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Página 1 a partir de 992 resultados
alpha-Tocopheryl succinate induces apoptosis in prostate cancer cells in part through inhibition of Bcl-xL/Bcl-2 function.
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Although the antitumor effect of alpha-tocopheryl succinate (vitamin E succinate) has been well demonstrated, its underlying mechanism remains elusive. This study provides evidence that inhibition of Bcl-xL/Bcl-2 function represents a major pathway whereby alpha-tocopheryl succinate mediates
Vitamin E succinate inhibits the function of androgen receptor and the expression of prostate-specific antigen in prostate cancer cells.
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Although epidemiological evidence indicates that a daily supplement of vitamin E may reduce the risk of prostate cancer, the detailed mechanism underlying this effect remains unclear. Here we demonstrate that alpha-tocopheryl succinate (VES) can suppress the expression of prostate-specific antigen
pH-sensitive nanoparticles of poly(L-histidine)-poly(lactide-co-glycolide)-tocopheryl polyethylene glycol succinate for anti-tumor drug delivery.
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A novel pH-sensitive polymer, poly(L-histidine)-poly(lactide-co-glycolide)-tocopheryl polyethylene glycol succinate (PLH-PLGA-TPGS), was synthesized to design a biocompatible drug delivery system for cancer chemotherapy. The structure of the PLH-PLGA-TPGS copolymer was confirmed by (1)H-NMR, FTIR
Capecitabine encapsulated chitosan succinate-sodium alginate macromolecular complex beads for colon cancer targeted delivery: in vitro evaluation.
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The present study aims to investigate the efficacy of the novel biopolymeric complex multiparticulate system consisting of chitosan succinate and alginate for the capecitabine-targeted delivery to colon cancer. A Box-Behnken design was used to optimize the CS-SA beads by considering the effect of
Vitamin E and prostate cancer: is vitamin E succinate a superior chemopreventive agent?
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There is convincing evidence that vitamin E succinate significantly reduces human prostate cancer growth in experimental models compared with alpha-tocopherol or tocopheryl acetate. Its intact delivery to cancer cells is questionable when administered orally; however, a study in transgenic mice
The potential of lactate and succinate to kill nutrient deprived tumor cells by intracellular acidification.
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We have investigated the ability of the weak acids, lactate, succinate, and the monomethylester of succinate, to cause intracellular acidification of EMT-6 and MGH-U1 cells. Each of the three substances caused a decrease of intracellular pH (pHi) when the cell lines were exposed at low extracellular
Endoplasmic reticulum stress contributes to vitamin E succinate-induced apoptosis in human gastric cancer SGC-7901 cells.
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Vitamin E succinate (RRR-alpha-tocopheryl succinate, VES), an efficient inducer of apoptosis, acts as a potent agent for cancer therapy. However, the mechanism by which VES mediates the effects are not yet fully understood. Here we studied the effect of endoplasmic reticulum (ER) stress and unfolded
alpha-Tocopheryl succinate sensitizes established tumors to vaccination with nonmatured dendritic cells.
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OBJECTIVE
Dendritic cells (DCs) are considered potential candidates for cancer immunotherapy due to their ability to process and present antigens to T cells and stimulate immune responses. However, DC-based vaccines have exhibited minimal effectiveness against established tumors in mice and human
Comparison of the subrenal capsule assay and succinate dehydrogenase inhibition test as drug sensitivity tests for cancer.
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The same chemotherapeutic agents were tested against fresh surgical explants of solid tumors obtained from 50 patients using the in vivo subrenal capsule (SRC) assay and the in vitro succinate dehydrogenase inhibition (SDI) test in comparison. Control growth adequate to meet evaluable assay criteria
Vitamin E succinate inhibits human prostate cancer cell growth via modulating cell cycle regulatory machinery.
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Several epidemiological studies have demonstrated that vitamin E is a chemopreventative agent for prostate cancer. alpha-Tocopheryl succinate (VES), a derivative of vitamin E, effectively modulates prostate cancer cell growth. However, little is known about the mechanisms regarding this action. Here
Vitamin E succinate (VES) induces Fas sensitivity in human breast cancer cells: role for Mr 43,000 Fas in VES-triggered apoptosis.
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Fas (CD95/APO-1) is an important mediator of apoptosis. We show that Fas-resistant MCF-7, MDA-MB-231, and MDA-MB-435 human breast cancer cells become responsive to anti-Fas (CD95) agonistic antibody-triggered apoptosis after pretreatment or cotreatment with vitamin E succinate (VES;
Evidence for role of transforming growth factor-beta in RRR-alpha-tocopheryl succinate-induced apoptosis of human MDA-MB-435 breast cancer cells.
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MDA-MB-435 human breast cancer cells treated with 10 micrograms/ml of RRR-alpha-tocopheryl succinate (vitamin E succinate, VES) for one, two, three, and four days exhibit 9%, 19%, 51%, and 73% apoptotic cells, respectively. Likewise, cells cultured for one, two, and three days with conditioned media
Peptide YY augments gross inhibition by vitamin E succinate of human pancreatic cancer cell growth.
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BACKGROUND
Vitamin E succinate (VES) significantly inhibits cell growth in vitro in breast, prostate, and skin cancer cell lines. Our study demonstrated similar inhibitory effects on Mia PaCa-2 pancreatic cancer cells at the same concentration of VES (10 pg/ml). Peptide YY (PYY) also inhibits
Prolonged lifespan and high incidence of neoplasms in NZB/NZW mice treated with hydrocortisone sodium succinate.
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This study investigated the effects of prolonged corticosteroid therapy on the course of spontaneous autoimmune disease and oncogenesis in NZB/NZW mice, an animal model of systemic lupus erythematosus. Twenty young female NZB/NZW mice were treated until death with low-dose hydrocortisone sodium
VCPA, a novel synthetic derivative of α-tocopheryl succinate, sensitizes human gastric cancer to doxorubicin-induced apoptosis via ROS-dependent mitochondrial dysfunction.
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Gastric carcinoma is a common malignant disease worldwide and has a dismal prognosis. Doxorubicin (DOX), one of the most widely used chemotherapeutic agents, has limited use because of its side effects and the development of tumor-cell resistance. Combinations of doxorubicin and non-cross-resistant
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