Displaying publications 1 - 20 of 908 in total

  1. Shafee N, AbuBakar S
    FEBS Lett., 2002 Jul 31;524(1-3):20-4.
    PMID: 12135735
    Dengue virus type 2 (DENV-2) infection induced apoptotic cellular DNA fragmentation in Vero cells within 8 days of infection. The addition of high concentrations of extracellular Zn(2+) but not Ca(2+), Mg(2+) or Mn(2+) to the cell culture medium hastened the detection of apoptosis to within 4 h after infection. No apoptotic cellular DNA fragmentation was detected in the cell culture treated with Zn(2+) alone or infected with heat- or ultraviolet light-inactivated DENV-2 in the presence of Zn(2+). These results suggest that (i) apoptosis is induced in African green monkey kidney cells infected with live DENV-2 and (ii) the addition of high extracellular Zn(2+) accelerates detection of apoptosis in the DENV-2-infected cells.
    Matched MeSH terms: Apoptosis/drug effects*; Apoptosis/physiology*
  2. Harith HH, Morris MJ, Kavurma MM
    Trends Endocrinol. Metab., 2013 Nov;24(11):578-87.
    PMID: 23948591 DOI: 10.1016/j.tem.2013.07.001
    Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has been extensively studied for its preferential ability to induce apoptosis of cancer cells. Beyond the cytotoxic capacity of TRAIL, new physiological and pathological roles for TRAIL have been identified, and there is now growing evidence supporting its involvement in the development of obesity and diabetes. This review summarizes the most recent findings associating TRAIL with obesity and diabetes in both humans and experimental settings. We also present and discuss some of the reported controversies behind TRAIL signaling and function. Understanding TRAIL mechanism(s) in vivo and its involvement in disease may lead to novel strategies to combat the growing pandemic of obesity and diabetes worldwide.
    Matched MeSH terms: TNF-Related Apoptosis-Inducing Ligand/metabolism*
  3. Shahdan, I.A., Rahman, M.T.
    The effectiveness of poultry stunning in producing swift slaughtering was analysed in response to the time needed for the chickens to become insensible upon neck cutting (Td) and the induction of myofiber apoptosis. In total, 49 chicken broilers (BW of 2.17 ± .24 kg) were sacrificed with pre-slaughter stunning, using a constant voltage stunner where the electric current varied between 7.2 to 124.3 mA, and without stunning. The electric current applied during stunning was found to have no effect on Td. Number of apoptotic myonuclei did not vary among stunned and unstunned meat. Apoptosis inducing factor (AIF) and caspase 3 expressions were also not detected in the meat samples of both stunned and unstunned groups at 1 d postmortem. Since the slaughtering process and stunning are associated with stress, the expression of 70 kDa-heat shock protein (Hsp70) was investigated. Moreover Hsp70 is also an inhibitor of apoptosis, by preventing the activation of AIF and apoptosome which stimulates caspase 3 activation. However, expression of Hsp70 was not induced in both stunned groups and unstunned groups. Together, this study found that poultry stunning does not affect Td and myofiber apoptosis.
    Matched MeSH terms: Apoptosis; Apoptosis Inducing Factor
  4. Ngai SC
    Curr Drug Targets, 2020;21(9):849-854.
    PMID: 32116190 DOI: 10.2174/1389450121666200302124426
    Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a natural protein expressed in a wide range of tissues in our body. It is a promising anti-cancer agent due to its selective killing of cancer cells, rendering normal cells unharmed. However, resistance occurs either intrinsically or develops over the course of TRAIL treatment. In view of its specificity to cancer cells, there is a pushing need to overcome TRAIL resistance. Curcumin (Cur), a natural active constituent of turmeric, has been evidenced to have anti-cancer properties. However, it is limited by its sparing solubility and low bioavailability. Combinational therapy is one of the most frequently used strategies to overcome these limitations, which has been proved to be more effective than monotherapy by achieving synergistic effects and reducing toxicity. This review aims to discuss TRAIL and its underlying apoptotic mechanisms, the combinational treatment of Cur and TRAIL in view of their respective limitations, and the underlying apoptotic mechanisms activated by the sensitization of cancers by Cur towards TRAIL-induced apoptosis. Finally, this review discusses the research gap and the author's insight into this research area in bridging the research gap from bench to bedside.
    Matched MeSH terms: Apoptosis; TNF-Related Apoptosis-Inducing Ligand
  5. Durani LW, Jaafar F, Tan JK, Tajul Arifin K, Mohd Yusof YA, Wan Ngah WZ, et al.
    Clin Ter, 2016;166(6):e365-73.
    PMID: 26794818 DOI: 10.7417/T.2015.1902
    Tocotrienols have been known for their antioxidant properties besides their roles in cellular signalling, gene expression, immune response and apoptosis. This study aimed to determine the molecular mechanism of tocotrienol-rich fraction (TRF) in preventing cellular senescence of human diploid fibroblasts (HDFs) by targeting the genes in senescence-associated signalling pathways.
    Matched MeSH terms: Apoptosis
  6. Ahmad Rohi Ghazali, Fazrina Hamzah, Wan Marahaini Wan Razali, Norizah Awang
    Alpinia conchigera (lengkuas kecil) merupakan sejenis tumbuhan herba yang sering digunakan sebagai rawatan alternatif
    dalam bidang perubatan tradisional. Kajian ini dijalankan untuk menilai kesan sitotoksik, genotoksik serta mod kematian
    sel yang disebabkan oleh ekstrak heksana A. conchigera ke atas sel hepar Chang. Asai MTT selama 24 jam telah dijalankan
    untuk mengenal pasti peratus viabiliti sel hepar Chang setelah dirawat dengan ekstrak heksana A. conchigera. Keputusan
    menunjukkan terdapat penurunan viabiliti sel secara signifi kan (p < 0.05) dengan nilai IC50 (8.6 μg/ml) berbanding kawalan
    negatif. Berdasarkan nilai IC50 ini, pewarnaan AO/PI dilakukan untuk menentukan mod kematian sel hepar Chang iaitu sama
    ada secara apoptosis atau nekrosis. Didapati bahawa terdapat perbezaan secara signifi kan (p < 0.05) bagi mod kematian
    sel hepar Chang secara apoptosis berbanding kawalan negatif. Dalam kajian ini, penentuan tahap kerosakan DNA sel
    hepar Chang turut dilakukan dengan menggunakan asai komet beralkali dengan nilai IC10 dan IC25 yang diperoleh daripada
    asai MTT (4 μg/ml dan 6 μg/ml) masing-masing. Setelah sel hepar Chang dirawat dengan ekstrak heksana A. conchigera
    selama 2 jam, didapati terdapat perbezaan secara signifi kan (p < 0.05) bagi peratus kerosakan DNA bagi kumpulan rawatan
    berbanding kawalan negatif. Kesimpulannya, ekstrak heksana A. conchigera memberi kesan sitotoksik dan genotoksik
    terhadap sel hepar Chang serta menyebabkan kematian sel secara apoptosis.
    Matched MeSH terms: Apoptosis
  7. Shahruzaman SH, Fakurazi S, Maniam S
    Cancer Manag Res, 2018;10:2325-2335.
    PMID: 30104901 DOI: 10.2147/CMAR.S167424
    Adaptive metabolic responses toward a low oxygen environment are essential to maintain rapid proliferation and are relevant for tumorigenesis. Reprogramming of core metabolism in tumors confers a selective growth advantage such as the ability to evade apoptosis and/or enhance cell proliferation and promotes tumor growth and progression. One of the mechanisms that contributes to tumor growth is the impairment of cancer cell metabolism. In this review, we outline the small-molecule inhibitors identified over the past decade in targeting cancer cell metabolism and the usage of some of these molecules in clinical trials.
    Matched MeSH terms: Apoptosis
  8. Norazizah S, Sazaly AB
    JUMMEC, 1997;2:19-21.
    Matched MeSH terms: Apoptosis
  9. Win TT, Yusuf Y, Jaafar H
    Malays J Med Sci, 2013 Mar;20(2):10-6.
    PMID: 23983572 MyJurnal
    Many studies on the role of apoptosis in cancer development and management have been undertaken. Apoptotic activity depends partly on the balance between anti-apoptotic (Bcl-2) and pro-apoptotic (Bax) activities. This study compared Bcl-2 and Bax expression in the tumour cells and endothelial cells of tumour blood vessels in soft tissue sarcoma, and examined the association of these with tumour characteristics.
    Matched MeSH terms: Apoptosis
  10. Wong SHM, Kong WY, Fang CM, Loh HS, Chuah LH, Abdullah S, et al.
    Crit. Rev. Oncol. Hematol., 2019 Nov;143:81-94.
    PMID: 31561055 DOI: 10.1016/j.critrevonc.2019.08.008
    Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions. Resistance to apoptosis is a hallmark of virtually all malignancies. Despite being a cause of pathological conditions, apoptosis could be a promising target in cancer treatment. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), also known as Apo-2 ligand (Apo2L), is a member of TNF cytokine superfamily. It is a potent anti-cancer agent owing to its specific targeting towards cancerous cells, while sparing normal cells, to induce apoptosis. However, resistance occurs either intrinsically or after multiple treatments which may explain why cancer therapy fails. This review summarizes the apoptotic mechanisms via extrinsic and intrinsic apoptotic pathways, as well as the apoptotic resistance mechanisms. It also reviews the current clinically tested recombinant human TRAIL (rhTRAIL) and TRAIL receptor agonists (TRAs) against TRAIL-Receptors, TRAIL-R1 and TRAIL-R2, in which the outcomes of the clinical trials have not been satisfactory. Finally, this review discusses the current strategies in overcoming resistance to TRAIL-induced apoptosis in pre-clinical and clinical settings.
    Matched MeSH terms: Apoptosis/drug effects; Receptors, TNF-Related Apoptosis-Inducing Ligand/agonists*; TNF-Related Apoptosis-Inducing Ligand/pharmacology; TNF-Related Apoptosis-Inducing Ligand/therapeutic use*
  11. Liew JC, Tan WS, Alitheen NB, Chan ES, Tey BT
    J Biosci Bioeng, 2010 Sep;110(3):338-44.
    PMID: 20547346 DOI: 10.1016/j.jbiosc.2010.02.017
    Serum deprivation inhibits cell growth and initiates apoptosis cell death in mammalian cell cultures. Since apoptosis is a genetically controlled cell death pathway, over-expression of anti-apoptotic proteins may provide a way to delay apoptosis. This study investigated the ability of the X-linked inhibitor of apoptosis protein (XIAP) to inhibit apoptosis induced by serum deprivation. Study includes evaluation of the ability of XIAP to prolong culture period and its effect on cell proliferation in serum-deprived media. The full length human XIAP was introduced into CHO-K1 cell lines and the effects of XIAP over-expression on the inhibition of apoptosis induced by serum-deprived conditions were examined. In batch cultures, cells over-expressing XIAP showed decreased levels of apoptosis and a higher number of viable cell under serum-deprived conditions compared to the control cell lines. The viability of control cells dropped to 40% after 2days of serum deprivation, the XIAP expressing cells still maintained at a viability higher than 90%. Further investigation revealed that the caspase-3 activity of the CHO-K1 cell line was inhibited as a result of XIAP expression.
    Matched MeSH terms: Apoptosis/physiology*; X-Linked Inhibitor of Apoptosis Protein/genetics; X-Linked Inhibitor of Apoptosis Protein/metabolism*
  12. Cheah SC, Appleton DR, Lee ST, Lam ML, Hadi AH, Mustafa MR
    Molecules, 2011 Mar 21;16(3):2583-98.
    PMID: 21441862 DOI: 10.3390/molecules16032583
    In the present study we investigated the effects of panduratin A, isolated from Boesenbergia rotunda, on proliferation and apoptosis in A549 human non-small cell lung cancer cells. Cell proliferation and induction of apoptosis was determined by the real-time cellular analyzer (RTCA), MTT assay and High Content Screening (HCS). The RTCA assay indicated that panduratin A exhibited cytotoxicity, with an IC₅₀ value of 4.4 µg/mL (10.8 µM). Panduratin A arrested cancer cells labeled with bromodeoxyuridine (BrdU) and phospho-Histone H3 in the mitotic phase. The cytotoxic effects of panduratin A were found to be accompanied by a dose-dependent induction of apoptosis, as assessed by DNA condensation, nuclear morphology and intensity, cell permeability, mitochondrial mass/ potential, F-actin and cytochrome c. In addition, treatment with an apoptosis-inducing concentration of panduratin A resulted in significant inhibition of Nuclear Factor-kappa Beta (NF-κB) translocation from cytoplasm to nuclei activated by tumor necrosis factor-alpha (TNF-α), as illustrated by the HCS assay. Our study provides evidence for cell growth inhibition and induction of apoptosis by panduratin A in the A549 cell line, suggesting its therapeutic potential as an NF-κB inhibitor.
    Matched MeSH terms: Apoptosis/drug effects*
  13. Wong RS
    PMID: 21943236 DOI: 10.1186/1756-9966-30-87
    Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions. It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely in human subjects.
    Matched MeSH terms: Apoptosis/drug effects*
  14. Fauzi AN, Norazmi MN, Yaacob NS
    Food Chem. Toxicol., 2011 Apr;49(4):871-8.
    PMID: 21167897 DOI: 10.1016/j.fct.2010.12.010
    Honey is reported to contain various compounds such as phenols, vitamins and antioxidants. The present study investigates the anticancer potential of Tualang honey (Agromas) (TH) in human breast (MCF-7 and MDA-MB-231) and cervical (HeLa) cancer cell lines; as well as in the normal breast epithelial cell line, MCF-10A. The cells were treated with increasing doses of TH (1-10%) for up to 72 h. Increase in lactate dehydrogenase (LDH) leakage from the cell membranes indicates that TH is cytotoxic to all three cancer cells with effective concentrations (EC(50)) of 2.4-2.8%. TH is however, not cytotoxic to the MCF-10A cells. Reactivity with annexin V fluorescence antibody and propidium iodide as analysed by flow cytometry and fluorescence microscopy shows that apoptosis occurred in these cancer cells. TH also reduced the mitochondrial membrane potential (Δψ(m)) in the cancer cell lines after 24h of treatment. The activation of caspase-3/7 and -9 was observed in all TH-treated cancer cells indicating the involvement of mitochondrial apoptotic pathway. This study shows that TH has significant anticancer activity against human breast and cervical cancer cell lines.
    Matched MeSH terms: Apoptosis*
  15. Goon JA, Noor Aini AH, Musalmah M, Yasmin Anum MY, Wan Ngah WZ
    Med J Malaysia, 2008 Oct;63(4):319-24.
    PMID: 19385493 MyJurnal
    Effect of Tai Chi exercise on the level of DNA damage using the comet assay, lymphocyte viability and frequency of sister chromatid exchange (SCE) were determined in adults aged above 45. Tai Chi participants of 7 years (n=35), showed higher level of normal DNA and lower level of mild and severely damaged DNA as compared to the sedentary subjects (n=35). The former are suggested to have effective DNA repair mechanism as their frequency of SCE was markedly lower. Higher lymphocyte apoptosis and proliferation found in the Tai Chi participants also indicated that the exercise promotes renewal and regeneration of lymphocytes.
    Matched MeSH terms: Apoptosis*
  16. Harith HH, Di Bartolo BA, Cartland SP, Genner S, Kavurma MM
    J Diabetes, 2016 Jul;8(4):568-78.
    PMID: 26333348 DOI: 10.1111/1753-0407.12339
    BACKGROUND: Insulin regulates glucose homeostasis but can also promote vascular smooth muscle (VSMC) proliferation, important in atherogenesis. Recently, we showed that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) stimulates intimal thickening via accelerated growth of VSMCs. The aim of the present study was to determine whether insulin-induced effects on VSMCs occur via TRAIL.

    METHODS: Expression of TRAIL and TRAIL receptor in response to insulin and glucose was determined by polymerase chain reaction. Transcriptional activity was assessed using wild-type and site-specific mutations of the TRAIL promoter. Chromatin immunoprecipitation studies were performed. VSMC proliferation and apoptosis was measured.

    RESULTS: Insulin and glucose exposure to VSMC for 24 h stimulated TRAIL mRNA expression. This was also evident at the transcriptional level. Both insulin- and glucose-inducible TRAIL transcriptional activity was blocked by dominant-negative specificity protein-1 (Sp1) overexpression. There are five functional Sp1-binding elements (Sp1-1, Sp1-2, Sp-5/6 and Sp1-7) on the TRAIL promoter. Insulin required the Sp1-1 and Sp1-2 sites, but glucose needed all Sp1-binding sites to induce transcription. Furthermore, insulin (but not glucose) was able to promote VSMC proliferation over time, associated with increased decoy receptor-2 (DcR2) expression. In contrast, chronic 5-day exposure of VSMC to 1 µg/mL insulin repressed TRAIL and DcR2 expression, and reduced Sp1 enrichment on the TRAIL promoter. This was associated with increased cell death.

    CONCLUSIONS: The findings of the present study provide a new mechanistic insight into how TRAIL is regulated by insulin. This may have significant implications at different stages of diabetes-associated cardiovascular disease. Thus, TRAIL may offer a novel therapeutic solution to combat insulin-induced vascular pathologies.

    Matched MeSH terms: Apoptosis/drug effects*; Receptors, TNF-Related Apoptosis-Inducing Ligand/genetics; Receptors, TNF-Related Apoptosis-Inducing Ligand/metabolism; TNF-Related Apoptosis-Inducing Ligand/genetics; TNF-Related Apoptosis-Inducing Ligand/metabolism*
  17. Gény C, Rivière G, Bignon J, Birlirakis N, Guittet E, Awang K, et al.
    J Nat Prod, 2016 Apr 22;79(4):838-44.
    PMID: 27008174 DOI: 10.1021/acs.jnatprod.5b00915
    Proteins of the Bcl-2 family are key targets in anticancer drug discovery. Disrupting the interaction between anti- and pro-apoptotic members of this protein family was the approach chosen in this study to restore apoptosis. Thus, a biological screening on the modulation of the Bcl-xL/Bak and Mcl-1/Bid interactions permitted the selection of Knema hookeriana for further phytochemical investigations. The ethyl acetate extract from the stem bark led to the isolation of six new compounds, three acetophenone derivatives (1-3) and three anacardic acid derivatives (4-6), along with four known anacardic acids (7-10) and two cardanols (11, 12). Their structures were elucidated by 1D and 2D NMR analysis in combination with HRMS experiments. The ability of these compounds to antagonize Bcl-xL/Bak and Mcl-1/Bid association was determined, using a protein-protein interaction assay, but only anacardic acid derivatives (4-10) exhibited significant binding properties, with Ki values ranging from 0.2 to 18 μM. Protein-ligand NMR experiments further revealed that anacardic acid 9, the most active compound, does not interact with the anti-apoptotic proteins Bcl-xL and Mcl-1 but instead interacts with pro-apoptotic protein Bid.
    Matched MeSH terms: Apoptosis; Apoptosis Regulatory Proteins
  18. Tay ST, Rohani MY, Ho TM, Devi S
    PMID: 12971561
    Using cultured mouse fibroblast L929 cells, this study demonstrated the hemolytic and cytotoxic activities and induction of apoptosis in cells infected with Orientia tsutsugamushi. Low levels of hemolytic activity were detected using heavily infected cells. No hemolysin or cytotoxin were detected in the infected culture fluid regardless of the pathogenicity of the O. tsutsugamushi strains in mice. Using propidium iodide uptake assay, acridine orange/ethidium bromide staining and terminal deoxynucleotide transferase-mediated dUTP-digoxigenin nick-end labeling assay, apoptosis was observed in L929 cells infected with Karp and Gilliam strains.
    Matched MeSH terms: Apoptosis*
  19. Tung J, Tew LS, Hsu YM, Khung YL
    Sci Rep, 2017 04 11;7(1):793.
    PMID: 28400564 DOI: 10.1038/s41598-017-00912-3
    Measuring at ~30 nm, a fully customizable holliday junction DNA nanoconstruct, was designed to simultaneously carry three unmodified SiRNA strands for apoptosis gene knockout in cancer cells without any assistance from commercial transfection kits. In brief, a holliday junction structure was intelligently designed to present one arm with a cell targeting aptamer (AS1411) while the remaining three arms to carry different SiRNA strands by means of DNA/RNA duplex for inducing apoptosis in cancer cells. By carrying the three SiRNA strands (AKT, MDM2 and Survivin) into triple negative breast MDA-MB-231 cancer cells, cell number had reduced by up to ~82% within 24 hours solely from one single administration of 32 picomoles. In the immunoblotting studies, up-elevation of phosphorylated p53 was observed for more than 8 hours while the three genes of interest were suppressed by nearly half by the 4-hour mark upon administration. Furthermore, we were able to demonstrate high cell selectivity of the nanoconstruct and did not exhibit usual morphological stress induced from liposomal-based transfection agents. To the best of the authors' knowledge, this system represents the first of its kind in current literature utilizing a short and highly customizable holliday DNA junction to carry SiRNA for apoptosis studies.
    Matched MeSH terms: Apoptosis/genetics*
  20. Rajandram R, Razack AH, Ng KL, Gobe GC
    J Kidney Cancer VHL, 2016;3(1):1-11.
    PMID: 28326275 DOI: 10.15586/jkcvhl.2016.47
    Although primary localised tumours of renal cell carcinoma (RCC) can be treated relatively successfully with surgery, metastatic RCC has poor prognosis because of late diagnosis and resistance to therapies. In the present study, we were interested in profiling the protein expression of "inhibitor of caspase-activated DNase" (ICAD), an apoptosis inhibitor, in kidney cancer and its paired normal kidney. Immunohistochemistry with automated batch staining and morphometry using digital pathology were used to compare ICAD in 121 RCC specimens with their paired normal kidney tissue. Tissue microarray of formalin-fixed, paraffin-embedded archival tissue was used. Intensity and localisation of ICAD were compared between normal and cancer samples, and against grading within the cancers. The results demonstrated that, in this cohort, ICAD was highly expressed in the proximal tubular epithelium of normal kidney, and significantly decreased in clear cell RCC tissue (p < 0.05) as well as other subtypes of RCC (p < 0.01) compared with normal kidney. There was a tendency towards nuclear localisation of ICAD in clear cell RCC, but not in other subtypes of RCC. No significant association was found between ICAD intensity and grade of RCC. In summary, down-regulation of ICAD occurs in RCC. ICAD normally inhibits DNA fragmentation and apoptosis; thus, its down-regulation was unexpected in a cancer known for its resistance to apoptosis. However, these RCC samples were from primary, not metastatic, RCC sites, and down-regulated ICAD may be part of a progressive pathway that promotes RCC metastasis.
    Matched MeSH terms: Apoptosis; Apoptosis Regulatory Proteins
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