Displaying publications 61 - 80 of 1087 in total

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  1. Boroumand Moghaddam A, Namvar F, Moniri M, Md Tahir P, Azizi S, Mohamad R
    Molecules, 2015;20(9):16540-65.
    PMID: 26378513 DOI: 10.3390/molecules200916540
    In the field of nanotechnology, the use of various biological units instead of toxic chemicals for the reduction and stabilization of nanoparticles, has received extensive attention. Among the many possible bio resources, biologically active products from fungi and yeast represent excellent scaffolds for this purpose. Since fungi and yeast are very effective secretors of extracellular enzymes and number of species grow fast and therefore culturing and keeping them in the laboratory are very simple. They are able to produce metal nanoparticles and nanostructure via reducing enzyme intracellularly or extracellularly. The focus of this review is the application of fungi and yeast in the green synthesis of inorganic nanoparticles. Meanwhile the domain of biosynthesized nanoparticles is somewhat novel; the innovative uses in nano medicine in different areas including the delivery of drug, cancer therapy, antibacterial, biosensors, and MRI and medical imaging are reviewed. The proposed signaling pathways of nanoparticles induced apoptosis in cancerous cells and anti-angiogenesis effects also are reviewed. In this article, we provide a short summary of the present study universally on the utilization of eukaryotes like yeast and fungi in the biosynthesis of nanoparticles (NPs) and their uses.
    Matched MeSH terms: Apoptosis
  2. Lye, H.M., Chiew, J.C., Siddique, M.M.
    MyJurnal
    The increasing and widespread use of synthetic food dyes raises health concerns and earlier reports suggest that certain food dyes might be harmful for human health. In this study, we have investigated the effect of three commonly used food dyes on human liver cell line, HepG2. Our findings suggest that these experimental food dyes significantly affect cell viability and this effect can be worsen in hyperglycemic condition. Accumulation of cellular fat was significantly higher in presence of these dyes. Expression pattern of the gene involved in regulating apoptosis suggests that that the observed cell death could be attributed to the activation of apoptotic pathway. These findings suggest that these experimental dyes might exert synergistic toxicity in hyperglycemia that need to be confirmed using suitable in vivo models.
    Matched MeSH terms: Apoptosis
  3. Gundamaraju R, Lu W, Manikam R
    Cancers (Basel), 2021 Jan 23;13(3).
    PMID: 33498743 DOI: 10.3390/cancers13030432
    The Warburg effect has immensely succored the study of cancer biology, especially in highlighting the role of mitochondria in cancer stemness and their benefaction to the malignancy of oxidative and glycolytic cancer cells. Mitochondrial genetics have represented a focal point in cancer therapeutics due to the involvement of mitochondria in programmed cell death. The mitochondrion has been well established as a switch in cell death decisions. The mitochondrion's instrumental role in central bioenergetics, calcium homeostasis, and translational regulation has earned it its fame in metastatic dissemination in cancer cells. Here, we revisit and review mechanisms through which mitochondria influence oncogenesis and metastasis by underscoring the oncogenic mitochondrion that is capable of transferring malignant capacities to recipient cells.
    Matched MeSH terms: Apoptosis
  4. Normah Awang, Siti Musslihah Shahidi, Asmah Hamid, Nurul Farahana Kamaludin
    MyJurnal
    Kesan sitotoksik sebatian organostanum (IV) terhadap pelbagai sel kanser telah dikaji oleh para saintis di seluruh dunia.Dalam kajian ini,dua sebatian baru organostanum (IV) iaitu difenilstanum (IV) etilfenilditiokarbamat (DFEF) dan difenilstanum (IV) butilfenilditiokarbamat (DFBF) telah diuji kesan sitotoksiknya terhadap sel eritroleukemia, K562. Sel eritroleukemia, K562 merupakan sel sasaran manakala, sel hepar Chang dan sel fibroblas V79 pula digunakan untuk menilai kesan kedua-dua sebatian ini terhadap sel bukan kanser. Kesan sitotoksik sebatian DFEF dan DFBF diuji menggunakan ujian asai 3-(4,5-dimetiltiazol-2-il)-2, 5-difeniltetrazolium bromida (MTT) dengan masa pendedahan 24 jam, 48 jam dan 72 jam pada kepekatan sebatian yang berbeza. Pemerhatian terhadap perubahan morfologi juga dilakukan menggunakan nilai IC50 yang diperolehi pada masa pendedahan seperti ujian asai MTT. Ujian sitotoksisiti telah menunjukkan sebatian DFEF dan DFBF adalah sangat toksik terhadap sel K562 dengan nilai IC50 kurang daripada 10 μM untuk ketiga-tiga masa pendedahan.Indeks pemilihan juga membuktikan bahawa kedua-dua sebatian memberikan kesan sitotoksik secara memilih terhadap sel K562 pada masa 48 jam dan 72 jam, tetapi pada masa 24 jam, sebatian ini bertindak secara tidak memilih terhadap sel K562 dan sel bukan kanser. Perubahan morfologi yang diperhatikan adalah menyerupai ciri-ciri apoptosis seperti pengecutan sel dan pembentukan jasad apoptotik dan juga nekrosis seperti sel lisis. Kesimpulannya, sebatian difenilstanum (IV) alkilfenilditiokarbamat berpotensi untuk dibangunkan sebagai agen antileukemia tetapi mekanisma khusus tindakan sebatian ini terhadap sel K562 perlu dikaji pada masa akan datang untuk menjelaskan potensi sebatian ini sebagai dadah antikanser yang baru.


    Matched MeSH terms: Apoptosis
  5. Fadaeinasab M, Karimian H, Omar H, Taha H, Khorasani A, Banisalam B, et al.
    J Asian Nat Prod Res, 2020 May;22(5):474-488.
    PMID: 30945944 DOI: 10.1080/10286020.2019.1588888
    One new indole alkaloid, reflexin A (1), and two known indoles, macusine B (2) and vinorine (3), were isolated from the bark of Rauvolfia reflexa. Their structures were elucidated by 1D and 2D NMR, UV, IR, and MS spectroscopic analyses. Compound 1 displayed anticancer activity against HCT-116 colon cancer cells with an IC50 value of 30.24 ± 0.75 µM. The results implied that the newly isolated 1 induced apoptosis in HCT-116 cells, suggesting its possible role as an anticancer agent. In vivo acute toxicity study was performed on compound 1 to evaluate its safety profile.
    Matched MeSH terms: Apoptosis
  6. Ang KP, Chan PF, Hamid RA
    J Biol Inorg Chem, 2021 10;26(7):833-853.
    PMID: 34476610 DOI: 10.1007/s00775-021-01892-6
    Tricyclohexylphosphanegold(I) n-mercaptobenzoate (n = 2, 3, 4) labelled as 1-3 were previously reported to significantly suppress thioredoxin reductase (TrxR) activities towards ovarian cancer cells, A2780, in vitro. Herein, we explored the role of 1-3 for their apoptosis inducing ability against A2780 cells. 1-3 exhibited IC50 values at 1.19 ± 0.03 µM, 2.28 ± 0.04 μM and 0.78 ± 0.01 μM, respectively, compared to cisplatin at 26.8 ± 0.15 µM. The compounds induced A2780 apoptosis via a caspase-dependent mitochondrion pathway as evidenced by ROS production, cytochrome c release, caspases-3/7, -8, -9 and -10 activation, APAF1 and BAX upregulation as well as BCL2A1 and BCL2 genes' downregulation. In addition, the death mode of 1-3 was also mediated via death receptor extrinsic pathway manifested by FAS, FASL, FADD, and TNFR1 genes' upregulation via Human Rt PCR analysis. In addition, 1-3 significantly caused A2780 arrest at S phase, which was associated with the upregulation of TP53, E2F1, RB1 and CDKN1A upregulation and downregulation of CDK1, CDK4, CDC25A and CDC25C genes. Based on these promising results, these phosphanegold(I) thiolate derivatives could act as feasible candidates for further advanced in vivo ovarian cancer studies to develop novel chemotherapeutic agents derived from metal-based agents.
    Matched MeSH terms: Apoptosis
  7. Shukla MK, Dubey A, Pandey S, Singh SK, Gupta G, Prasher P, et al.
    Curr Pharm Des, 2022;28(39):3202-3211.
    PMID: 35422206 DOI: 10.2174/1381612828666220413103831
    Several factors exist that limit the efficacy of lung cancer treatment. These may be tumor-specific delivery of therapeutics, airway geometry, humidity, clearance mechanisms, presence of lung diseases, and therapy against tumor cell resistance. Advancements in drug delivery using nanotechnology based multifunctional nanocarriers, have emerged as a viable method for treating lung cancer with more efficacy and fewer adverse effects. This review does a thorough and critical examination of effective nano-enabled approaches for lung cancer treatment, such as nano-assisted drug delivery systems. In addition, to therapeutic effectiveness, researchers have been working to determine several strategies to produce nanotherapeutics by adjusting the size, drug loading, transport, and retention. Personalized lung tumor therapies using sophisticated nano modalities have the potential to provide great therapeutic advantages based on individual unique genetic markers and disease profiles. Overall, this review provides comprehensive information on newer nanotechnological prospects for improving the management of apoptosis in lung cancer.
    Matched MeSH terms: Apoptosis
  8. Abdul Ghani MA, Ugusman A, Latip J, Zainalabidin S
    Int J Mol Sci, 2023 Mar 10;24(6).
    PMID: 36982410 DOI: 10.3390/ijms24065339
    One in every three deaths worldwide is caused by cardiovascular diseases (CVDs), estimating a total of 17.9 million deaths annually. By 2030, it is expected that more than 24 million people will die from CVDs related complications. The most common CVDs are coronary heart disease, myocardial infarction, stroke, and hypertension. A plethora of studies has shown inflammation causing both short-term and long-term damage to the tissues in many organ systems, including the cardiovascular system. In parallel to inflammation processes, it has been discovered that apoptosis, a mode of programmed cell death, may also contribute to CVD development due to the loss of cardiomyocytes. Terpenophenolic compounds are comprised of terpenes and natural phenols as secondary metabolites by plants and are commonly found in the genus Humulus and Cannabis. A growing body of evidence has shown that terpenophenolic compounds exhibit protective properties against inflammation and apoptosis within the cardiovascular system. This review highlights the current evidence elucidating the molecular actions of terpenophenolic compounds in protecting the cardiovascular system, i.e., bakuchiol, ferruginol, carnosic acid, carnosol, carvacrol, thymol and hinokitiol. The potential of these compounds is discussed as the new nutraceutical drugs that may help to decrease the burden of cardiovascular disorders.
    Matched MeSH terms: Apoptosis
  9. Law D, Abdulkareem Najm A, Chong JX, K'ng JZY, Amran M, Ching HL, et al.
    PeerJ, 2023;11:e15651.
    PMID: 37483971 DOI: 10.7717/peerj.15651
    A previous study has shown that synthetic antimicrobial peptides (AMPs) derived from Anabas testudineus (ATMP1) could in-vitro inhibit the progression of breast cancer cell lines. In this study, we are interested in studying altered versions of previous synthetic AMPs to gain some insight into the peptides functions. The AMPs were altered and subjected to bioinformatics prediction using four databases (ADP3, CAMP-R3, AMPfun, and ANTICP) to select the highest anticancer activity. The bioinformatics in silico analysis led to the selection of two AMPs, which are ATMP5 (THPPTTTTTTTTTTTYTAAPATTT) and ATMP6 (THPPTTTTTTTTTTTTTAAPARTT). The in silico analysis predicted that ATMP5 and ATMP6 have anticancer activity and lead to cell death. The ATMP5 and ATMP6 were submitted to deep learning databases (ToxIBTL and ToxinPred2) to predict the toxicity of the peptides and to (AllerTOP & AllergenFP) check the allergenicity. The results of databases indicated that AMPs are non-toxic to normal human cells and allergic to human immunoglobulin. The bioinformatics findings led to select the highest active peptide ATMP5, which was synthesised and applied for in-vitro experiments using cytotoxicity assay MTT Assay, apoptosis detection using the Annexin V FTIC-A assay, and gene expression using Apoptosis PCR Array to evaluate the AMP's anticancer activity. The antimicrobial activity is approved by the disc diffusion method. The in-vitro experiments analysis showed that ATMP5 had the activity to inhibit the growth of the breast cancer cell line (MDA-MB-231) after 48 h and managed to arrest the cell cycle of the MDA-MB-231, apoptosis induction, and overexpression of the p53 by interaction with the related apoptotic genes. This research opened up new opportunities for developing potential and selective anticancer agents relying on antimicrobial peptide properties.
    Matched MeSH terms: Apoptosis
  10. Al-Shami SA, Al-Kaabi MM, Mahdi AK, Al-Attar Z
    Malays J Pathol, 2023 Aug;45(2):229-236.
    PMID: 37658532
    INTRODUCTION: Ovarian cancer is one of leading causes of cancer related death in gynecology. CD117 is a tyrosine kinase receptor that plays an important role in regulation of apoptosis, cell proliferation and adhesion by binding to its ligand-stem cell factor. Recent studies demonstrated its aberrant overexpression in various malignancies and concluded that it may play a pivotal role in carcinogenesis.

    AIM: To evaluate CD117 expression in ovarian surface epithelial tumours.

    MATERIALS AND METHODS: This retrospective study included 30 ovarian epithelial borderline, low and highly malignant tumours' formalin-fixed paraffin-blocks (FFPE) tissue blocks. Tissue sections were subjected to the routine haematoxylin-eosin stain and with the anti-CD117 immunohistochemically.

    RESULTS: There is a high significant difference in CD117 expression between borderline and malignant groups (P = 0.001). Additionally, there was significant difference in expression in relation to histopathological type (serous versus non-serous) in low-grade and the high-grade ovarian surface epithelial tumours (p=0.04, p=0.035 respectively). Tumour grade and stage strongly correlates with CD117 expression (p=0.014, p=0.019 respectively).

    CONCLUSION: We concluded that CD117 expression was significantly correlated with higher ovarian tumour grade and stage.

    Matched MeSH terms: Apoptosis
  11. Yue X, Ling Ma N, Zhong J, Yang H, Chen H, Yang Y, et al.
    Environ Res, 2024 Jan 15;241:117474.
    PMID: 37879390 DOI: 10.1016/j.envres.2023.117474
    Here, we collected 154 plant species in China ancient forests looking for novel efficient bioactive compounds for cancer treatments. We found 600 bioactive phyto-chemicals that induce apoptosis of liver cancer cell in vitro. First, we screen the plant extract's in vitro cytotoxicity inhibition of cancer cell growth using in vitro HepG2 cell lines and MTT cytotoxicity. The results from these initial MTT in vitro cytotoxicity tests show that the most efficient plants towards hepatoma cytoxicity is Cephalotaxus sinensis, mint bush (Elsholtzia stauntonii) and winged spindle tree (Euonymus alatus). We then used in cell-counting kit-8 (CCK-8) to further understand in vivo tumor growth using nude mice and GC-MS and LC-QTOF-MS to analyze the composition of compounds in the extracts. Extracted chemically active molecules analyzed by network pharmacology showed inhibition on the growth of liver cancer cells by acting on multiple gene targets, which is different from the currently used traditional drugs acting on only one target of liver cancer cells. Extracts from Cephalotaxus sinensis, mint bush (Elsholtzia stauntonii) and winged spindle tree (Euonymus alatus) induce apoptosis in hepatoma cancer cell line HepG2 with a killing rate of more than 83% and a tumor size decrease by 62-67% and a killing rate of only 6% of normal hepatocyte LO2. This study highlight efficient candidate species for cancer treatment providing a basis for future development of novel plant-based drugs to help meeting several of the UN SDGs and planetary health.
    Matched MeSH terms: Apoptosis
  12. Li Y, Ye Y, Yuan H, Rihan N, Han M, Liu X, et al.
    Sci Total Environ, 2024 Apr 01;919:170924.
    PMID: 38360329 DOI: 10.1016/j.scitotenv.2024.170924
    Nanoplastics (NPs) are widely distributed environmental pollutants that can disrupt intestinal immunity of crustaceans. In this study, the effects of NPs on gut immune enzyme activities, cell morphology, apoptosis, and microbiota diversity of Litopenaeus vannamei were investigated. L. vannamei was exposed to five concentrations of NPs (0, 0.1, 1, 5, and 10 mg/L) for 28 days. The results showed that higher concentrations of NPs damaged the intestinal villi, promoted formation of autophagosomes, increased intestinal non-specific immunoenzyme activities, and significantly increased apoptosis at 10 mg/L. In response to exposure to NPs, the expression levels of ATG3, ATG4, ATG12, Caspase-3, p53, and TNF initially increased and then decreased. In addition, the concentration of NPs was negatively correlated to the expression levels of the genes of interest and intestinal enzyme activities, suggesting that exposure to NPs inhibited apoptosis and immune function. The five dominant phyla of the gut microbiota (Proteobacteria, Firmicutes, Bacteroidetes, Acidobacteria, and Actinomycetes) were similar among groups exposed to different concentrations of NPs, but the abundances tended to differ. Notably, exposure to NPs increased the abundance of pathogenic bacteria. These results confirm that exposure to NPs negatively impacted intestinal immune function of L. vannamei. These findings provide useful references for efficient breeding of L. vannamei.
    Matched MeSH terms: Apoptosis
  13. Yusof YA, Saad SM, Makpol S, Shamaan NA, Ngah WZ
    Clinics (Sao Paulo), 2010;65(12):1371-7.
    PMID: 21340229
    OBJECTIVES: The aim of this study was to determine the antiproliferative and apoptotic effects of hot water extracts of Chlorella vulgaris on hepatoma cell line HepG2.

    INTRODUCTION: The search for food and spices that can induce apoptosis in cancer cells has been a major study interest in the last decade. Chlorella vulgaris, a unicellular green algae, has been reported to have antioxidant and anti-cancer properties. However, its chemopreventive effects in inhibiting the growth of cancer cells have not been studied in great detail.

    METHODS: HepG2 liver cancer cells and WRL68 normal liver cells were treated with various concentrations (0-4 mg/ml) of hot water extract of C. vulgaris after 24 hours incubation. Apoptosis rate was evaluated by TUNEL assay while DNA damage was assessed by Comet assay. Apoptosis proteins were evaluated by Western blot analysis.

    RESULTS: Chlorella vulgaris decreased the number of viable HepG2 cells in a dose dependent manner (p < 0.05), with an IC50 of 1.6 mg/ml. DNA damage as measured by Comet assay was increased in HepG2 cells at all concentrations of Chlorella vulgaris tested. Evaluation of apoptosis by TUNEL assay showed that Chlorella vulgaris induced a higher apoptotic rate (70%) in HepG2 cells compared to normal liver cells, WRL68 (15%). Western blot analysis showed increased expression of pro-apoptotic proteins P53, Bax and caspase-3 in the HepG2 cells compared to normal liver cells WRL68, and decreased expression of the anti-apoptotic protein Bcl-2.

    CONCLUSIONS: Chlorella vulgaris may have anti-cancer effects by inducing apoptosis signaling cascades via an increased expression of P53, Bax and caspase-3 proteins and through a reduction of Bcl-2 protein, which subsequently lead to increased DNA damage and apoptosis.

    Matched MeSH terms: Apoptosis/drug effects*; Apoptosis Regulatory Proteins/metabolism
  14. See WZC, Naidu R, Tang KS
    Curr Neuropharmacol, 2024;22(1):140-151.
    PMID: 36703582 DOI: 10.2174/1570159X21666230126161524
    Parkinson's disease (PD) is a heterogeneous disease involving a complex interaction between genes and the environment that affects various cellular pathways and neural networks. Several studies have suggested that environmental factors such as exposure to herbicides, pesticides, heavy metals, and other organic pollutants are significant risk factors for the development of PD. Among the herbicides, paraquat has been commonly used, although it has been banned in many countries due to its acute toxicity. Although the direct causational relationship between paraquat exposure and PD has not been established, paraquat has been demonstrated to cause the degeneration of dopaminergic neurons in the substantia nigra pars compacta. The underlying mechanisms of the dopaminergic lesion are primarily driven by the generation of reactive oxygen species, decrease in antioxidant enzyme levels, neuroinflammation, mitochondrial dysfunction, and ER stress, leading to a cascade of molecular crosstalks that result in the initiation of apoptosis. This review critically analyses the crucial upstream molecular pathways of the apoptotic cascade involved in paraquat neurotoxicity, including mitogenactivated protein kinase (MAPK), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/AKT, mammalian target of rapamycin (mTOR), and Wnt/β-catenin signaling pathways.
    Matched MeSH terms: Apoptosis
  15. Vijayarathna S, Sasidharan S
    Asian Pac J Cancer Prev, 2014;15(13):5499-500.
    PMID: 25041025
    Matched MeSH terms: Apoptosis/drug effects*; Apoptosis/genetics*
  16. Lai CS, Mas RH, Nair NK, Mansor SM, Navaratnam V
    J Ethnopharmacol, 2010 Feb 3;127(2):486-94.
    PMID: 19833183 DOI: 10.1016/j.jep.2009.10.009
    Typhonium flagelliforme is an indigenous plant of Malaysia and is used by the local communities to treat cancer. This study aims to identify the chemical constituents of Typhonium flagelliforme particularly those which have antiproliferative properties towards human cancer cell lines.
    Matched MeSH terms: Apoptosis/drug effects; Apoptosis/physiology
  17. Herlambang Devianto, Desiana Radithia, Bagus Soebadi, Adiastuti Endah Parmadiati, Rosnah Zain
    MyJurnal
    Introduction: One of the risk factors for cancer is the habit of smoking. Some carcinogenic substances in ciga-rettes are nicotine and nitrosamine. In cigarette smoke there are free radical molecules or Reactive Oxygen Species (ROS) that can cause DNA mutations that can disrupt the balance of cell metabolism. One of them is the apoptosis, apoptosis is a programmed cell death mechanism. In cancer conditions there are apoptotic disorders and excessive proliferation of cells. The process of apoptosis is influenced by the death receptor, Tumor Necrosis Factor apoptosis inducing ligand R1 (TRAIL R1). This study aims to determine the effect of smoke exposure to expression of TRAIL R1 on the mucosal epithelium of the tongue of the Wistar rat (Rattus Novergicus). Methods: The subjects of this study were 24 male Rattus Novergicus with the age range of 12-14 weeks and weighing ± 170 grams. Divided into 4 groups with 2 control groups 4 weeks (K4), 8 weeks (K8) and 2 treatment groups each given 2 cigarettes / day ex-posure to cigarette smoke for each rat for 4 weeks (P4) and 8 weeks (P8). Results: The results showed that exposure to cigarette smoke can cause interference with TRAIL R1 expression. There was a significant difference in TRAIL R1 expression between the control and treatment groups and there was a significant difference in TRAIL R1 expression between the duration of cigarette smoke exposure (P4 and P8). Conclusion: Exposure to cigarette smoke can interfere with the process of apoptosis.
    Matched MeSH terms: Apoptosis; Apoptosis Inducing Factor; Receptors, TNF-Related Apoptosis-Inducing Ligand
  18. Inayat-Hussain SH, Cohen GM, Cain K
    Cell Biol Toxicol, 1999;15(6):381-7.
    PMID: 10811533
    There is now a wealth of information regarding the apoptotic mode of cell death and its importance in toxicological studies in many mammalian organs including the liver. In this study, we investigated the modulatory effects of the heavy metal Zn2+ on transforming growth factor-beta1 (TGF-beta1)-induced apoptosis in primary rat hepatocytes. Apoptosis induced by TGF-beta1 (1 ng/ml) in hepatocytes was accompanied by nuclear condensation as assessed morphologically by staining with Hoechst 33258 and DNA cleavage as detected biochemically by in situ end-labeling, field inversion and conventional gel electrophoresis. Pretreatment with 100 micromol/L Zn2+ abrogated the nuclear condensation, in situ end-labeling, and DNA laddering in TGF-beta1-treated hepatocytes. Surprisingly, Zn2+ did not inhibit the formation of high-molecular-weight DNA fragments (30-50 kbp to 250-300 kbp). These data provide evidence that Zn2+ exerts its effects on the endonucleases that act downstream in the execution phase of TGF-beta1-induced apoptosis in hepatocytes.
    Matched MeSH terms: Apoptosis/drug effects; Apoptosis/physiology*
  19. Othman N, Nagoor NH
    Biomed Res Int, 2014;2014:318030.
    PMID: 24999473 DOI: 10.1155/2014/318030
    Lung cancer remains to be one of the most common and serious types of cancer worldwide. While treatment is available, the survival rate of this cancer is still critically low due to late stage diagnosis and high frequency of drug resistance, thus highlighting the pressing need for a greater understanding of the molecular mechanisms involved in lung carcinogenesis. Studies in the past years have evidenced that microRNAs (miRNAs) are critical players in the regulation of various biological functions, including apoptosis, which is a process frequently evaded in cancer progression. Recently, miRNAs were demonstrated to possess proapoptotic or antiapoptotic abilities through the targeting of oncogenes or tumor suppressor genes. This review examines the involvement of miRNAs in the apoptotic process of lung cancer and will also touch on the promising evidence supporting the role of miRNAs in regulating sensitivity to anticancer treatment.
    Matched MeSH terms: Apoptosis/drug effects; Apoptosis/genetics*
  20. Barathan M, Gopal K, Mohamed R, Ellegård R, Saeidi A, Vadivelu J, et al.
    Apoptosis, 2015 Apr;20(4):466-80.
    PMID: 25577277 DOI: 10.1007/s10495-014-1084-y
    Persistent hepatitis C virus (HCV) infection appears to trigger the onset of immune exhaustion to potentially assist viral persistence in the host, eventually leading to hepatocellular carcinoma. The role of HCV on the spontaneous expression of markers suggestive of immune exhaustion and spontaneous apoptosis in immune cells of chronic HCV (CHC) disease largely remain elusive. We investigated the peripheral blood mononuclear cells of CHC patients to determine the spontaneous recruitment of cellular reactive oxygen species (cROS), immunoregulatory and exhaustion markers relative to healthy controls. Using a commercial QuantiGenePlex(®) 2.0 assay, we determined the spontaneous expression profile of 80 different pro- and anti-apoptotic genes in persistent HCV disease. Onset of spontaneous apoptosis significantly correlated with the up-regulation of cROS, indoleamine 2,3-dioxygenase (IDO), cyclooxygenase-2/prostaglandin H synthase (COX-2/PGHS), Foxp3, Dtx1, Blimp1, Lag3 and Cd160. Besides, spontaneous differential surface protein expression suggestive of T cell inhibition viz., TRAIL, TIM-3, PD-1 and BTLA on CD4+ and CD8+ T cells, and CTLA-4 on CD4+ T cells was also evident. Increased up-regulation of Tnf, Tp73, Casp14, Tnfrsf11b, Bik and Birc8 was observed, whereas FasLG, Fas, Ripk2, Casp3, Dapk1, Tnfrsf21, and Cflar were moderately up-regulated in HCV-infected subjects. Our observation suggests the spontaneous onset of apoptosis signaling and T cell exhaustion in chronic HCV disease.
    Matched MeSH terms: Apoptosis*; Apoptosis Regulatory Proteins/genetics*; Apoptosis Regulatory Proteins/metabolism
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