Induction of apoptosis by hexamethylene bisacetamide is p53-dependent associated with telomerase activity but not with terminal differentiation.

Zhang, Zichen; Liong, Emily C.; Lau, Tyh; Leung, Ka Man; Fung, Phoenix; Tipoe, GL

doi:10.3892/ijo.16.5.887

Cited by 7 publications

(6 citation statements)

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“…The human colon adenocarcinoma cell lines SW1116 and HT‐29, which harbour mutant p53 genes ( Shao et al ., 1996 ; Zhang et al ., 2000 ), were purchased from American Type Culture Collection (Manassas, VA, USA). SW1116 and HT‐29 cells were maintained in RPMI‐1640 containing 10% fetal bovine serum (FBS), 100 μ mL −1 penicillin G, 100 μg mL −1 streptomycin and maintained at 37 °C, 95% humidity, and 5% carbon dioxide.…”

Section: Methodsmentioning

confidence: 99%

Bone morphogenetic protein signalling is required for the anti‐mitogenic effect of the proteasome inhibitor MG‐132 on colon cancer cells

Sung

et al. 2008

British J Pharmacology

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Background and purpose: Inhibition of proteasome has been emerging as a promising approach in pathway-directed cancer therapy. Bone morphogenetic protein (BMP) signalling, which is known to be regulated by the ubiquitin-proteasome pathway in osteoblasts, plays a crucial role in the suppression of gastrointestinal carcinogenesis. Here we sought to elucidate the antimitogenic effect of a proteasome inhibitor in relation to BMP signalling in colon cancer.

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Section: Methodsmentioning

confidence: 99%

Bone morphogenetic protein signalling is required for the anti‐mitogenic effect of the proteasome inhibitor MG‐132 on colon cancer cells

Sung

et al. 2008

British J Pharmacology

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“…This compound causes tumor cell lines to progressively accumulate in the G 1 phase of the cell cycle and undergo terminal differentiation or apoptosis (72). A decline in telomerase activity, which precedes the appearance of differentiated or apoptotic cells, has also been noted (60,61). The primary mechanism of action of this compound is unclear (73), but its actions result in changes in the activities of various genes whose products are involved in cell division and differentiation, including down-regulation of c-myc transcriptional activity (reviewed in Ref.…”

Section: Discussionmentioning

confidence: 99%

“…The reduction in telomerase activity was of slow onset and reached a maximum between 24-and 48-h exposure to HMBA (data not shown). This compound was tested because of its ability to induce terminal differentiation (59) and loss of telomerase activity (60,61) in tumor cell lines.…”

Section: Suppression Of Telomerase Activity In Tumor Cell Lines With mentioning

confidence: 99%

Induction of Telomerase Activity During Development of Human Mast Cells from Peripheral Blood CD34+ Cells: Comparisons with Tumor Mast-Cell Lines

Chaves-Dias

Hundley

Gilfillan

et al. 2001

The Journal of Immunology

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To further characterize the development of mast cells from human hemopoietic pluripotent cells we have investigated the expression of telomerase activity in cultured human peripheral blood CD34+ cells, and CD34+/CD117+/CD13+ progenitor mast cells selected therefrom, with the idea that induction of telomerase is associated with clonal expansion of CD34+/CD117+/CD13+ cells. A rapid increase in telomerase activity preceded proliferation of both populations of cells in the presence of stem cell factor and either IL-3 or IL-6. The induction was transient, and telomerase activity declined to basal levels well before the appearance of mature mast cells. Studies with pharmacologic inhibitors suggested that this induction was initially dependent on the p38 mitogen-activated protein kinase and phosphatidylinositol 3′-kinase, but once cell replication was underway telomerase activity, but not cell replication, became resistant to the effects of inhibitors. Tumor mast cell lines, in contrast, expressed persistently high telomerase activity throughout the cell cycle, and this expression was unaffected by inhibitors of all known signaling pathways in mast cells even when cell proliferation was blocked for extended periods. These results suggest that the transient induction of telomerase activity in human progenitor mast cells was initially dependent on growth factor-mediated signals, whereas maintenance of high activity in tumor mast cell lines was not dependent on intracellular signals or cell replication.

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“…NF-kB activation can lead to the enhanced expression of proinflammatory cytokines, chemokines, adhesion molecules, inflammatory receptors, and inflammatory enzymes such as iNOS and COX-2. [37][38][39] Therefore, the modulation of NF-kB activation may provide a direct way of inhibiting inflammatory mediators. 40) In our study, the hepatic TBA-reactive substance and ROS levels in db/db mice were 2.1 and 1.7 times higher than those of m/m mice, respectively (Figs.…”

Section: Discussionmentioning

confidence: 99%

The Beneficial Effects of Morroniside on the Inflammatory Response and Lipid Metabolism in the Liver of <i>db</i>/<i>db</i> Mice

Park

Yamabe

Noh

et al. 2009

Biological & Pharmaceutical Bulletin

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Diabetes mellitus is a major cause of mortality and morbidity worldwide, and its prevalence is increasing at an alarming rate. Hyperglycemia and dyslipidemia lead to complications associated with diabetes mellitus, and, also, the attenuation of oxidative stress and regulation of stress-sensitive signaling pathways have been considered as ways to alleviate diabetes. [1][2][3][4] Hyperglycemia causes oxidative stress by two mechanisms: first, by decreasing the regeneration of the important cellular antioxidant, reduced glutathione (GSH) from oxidized glutathione (GSSG), and second, by decreasing the availability of reduced nicotinamide adenine dinucleotide phosphate (NADPH). Furthermore, hyperglycemia-induced reactive oxygen species (ROS) stimulate the activation of protein kinase C (PKC), formation of advanced glycation endproducts (AGE), and sorbitol accumulation. Also, increased ROS lead to the activation of nuclear factor-kappa B (NF-kB), and activated NF-kB can enhance the expression of proinflammatory cytokines, chemokines, adhesion molecules, inflammatory receptors, and inflammatory enzymes such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). 5-7)Dyslipidemia is the abnormal state of elevated cholesterol, triglyceride, and low-density lipoprotein or decreased highdensity lipoprotein in the plasma level that contribute to the development of atherosclerosis. Dyslipidemia is a risk factor for coronary artery disease, a leading cause of mortality in patients with diabetes mellitus. [8][9][10] Triglyceride is involved in the ectopic accumulation of lipid stores in the liver and are associated with a number of diseases such as metabolic syndrome and type 2 diabetes. Critical players in potentiating the promoting effect of hyperinsulinemia on hepatic lipid accumulation are the anabolic transcription factor peroxisome proliferator activated receptor a (PPARa) and sterol regulatory element binding proteins (SREBPs), which upregulate genes such as those for fatty acid synthase and cholesterol levels. [11][12][13] Corni Fructus (Cornus officinalis SIEB. et ZUCC.) is a rich source of iridoid glycosides in traditional medicine.14) Iridoids are a group of natural products belonging to the terpenoids, which are ubiquitous in plants. However, only a limited number of taxa possess the enzymes that give rise to the cyclopentane ring that is characteristic of the carbocyclic iridoids.15) Morroniside is a carbocyclic iridoid glycoside which has been reported to exhibit marked antioxidant activity. 16) In our previous studies, we reported the beneficial effect of morroniside on streptozotocin-induced type 1 diabetic renal damage. The administration of morroniside could ameliorate hyperglycemia, renal oxidative stress, and inflammation in diabetic rats. 17) However, the effect of morroniside on the type 2 diabetic liver, especially in dyslipidemia, has not yet been determined. The liver is an important organ for maintaining glucose metabolism and lipid homeostasis, since it can store (via glycogen synthes...

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Induction of apoptosis by hexamethylene bisacetamide is p53-dependent associated with telomerase activity but not with terminal differentiation.

Cited by 7 publications

References 0 publications

Bone morphogenetic protein signalling is required for the anti‐mitogenic effect of the proteasome inhibitor MG‐132 on colon cancer cells

Bone morphogenetic protein signalling is required for the anti‐mitogenic effect of the proteasome inhibitor MG‐132 on colon cancer cells

Induction of Telomerase Activity During Development of Human Mast Cells from Peripheral Blood CD34+ Cells: Comparisons with Tumor Mast-Cell Lines

The Beneficial Effects of Morroniside on the Inflammatory Response and Lipid Metabolism in the Liver of <i>db</i>/<i>db</i> Mice

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