Effect of Coffee-like Green Tea Preparation on Cytotoxicity of Human Cancer and Normal Cells

Cancer cells, relative to normal cells, demonstrate increased sensitivity to glucose-deprivation-induced cytotoxicity. To determine whether oxidative stress mediated by O2•− and hydroperoxides contributed to the differential susceptibility of human epithelial cancer cells to glucose deprivation, the oxidation of DHE (dihydroethidine; for O2•−) and CDCFH2 [5- (and 6-)carboxy-2′,7′-dichlorodihydrofluorescein diacetate; for hydroperoxides] was measured in human colon and breast cancer cells (HT29, HCT116, SW480 and MB231) and compared with that in normal human cells [FHC cells, 33Co cells and HMECs (human mammary epithelial cells)]. Cancer cells showed significant increases in DHE (2–20-fold) and CDCFH2 (1.8–10-fold) oxidation, relative to normal cells, that were more pronounced in the presence of the mitochondrial electron-transport-chain blocker, antimycin A. Furthermore, HCT116 and MB231 cells were more susceptible to glucose-deprivation-induced cytotoxicity and oxidative stress, relative to 33Co cells and HMECs. HT29 cells were also more susceptible to 2DG (2-deoxyglucose)-induced cytotoxicity, relative to FHC cells. Overexpression of manganese SOD (superoxide dismutase) and mitochondrially targeted catalase significantly protected HCT116 and MB231 cells from glucose-deprivation-induced cytotoxicity and oxidative stress and also protected HT29 cells from 2DG-induced cytotoxicity. These results show that cancer cells (relative to normal cells) demonstrate increased steady-state levels of ROS (reactive oxygen species; i.e. O2•− and H2O2) that contribute to differential susceptibility to glucose-deprivation-induced cytotoxicity and oxidative stress. These studies support the hypotheses that cancer cells increase glucose metabolism to compensate for excess metabolic production of ROS and that inhibition of glucose and hydroperoxide metabolism may provide a biochemical target for selectively enhancing cytotoxicity and oxidative stress in human cancer cells.

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Identification of Parasporin Genes in Vietnamese Isolates of Bacillus thuringiensis

Zeitschrift für Naturforschung C ◽

10.1515/znc-2008-1-225 ◽

2008 ◽

Vol 63 (1-2) ◽

pp. 139-143 ◽

Cited By ~ 7

Author(s):

Koichi Yasutake ◽

Akiko Uemori ◽

Ngo D. Binh ◽

Eiichi Mizuki ◽

Michio Ohba

Keyword(s):

Bacillus Thuringiensis ◽

Cancer Cells ◽

Human Cancer ◽

Nucleotide Sequence Analysis ◽

Hep G2 ◽

Normal Cells ◽

Proteolytic Activation ◽

Human Cancer Cells ◽

Genes Encoding

Four genes encoding parasporins, cytotoxins preferentially killing human cancer cells in vitro, were isolated from four Vietnamese strains of Bacillus thuringiensis. Nucleotide sequence analysis revealed that: (1) three genes fall into the two known classes, ps1Aa and ps1Ab, and (2) another one belongs to ps1Ac, a novel gene class established in this study. Upon proteolytic activation, parasporal protein of the organism with ps1Ac exhibited strong cytocidal activity against human cancer cells, HeLa and Hep G2, but not to non-cancer normal cells, UtSMC and HC.

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Green Tea Polyphenol Epigallocatechin-3-Gallate Differentially Modulates Nuclear Factor κB in Cancer Cells versus Normal Cells

Archives of Biochemistry and Biophysics ◽

10.1006/abbi.2000.1742 ◽

2000 ◽

Vol 376 (2) ◽

pp. 338-346 ◽

Cited By ~ 302

Author(s):

Nihal Ahmad ◽

Sanjay Gupta ◽

Hasan Mukhtar

Keyword(s):

Cancer Cells ◽

Green Tea ◽

Nuclear Factor Κb ◽

Nuclear Factor ◽

Tea Polyphenol ◽

Normal Cells ◽

Green Tea Polyphenol

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Epicatechins Purified from Green Tea (Camellia sinensis) Differentially Suppress Growth of Gender-Dependent Human Cancer Cell Lines

Evidence-based Complementary and Alternative Medicine ◽

10.1093/ecam/nel003 ◽

2006 ◽

Vol 3 (2) ◽

pp. 237-247 ◽

Cited By ~ 48

Author(s):

Mepur H. Ravindranath ◽

Thiruverkadu S. Saravanan ◽

Clarence C. Monteclaro ◽

Naftali Presser ◽

Xing Ye ◽

...

Keyword(s):

Prostate Cancer ◽

Ovarian Cancer ◽

Epithelial Ovarian Cancer ◽

Cell Lines ◽

Green Tea ◽

Cancer Cell ◽

Human Cancer ◽

Biological Effects ◽

Cancer Cell Lines

The anticancer potential of catechins derived from green tea is not well understood, in part because catechin-related growth suppression and/or apoptosis appears to vary with the type and stage of malignancy as well as with the type of catechin. Thisin vitrostudy examined the biological effects of epicatechin (EC), epigallocatechin (EGC), EC 3-gallate (ECG) and EGC 3-gallate (EGCG) in cell lines from human gender-specific cancers. Cell lines developed from organ-confined (HH870) and metastatic (DU145) prostate cancer, and from moderately (HH450) and poorly differentiated (HH639) epithelial ovarian cancer were grown with or without EC, EGC, ECG or EGCG. When untreated cells reached confluency, viability and doubling time were measured for treated and untreated cells. Whereas EC treatment reduced proliferation of HH639 cells by 50%, EGCG suppressed proliferation of all cell lines by 50%. ECG was even more potent: it inhibited DU145, HH870, HH450 and HH639 cells at concentrations of 24, 27, 29 and 30 µM, whereas EGCG inhibited DU145, HH870, HH450 and HH639 cells at concentrations 89, 45, 62 and 42 µM. When compared with EGCG, ECG more effectively suppresses the growth of prostate cancer and epithelial ovarian cancer cell lines derived from tumors of patients with different stages of disease.

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LN-6: a monoclonal antibody to vimentin expressed in non-hematopoietic mesenchymal cells and derived tumors and reactive in B5-fixed, paraffin-embedded tissues.

Journal of Histochemistry & Cytochemistry ◽

10.1177/37.9.2671152 ◽

1989 ◽

Vol 37 (9) ◽

pp. 1363-1370 ◽

Cited By ~ 4

Author(s):

E Stathopoulos ◽

G S Naeve ◽

C R Taylor ◽

A L Epstein

Keyword(s):

Monoclonal Antibody ◽

Human Cancer ◽

Wide Spectrum ◽

Mesenchymal Cells ◽

Lymphoid Cells ◽

Normal Cells ◽

Immunohistochemical Diagnosis ◽

Pathological Tissues

We generated a monoclonal antibody (MAb), designated LN-6, directed against human vimentin, which retains its immunoreactivity in B5-fixed, paraffin-embedded tissues. Like other anti-vimentin MAb, LN-6 was found to be reactive with a wide spectrum of human sarcomas and normal cells of mesenchymal derivation. However, unlike other similar reagents, LN-6 was unreactive with normal and malignant human lymphoid cells and therefore displays a more restricted immunoreactivity. Because of its ability to stain routinely processed pathological tissues and its marked reactivity with human sarcomas, LN-6 is a unique reagent for the immunohistochemical diagnosis of human cancer.

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Revisiting Szent-Györgyi's Cancer Hypothesis

10.21203/rs.3.rs-754303/v1 ◽

2021 ◽

Author(s):

Morris Alfred Johnson ◽

Michael Smits

Keyword(s):

Cell Lines ◽

Strong Interaction ◽

Human Cancer ◽

Glyoxalase I ◽

Human Cancer Cell ◽

Normal Cells ◽

Human Cancer Cell Lines ◽

Mouse Lymphoma Cells ◽

Near Term ◽

Mouse Lymphoma

Abstract Rationale for this communication • -The promine/retine hypothesis on the control of cancer never reached a definite conclusion.• -The chemical natures of promine and retine remain unsettled though usually assumed to be glyoxalases and methylglyoxal.• -Many years ago we published some data that indicated the hypothesis may be operating in plants in which glyoxalase I may exist in normal cells in an inhibited state rather than compartmentalized as in early versions of the hypothesis.• -Manju Ray in India has published many papers claiming that methylglyoxal can be used to successfully treat cancer in humans.• -We present here previously unpublished data that shows depriving glyoxalase I of GSH allows methylglyoxal to kill mouse lymphoma cells. During treatment of two human cancer cell lines, killing of one line was enhanced by blocking thioredoxin as well as GSH.It is hoped that what is conveyed here may reignite interest in the near term. Nuclear methodology and statistics can be found in Figure 1. The data show a strong interaction between the hypothesis and thiols. It is concluded that the hypothesis has yet to be thoroughly investigated.

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EGCG, green tea polyphenols and their synthetic analogs and prodrugs for human cancer prevention and treatment

Advances in Clinical Chemistry ◽

10.1016/b978-0-12-385855-9.00007-2 ◽

2011 ◽

pp. 155-177 ◽

Cited By ~ 116

Author(s):

Di Chen ◽

Sheng Biao Wan ◽

Huanjie Yang ◽

Jian Yuan ◽

Tak Hang Chan ◽

...

Keyword(s):

Cancer Prevention ◽

Green Tea ◽

Human Cancer ◽

Tea Polyphenols ◽

Green Tea Polyphenols ◽

Synthetic Analogs ◽

Prevention And Treatment

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Activation of PTHrP-cAMP-CREB1 signaling following p53 loss is essential for osteosarcoma initiation and maintenance

eLife ◽

10.7554/elife.13446 ◽

2016 ◽

Vol 5 ◽

Cited By ~ 22

Author(s):

Mannu K Walia ◽

Patricia MW Ho ◽

Scott Taylor ◽

Alvin JM Ng ◽

Ankita Gupte ◽

...

Keyword(s):

Human Cancer ◽

Point Mutations ◽

Therapeutic Targets ◽

Complete Loss ◽

Osteoblastic Cells ◽

Normal Cells ◽

P53 Pathway ◽

Common Cancer ◽

Frequent Event ◽

Camp Levels

Mutations in the P53 pathway are a hallmark of human cancer. The identification of pathways upon which p53-deficient cells depend could reveal therapeutic targets that may spare normal cells with intact p53. In contrast to P53 point mutations in other cancer, complete loss of P53 is a frequent event in osteosarcoma (OS), the most common cancer of bone. The consequences of p53 loss for osteoblastic cells and OS development are poorly understood. Here we use murine OS models to demonstrate that elevated Pthlh (Pthrp), cAMP levels and signalling via CREB1 are characteristic of both p53-deficient osteoblasts and OS. Normal osteoblasts survive depletion of both PTHrP and CREB1. In contrast, p53-deficient osteoblasts and OS depend upon continuous activation of this pathway and undergo proliferation arrest and apoptosis in the absence of PTHrP or CREB1. Our results identify the PTHrP-cAMP-CREB1 axis as an attractive pathway for therapeutic inhibition in OS.

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