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  1. Malays Orthop J, 2021 Mar;15(1):156.
    PMID: 33880167
    [This corrects the article DOI: 10.5704/MOJ.2011.019.][This corrects the article DOI: 10.5704/MOJ.1611.015.].
    Matched MeSH terms: Apoptosis
  2. 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*
  3. 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*
  4. Shahdan, I.A., Rahman, M.T.
    MyJurnal
    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
  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
    MyJurnal
    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. 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
  9. Norazizah S, Sazaly AB
    JUMMEC, 1997;2:19-21.
    Matched MeSH terms: Apoptosis
  10. Break MKB, Chiang M, Wiart C, Chin CF, Khoo ASB, Khoo TJ
    Nutr Cancer, 2021;73(3):473-483.
    PMID: 32270712 DOI: 10.1080/01635581.2020.1751217
    Boesenbergia rotunda (L.) Mansf. is an edible herb that is commonly used in the cuisine of several Asian countries. Studies have shown that it possesses high bioactivity against a variety of cancer cells. In this study, we investigated the cytotoxic activity of Boesenbergia rotunda rhizomes and some of its constituents on nasopharyngeal carcinoma cells (HK1). MTT assay results showed that the methanolic and hexane extracts of Boesenbergia rotunda decreased HK1 cell viability with IC50 values of 136 µg/ml and 66 µg/ml, respectively. Cardamonin, a constituent of Boesenbergia rotunda, exhibited the highest cytotoxic activity with an IC50 value of 27 μg/ml. Further studies on cardamonin revealed that it inhibited the migration of HK1 cells, caused G2/M-phase arrest and induced apoptosis. Apoptosis was induced via activating caspase-8 and caspase-3, but independent of caspase-9. This indicated that cardamonin induced extrinsic apoptosis. Western blot analysis further showed that cardamonin caused extrinsic apoptosis, as the expression levels of intrinsic apoptosis-related proteins (Bcl-XL, Bcl-2 and Bax), were not affected. Finally, JC-1 staining of HK1 cells revealed an increase in the mitochondrial membrane potential after treatment, further proving that cardamonin did not induce apoptosis via the intrinsic pathway. These results reflect cardamonin's potential as an anticancer agent.
    Matched MeSH terms: Apoptosis
  11. 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/drug effects*; TNF-Related Apoptosis-Inducing Ligand/pharmacology*
  12. Azman KF, Safdar A, Zakaria R
    Exp Gerontol, 2021 07 15;150:111372.
    PMID: 33905879 DOI: 10.1016/j.exger.2021.111372
    Aging is associated with a variety of morphological and functional changes in the liver. Oxidative stress and inflammation are now widely accepted as the main mechanisms involved in the aging process that may subsequently cause severe injury to mitochondrial DNA which leads to apoptosis. As aging may increase the risks for various liver diseases and plays as an adverse prognostic factor increasing the mortality rate, knowledge regarding the mechanisms of age-related liver susceptibility and the possible therapeutic interventions is imperative. Due to cost and time constraints, a mimetic aging model is generally preferred to naturally aged animals to study the underlying mechanisms of aging liver. The use of D-galactose in aging research is dated back to 1962 and has since been used widely. This review aims to comprehensively summarize the effects of D-galactose-induced aging on the liver and the underlying mechanisms involved. Its potential therapeutic interventions are also discussed. It is hoped that this invaluable information may facilitate researchers in choosing the appropriate aging model and provide a valuable platform for testing potential therapeutic strategies for the prevention and treatment of age-related liver diseases.
    Matched MeSH terms: Apoptosis
  13. 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*
  14. 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*
  15. Chaudhry GE, Sohimi NKA, Mohamad H, Zafar MN, Ahmed A, Sung YY, et al.
    Asian Pac J Cancer Prev, 2021 Feb 01;22(S1):17-24.
    PMID: 33576208 DOI: 10.31557/APJCP.2021.22.S1.17
    OBJECTIVE: Liver cancer is one of the most common causes of cancer death, with reduced survival rates. The development of new chemotherapeutic agents is essential to find effective cytotoxic drugs that give minimum side effects to the surrounding healthy tissues. The main objective of the present study was to evaluate the cytotoxic effects and mechanism of cell death induced by the crude and diethyl ether extract of Xylocarpus mouccensis on the human hepatocellular carcinoma cell line.

    METHODS: The cytotoxicity activity was measured using the MTS assay. The mode of cell death determined by the apoptosis study, DNA fragmentation analysis done by using the TUNEL system. The pathway study or mechanism of apoptosis observed by study caspases 8, 9, 3/7 Glo-caspases method.

    RESULTS: In this study, the methanol extracts prepared from leaf Xylocarpus mouccensis leaf produced cytotoxicity effect with IC50 (72hr) < 30µg/ml. The IC50 value at 72 hours exerted by diethyl ether extract of Xylocarpus moluccensis leaf was 0.22 µg/ml, which was more cytotoxic than to that of crude methanol extract. The results obtained by the colorimetric TUNEL system suggest that methanol crude extract of Xylocarpus moluccensis (leaf), diethyl ether extract of Xylocarpus moluccensis (leaf) and methanol extract of Xylocarpus granatum (bark) induced DNA fragmentation in the HepG2 cell line. Besides, the caspase-Glo assay demonstrated that diethyl ether leaf extract of Xylocarpus moluccensis triggered apoptotic cell death via activation of caspases -8, and -3/7 However, no visible activation was noticed for caspase -9. Furthermore, TLC indicates the presence of potential metabolites in an extract of Xylocarpus moluccensis.

    CONCLUSION: Thus, the present study suggests the remarkable potential of active metabolites in the extract of Xylocarpus moluccensis as a future therapeutic agent for the treatment of cancer.
    .

    Matched MeSH terms: Apoptosis*; Apoptosis Regulatory Proteins/genetics; Apoptosis Regulatory Proteins/metabolism*
  16. 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*
  17. 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*
  18. 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*
  19. 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*
  20. 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
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