor role in cell death in most cell lines. Based on our results, apoptosis is the predominant death mechanism following mTHPC-mediated PDT. Autophagy can occur in parallel to apoptosis or the former can be dominant first, yet ultimately leading to autophagy-associated apoptosis. The death of the cells is in some cases accompanied by DNA fragmentation and a G2/M phase arrest. In general, the overall phototoxic effects and the concentrations as well as the time to establish these effects varies between cell lines, suggesting that the cancer cells are not all dying by one defined mechanism, but rather succumb to an individual interplay of different cell death mechanisms. Besides the evaluation of the underlying cell death mechanisms, we focused on the comparison of results in a set of five identically treated cell lines in this study. Although cells were treated under equitoxic conditions and PDT acts via a rather unspecific ROS formation, very heterogeneous results were obtained with different cell lines. This study shows that general conclusions after PDT in vitro require testing on several cell lines to be reliable, which has too often been ignored in the past.

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