Displaying publications 1 - 20 of 701 in total

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  1. Fulltext Cholesterol accumulation in ccRCC: the role of ccRCC-initiating VHL-HIFα pathway
    Mohtar MA, Hasanah Mohd Yusuf SN, Syafruddin SE
    EBioMedicine, 2024 May;103:105112.
    PMID: 38599011 DOI: 10.1016/j.ebiom.2024.105112
    Matched MeSH terms: Signal Transduction*
  2. Fulltext Exosomal mediated signal transduction through artificial microRNA (amiRNA): A potential target for inhibition of SARS-CoV-2
    Vadivalagan C, Shitut A, Kamalakannan S, Chen RM, Serrano-Aroca Á, Mishra V, et al.
    Cell Signal, 2022 Jul;95:110334.
    PMID: 35461900 DOI: 10.1016/j.cellsig.2022.110334
    Exosome trans-membrane signals provide cellular communication between the cells through transport and/or receiving the signal by molecule, change the functional metabolism, and stimulate and/or inhibit receptor signal complexes. COVID19 genetic transformations are varied in different geographic positions, and single nucleotide polymorphic lineages were reported in the second waves due to the fast mutational rate and adaptation. Several vaccines were developed and in treatment practice, but effective control has yet to reach in cent presence. It was initially a narrow immune-modulating protein target. Controlling these diverse viral strains may inhibit their transuding mechanisms primarily to target RNA genes responsible for COVID19 transcription. Exosomal miRNAs are the main sources of transmembrane signals, and trans-located miRNAs can directly target COVID19 mRNA transcription. This review discussed targeted viral transcription by delivering the artificial miRNA (amiRNA) mediated exosomes in the infected cells and significant resources of exosome and their efficacy.
    Matched MeSH terms: Signal Transduction
  3. Fulltext Quorum quenching revisited--from signal decays to signalling confusion
    Hong KW, Koh CL, Sam CK, Yin WF, Chan KG
    Sensors (Basel), 2012;12(4):4661-96.
    PMID: 22666051 DOI: 10.3390/s120404661
    In a polymicrobial community, while some bacteria are communicating with neighboring cells (quorum sensing), others are interrupting the communication (quorum quenching), thus creating a constant arms race between intercellular communication. In the past decade, numerous quorum quenching enzymes have been found and initially thought to inactivate the signalling molecules. Though this is widely accepted, the actual roles of these quorum quenching enzymes are now being uncovered. Recent evidence extends the role of quorum quenching to detoxification or metabolism of signalling molecules as food and energy source; this includes "signalling confusion", a term coined in this paper to refer to the phenomenon of non-destructive modification of signalling molecules. While quorum quenching has been explored as a novel anti-infective therapy targeting, quorum sensing evidence begins to show the development of resistance against quorum quenching.
    Matched MeSH terms: Signal Transduction*
  4. Fulltext Organ defects of the Usp7K444R mutant mouse strain indicate the essential role of K63-polyubiquitinated Usp7 in organ formation
    Wu HT, Lin YT, Chew SH, Wu KJ
    Biomed J, 2023 Feb;46(1):122-133.
    PMID: 35183794 DOI: 10.1016/j.bj.2022.02.002
    BACKGROUND: K63-linked polyubiquitination of proteins have nonproteolytic functions and regulate the activity of many signal transduction pathways. USP7, a HIF1α deubiquitinase, undergoes K63-linked polyubiquitination under hypoxia. K63-polyubiquitinated USP7 serves as a scaffold to anchor HIF1α, CREBBP, the mediator complex, and the super elongation complex to enhance HIF1α-induced gene transcription. However, the physiological role of K63-polyubiquitinated USP7 remains unknown.

    METHODS: Using a Usp7K444R point mutation knock-in mouse strain, we performed immunohistochemistry and standard molecular biological methods to examine the organ defects of liver and kidney in this knock-in mouse strain. Mechanistic studies were performed by using deubiquitination, immunoprecipitation, and quantitative immunoprecipitations (qChIP) assays.

    RESULTS: We observed multiple organ defects, including decreased liver and muscle weight, decreased tibia/fibula length, liver glycogen storage defect, and polycystic kidneys. The underlying mechanisms include the regulation of protein stability and/or modulation of transcriptional activation of several key factors, leading to decreased protein levels of Prr5l, Hnf4α, Cebpα, and Hnf1β. Repression of these crucial factors leads to the organ defects described above.

    CONCLUSIONS: K63-polyubiquitinated Usp7 plays an essential role in the development of multiple organs and illustrates the importance of the process of K63-linked polyubiquitination in regulating critical protein functions.

    Matched MeSH terms: Signal Transduction*
  5. Fulltext Insights on Quorum-Quenching Properties of Lysinibacillus fusiformis Strain RB21, a Malaysian Municipal Solid-Waste Landfill Soil Isolate, via Complete Genome Sequence Analysis
    Yong D, Ee R, Lim YL, Chang CY, Yin WF, Chan KG
    Genome Announc, 2015;3(3).
    PMID: 25953192 DOI: 10.1128/genomeA.00409-15
    Lysinibacillus fusiformis strain RB21 is a quorum-quenching bacterium that is able to degrade quorum-sensing signaling molecules. Here, we present the first complete genome sequence of L. fusiformis strain RB21. The finished genome is 4.8 Mbp in size, and the quorum-quenching gene was identified.
    Matched MeSH terms: Signal Transduction
  6. Fulltext Optimal Device Independent Quantum Key Distribution
    Kamaruddin S, Shaari JS
    Sci Rep, 2016 08 03;6:30959.
    PMID: 27485160 DOI: 10.1038/srep30959
    We consider an optimal quantum key distribution setup based on minimal number of measurement bases with binary yields used by parties against an eavesdropper limited only by the no-signaling principle. We note that in general, the maximal key rate can be achieved by determining the optimal tradeoff between measurements that attain the maximal Bell violation and those that maximise the bit correlation between the parties. We show that higher correlation between shared raw keys at the expense of maximal Bell violation provide for better key rates for low channel disturbance.
    Matched MeSH terms: Signal Transduction
  7. Fulltext Counterfactual protocol within device independent framework and its insecurity
    Kamaruddin S, Shaari JS, Kolenderski P
    Sci Rep, 2020 Apr 03;10(1):5847.
    PMID: 32246055 DOI: 10.1038/s41598-020-62812-3
    We consider the counterfactual protocol proposed in Phys. Rev. Lett., 103, 230501 (2009) within a device independent framework and show how its security can easily be compromised. Capitalising on the fact that the protocol is based on the use of a single photon entanglement phenomenon, we propose an equivalent protocol. It can be made secure within such a pessimistic framework against a supra-quantum Eve limited only by the no-signalling principle. The equivalence the protocol demonstrates the possibility of device independent framework for counterfactual quantum cryptography.
    Matched MeSH terms: Signal Transduction
  8. [Exploring molecular mechanisms of fucoidan in improving human proximal renal tubular epithelial cells aging by targeting autophagy signaling pathways]
    Fang QJ, Liu JJ, Wan YG, Liu BH, Tu Y, Wu W, et al.
    Zhongguo Zhong Yao Za Zhi, 2020 Dec;45(24):6003-6011.
    PMID: 33496141 DOI: 10.19540/j.cnki.cjcmm.20200709.401
    Fucoidan(FPS) is an effective component of the Chinese patent medicine named Haikun Shenxi, which treats schronic renal failure in clinics, and has the potential anti-aging effects. However, it is still unclear whether FPS can improve renal aging, especially the molecular mechanism of its anti-aging. The human proximal renal tubular epithelial cells(HK-2) in vitro were divided into normal group(N), D-gal model group(D), low dose of FPS group(L-FPS), high dose of FPS group(H-FPS) and vitamin E group(VE), and treated by the different measures, respectively. More specifically, the HK-2 cells in each group were separately treated by 1 mL of 1% fetal bovine serum(FBS) or D-galactose(D-gal, 75 mmol·L~(-1)) or D-gal(75 mmol·L~(-1))+FPS(25 μg·mL~(-1)) or D-gal(75 mmol·L~(-1))+FPS(50 μg·mL~(-1)) or D-gal(75 mmol·L~(-1))+VE(50 μg·mL~(-1)). After the treatment for 24 h, firstly, the effects of D-gal on senescence-associated β-galactosidase(SA-β-gal) staining characteristics and klotho, P53 and P21 protein expression le-vels, as well as adenosine monophosphate activated protein kinase(AMPK)-uncoordinated 51-like kinase 1(ULK1) signaling pathway activation in the HK-2 cells were detected, respectively. Secondly, the effects of FPS and VE on SA-β-gal staining characteristics and klotho, P53 and P21 protein expression levels in the HK-2 cells exposed to D-gal were investigated, respectively. Finally, the effects of FPS and VE on microtubule-associated protein 1 light chain 3(LC3) protein expression level and AMPK-ULK1 signaling pathway activation in the HK-2 cells exposed to D-gal were examined severally. The results indicated that, for the HK-2 cells, the dose of 75 mmol·L~(-1) D-gal could induce the changes of SA-β-gal staining characteristics and klotho, P53 and P21 protein expression levels. That is causing cells aging. FPS and VE could both ameliorate the changes of SA-β-gal staining characteristics and klotho, P53 and P21 protein expression levels in the HK-2 cells exposed to D-gal. That is anti-cells aging, here, the functions of FPS and VE are similar. D-gal could not only induce cell aging but also increase LC3Ⅱ, phosphorylated-AMPK(p-AMPK) and phosphorylated-ULK1(p-ULK1) protein expressions, and activate autophagy-related AMPK-ULK1 signaling pathway. FPS and VE could both improve the changes of LC3Ⅱ, p-AMPK and p-ULK1 protein expression levels in the HK-2 cells exposed to D-gal. That is inhibiting autophagy-related AMPK-ULK1 signaling pathway activation. On the whole, for the human proximal renal tubular epithelial cells aging models induced by D-gal, FPS similar to VE, can ameliorate renal cells aging by possibly inhibiting autophagy-related AMPK-ULK1 signaling pathway activation. This finding provides the preliminary pharmacologic evidences for FPS protecting against renal aging.
    Matched MeSH terms: Signal Transduction*
  9. Fulltext Using the Proteomics Toolbox to Resolve Topology and Dynamics of Compartmentalized cAMP Signaling
    Kovanich D, Low TY, Zaccolo M
    Int J Mol Sci, 2023 Feb 28;24(5).
    PMID: 36902098 DOI: 10.3390/ijms24054667
    cAMP is a second messenger that regulates a myriad of cellular functions in response to multiple extracellular stimuli. New developments in the field have provided exciting insights into how cAMP utilizes compartmentalization to ensure specificity when the message conveyed to the cell by an extracellular stimulus is translated into the appropriate functional outcome. cAMP compartmentalization relies on the formation of local signaling domains where the subset of cAMP signaling effectors, regulators and targets involved in a specific cellular response cluster together. These domains are dynamic in nature and underpin the exacting spatiotemporal regulation of cAMP signaling. In this review, we focus on how the proteomics toolbox can be utilized to identify the molecular components of these domains and to define the dynamic cellular cAMP signaling landscape. From a therapeutic perspective, compiling data on compartmentalized cAMP signaling in physiological and pathological conditions will help define the signaling events underlying disease and may reveal domain-specific targets for the development of precision medicine interventions.
    Matched MeSH terms: Signal Transduction/physiology
  10. Fulltext An Insight into the Anti-Angiogenic and Anti-Metastatic Effects of Oridonin: Current Knowledge and Future Potential
    Abdullah NA, Md Hashim NF, Ammar A, Muhamad Zakuan N
    Molecules, 2021 Feb 03;26(4).
    PMID: 33546106 DOI: 10.3390/molecules26040775
    Cancer is one of the leading causes of death worldwide, with a mortality rate of more than 9 million deaths reported in 2018. Conventional anti-cancer therapy can greatly improve survival however treatment resistance is still a major problem especially in metastatic disease. Targeted anti-cancer therapy is increasingly used with conventional therapy to improve patients' outcomes in advanced and metastatic tumors. However, due to the complexity of cancer biology and metastasis, it is urgent to develop new agents and evaluate the anti-cancer efficacy of available treatments. Many phytochemicals from medicinal plants have been reported to possess anti-cancer properties. One such compound is known as oridonin, a bioactive component of Rabdosia rubescens. Several studies have demonstrated that oridonin inhibits angiogenesis in various types of cancer, including breast, pancreatic, lung, colon and skin cancer. Oridonin's anti-cancer effects are mediated through the modulation of several signaling pathways which include upregulation of oncogenes and pro-angiogenic growth factors. Furthermore, oridonin also inhibits cell migration, invasion and metastasis via suppressing epithelial-to-mesenchymal transition and blocking downstream signaling targets in the cancer metastasis process. This review summarizes the recent applications of oridonin as an anti-angiogenic and anti-metastatic drug both in vitro and in vivo, and its potential mechanisms of action.
    Matched MeSH terms: Signal Transduction/drug effects
  11. Comparative aspects of kisspeptin gene regulation
    Kitahashi T, Parhar IS
    Gen Comp Endocrinol, 2013 Jan 15;181:197-202.
    PMID: 23089246 DOI: 10.1016/j.ygcen.2012.10.003
    Kisspeptin plays an important role in the onset of puberty through stimulation of gonadotropin-releasing hormone (GnRH), a master molecule of reproduction. Furthermore, the existence of multiple kisspeptins is evident in most vertebrate species. Therefore, elucidating the regulatory mechanisms of the kisspeptin genes is important to understand the functions of multiple kisspeptin forms in the brain. This review focuses on the comparative aspects of kisspeptin gene regulation with an emphasis on the role of environmental signals including gonadal steroids, photoperiods and metabolic signals. These environmental signals differently regulate the kisspeptin genes distinctively in each species. In addition, photoperiodic regulation of the kisspeptin genes alters during sexual maturational, suggesting interactions between the gonadal hormone pathway and the photoperiod pathway. Further studies of the regulatory mechanisms of kisspeptin genes especially in teleosts which possess multiple kisspeptin/kisspeptin receptor systems will help to understand the precise role of multiple kisspeptin forms in different species.
    Matched MeSH terms: Signal Transduction/genetics; Signal Transduction/physiology
  12. Fulltext Simulation of a Petri net-based model of the terpenoid biosynthesis pathway
    Hawari AH, Mohamed-Hussein ZA
    BMC Bioinformatics, 2010;11:83.
    PMID: 20144236 DOI: 10.1186/1471-2105-11-83
    The development and simulation of dynamic models of terpenoid biosynthesis has yielded a systems perspective that provides new insights into how the structure of this biochemical pathway affects compound synthesis. These insights may eventually help identify reactions that could be experimentally manipulated to amplify terpenoid production. In this study, a dynamic model of the terpenoid biosynthesis pathway was constructed based on the Hybrid Functional Petri Net (HFPN) technique. This technique is a fusion of three other extended Petri net techniques, namely Hybrid Petri Net (HPN), Dynamic Petri Net (HDN) and Functional Petri Net (FPN).
    Matched MeSH terms: Signal Transduction*
  13. Gibberellins - a multifaceted hormone in plant growth regulatory network
    Gantait S, Sinniah UR, Ali MN, Sahu NC
    Curr Protein Pept Sci, 2015;16(5):406-12.
    PMID: 25824386
    Plants tend to acclimatize to unfavourable environs by integrating growth and development to environmentally activated signals. Phytohormones strongly regulate convergent developmental and stress adaptive procedures and synchronize cellular reaction to the exogenous and endogenous conditions within the adaptive signaling networks. Gibberellins (GA), a group of tetracyclic diterpenoids, being vital regulators of plant growth, are accountable for regulating several aspects of growth and development of higher plants. If the element of reproduction is considered as an absolute requisite then for a majority of the higher plants GA signaling is simply indispensable. Latest reports have revealed unique conflicting roles of GA and other phytohormones in amalgamating growth and development in plants through environmental signaling. Numerous physiological researches have detailed substantial crosstalk between GA and other hormones like abscisic acid, auxin, cytokinin, and jasmonic acid. In this review, a number of explanations and clarifications for this discrepancy are explored based on the crosstalk among GA and other phytohormones.
    Matched MeSH terms: Signal Transduction*
  14. [Molecular mechanisms of insulin resistance and interventional effects of Chinese herbal medicine]
    Yee HY, Yang JJ, Wan YG, Chong FL, Wu W, Long Y, et al.
    Zhongguo Zhong Yao Za Zhi, 2019 Apr;44(7):1289-1294.
    PMID: 31090283 DOI: 10.19540/j.cnki.cjcmm.20181105.003
    It is considered that insulin resistance(IR)and its signaling pathway disorder are one of pathogenesis that causes insulin target-organs/issues lesions and their slow progression. The clinical diagnosis index of IR is the homeostatic model of insulin resistance(HOMA-IR)based on fasting blood-glucose and fasting serum insulin. Furthermore, the emerging IR biomarkers including adiponectin may be the references for clinical diagnosis. The influence factors of IR are obesity, chronic microinflammation and a lack of exercise. The major signaling pathways of IR include insulin receptor substrate 1(IRS1)/phosphatidylinositiol-3-kinase(PI3 K)/serine-threonine kinase(Akt)pathway, mitogen-activated protein kinase(MAPK)pathway and Smad3 pathway. In clinics, insulin sensibility and IR could be increased and improved via promoting insulin secretion and enhancing insulin signaling activation. At present, insulin sensitizers treating IR not only have the classic thiazolidinediones and its ramifications but also have the newly discovered metformin and vitamin D. In addition, it is reported that some extracts from single Chinese herbal medicine(CHM)and Chinese herbal compound prescription such as total flavone from the flowers of Abelmoschl manihot, berberine, astragalus polysaccharides and Huang-qi decoction also have the beneficial effects in ameliorating IR. In the field of chronic kidney disease, targeting a common insulin target-organs/issues lesion, the early renal damage in diabetic mellitus, the intervention studies regarding to regulating podocyte IR signaling pathways by CHM will be one of the significant directions in the future.
    Matched MeSH terms: Signal Transduction*
  15. Fulltext Bile Acids: Physiological Activity and Perspectives of Using in Clinical and Laboratory Diagnostics
    Shansky Y, Bespyatykh J
    Molecules, 2022 Nov 13;27(22).
    PMID: 36431930 DOI: 10.3390/molecules27227830
    Bile acids play a significant role in the digestion of nutrients. In addition, bile acids perform a signaling function through their blood-circulating fraction. They regulate the activity of nuclear and membrane receptors, located in many tissues. The gut microbiota is an important factor influencing the effects of bile acids via enzymatic modification. Depending on the rate of healthy and pathogenic microbiota, a number of bile acids may support lipid and glucose homeostasis as well as shift to more toxic compounds participating in many pathological conditions. Thus, bile acids can be possible biomarkers of human pathology. However, the chemical structure of bile acids is similar and their analysis requires sensitive and specific methods of analysis. In this review, we provide information on the chemical structure and the biosynthesis of bile acids, their regulation, and their physiological role. In addition, the review describes the involvement of bile acids in various diseases of the digestive system, the approaches and challenges in the analysis of bile acids, and the prospects of their use in omics technologies.
    Matched MeSH terms: Signal Transduction/physiology
  16. Fulltext Activating RAC1 variants in the switch II region cause a developmental syndrome and alter neuronal morphology
    Banka S, Bennington A, Baker MJ, Rijckmans E, Clemente GD, Ansor NM, et al.
    Brain, 2022 Dec 19;145(12):4232-4245.
    PMID: 35139179 DOI: 10.1093/brain/awac049
    RAC1 is a highly conserved Rho GTPase critical for many cellular and developmental processes. De novo missense RAC1 variants cause a highly variable neurodevelopmental disorder. Some of these variants have previously been shown to have a dominant negative effect. Most previously reported patients with this disorder have either severe microcephaly or severe macrocephaly. Here, we describe eight patients with pathogenic missense RAC1 variants affecting residues between Q61 and R68 within the switch II region of RAC1. These patients display variable combinations of developmental delay, intellectual disability, brain anomalies such as polymicrogyria and cardiovascular defects with normocephaly or relatively milder micro- or macrocephaly. Pulldown assays, NIH3T3 fibroblast spreading assays and staining for activated PAK1/2/3 and WAVE2 suggest that these variants increase RAC1 activity and over-activate downstream signalling targets. Axons of neurons isolated from Drosophila embryos expressing the most common of the activating variants are significantly shorter, with an increased density of filopodial protrusions. In vivo, these embryos exhibit frequent defects in axonal organization. Class IV dendritic arborization neurons expressing this variant exhibit a significant reduction in the total area of the dendritic arbour, increased branching and failure of self-avoidance. RNAi knock down of the WAVE regulatory complex component Cyfip significantly rescues these morphological defects. These results establish that activating substitutions affecting residues Q61-R68 within the switch II region of RAC1 cause a developmental syndrome. Our findings reveal that these variants cause altered downstream signalling, resulting in abnormal neuronal morphology and reveal the WAVE regulatory complex/Arp2/3 pathway as a possible therapeutic target for activating RAC1 variants. These insights also have the potential to inform the mechanism and therapy for other disorders caused by variants in genes encoding other Rho GTPases, their regulators and downstream effectors.
    Matched MeSH terms: Signal Transduction/genetics
  17. Interferon-gamma (IFN-γ): Reviewing its mechanisms and signaling pathways on the regulation of endothelial barrier function
    Ng CT, Fong LY, Abdullah MNH
    Cytokine, 2023 Jun;166:156208.
    PMID: 37088004 DOI: 10.1016/j.cyto.2023.156208
    Interferon-gamma (IFN-γ) is a pleiotropic cytokine that plays a critical role in mediating an array of immune responses including promotes antiviral activity, facilitates macrophage activation, controls Th1/Th2 balance, and regulates cellular apoptosis and proliferation. A few articles have previously reviewed the effects of IFN-γ in the regulation of barrier permeability, but none of these articles focuses on barrier function of endothelial cells. This review aims to discuss the regulatory mechanisms of IFN-γ on endothelial barrier function and its underlying signaling pathways. Articles were retrieved from electronic databases such as PubMed and Google Scholar using keywords "Interferon-gamma", "endothelial cells", "barrier function", and "signaling pathway". The articles published between 2000 and 2022 that are related to the aforementioned topics were selected. A few journals published beyond this period were also included due to limited information available. The results showed that IFN-γ modulates endothelial barrier function, mainly involves small GTPases, STAT1-dependent pathway, p38 MAPK and nitric oxide. In conclusion, more in depth cellular and molecular studies are needed to elucidate the pathways of IFN-γ in the regulation of endothelial barrier function.
    Matched MeSH terms: Signal Transduction*
  18. MALAT1: A key regulator in lung cancer pathogenesis and therapeutic targeting
    Bhat AA, Afzal O, Afzal M, Gupta G, Thapa R, Ali H, et al.
    Pathol Res Pract, 2024 Jan;253:154991.
    PMID: 38070223 DOI: 10.1016/j.prp.2023.154991
    Lung cancer remains a formidable global health burden, necessitating a comprehensive understanding of the underlying molecular mechanisms driving its progression. Recently, lncRNAs have become necessary controllers of various biological functions, including cancer development. MALAT1 has garnered significant attention due to its multifaceted role in lung cancer progression. Lung cancer, among other malignancies, upregulates MALAT1. Its overexpression has been associated with aggressive tumor behavior and poor patient prognosis. MALAT1 promotes cellular proliferation, epithelial-mesenchymal transition (EMT), and angiogenesis in lung cancer, collectively facilitating tumor growth and metastasis. Additionally, MALAT1 enhances cancer cell invasion by interacting with numerous signaling pathways. Furthermore, MALAT1 has been implicated in mediating drug resistance in lung cancer, contributing to the limited efficacy of conventional therapies. Recent advancements in molecular biology and high-throughput sequencing technologies have offered fresh perspectives into the regulatory networks of MALAT1 in lung cancer. It exerts its oncogenic effects by acting as a ceRNA to sponge microRNAs, thereby relieving their inhibitory effects on target genes. Moreover, MALAT1 also influences chromatin remodeling and post-translational modifications to modulate gene expression, further expanding its regulatory capabilities. This review sheds light on the multifaceted roles of MALAT1 in lung cancer progression, underscoring its potential as an innovative therapeutic target and diagnostic biomarker. Targeting MALAT1 alone or combined with existing therapies holds promise to mitigate lung cancer progression and improve patient outcomes.
    Matched MeSH terms: Signal Transduction/genetics
  19. Insights into the molecular mechanisms and signalling pathways of epithelial to mesenchymal transition (EMT) in colorectal cancer: A systematic review and bioinformatic analysis of gene expression
    Azizan S, Cheng KJ, Mejia Mohamed EH, Ibrahim K, Faruqu FN, Vellasamy KM, et al.
    Gene, 2024 Feb 20;896:148057.
    PMID: 38043836 DOI: 10.1016/j.gene.2023.148057
    Colorectal cancer (CRC) is ranked as the second leading cause of mortality worldwide, mainly due to metastasis. Epithelial to mesenchymal transition (EMT) is a complex cellular process that drives CRC metastasis, regulated by changes in EMT-associated gene expression. However, while numerous genes have been identified as EMT regulators through various in vivo and in vitro studies, little is known about the genes that are differentially expressed in CRC tumour tissue and their signalling pathway in regulating EMT. Using an integration of systematic search and bioinformatic analysis, gene expression profiles of CRC tumour tissues were compared to non-tumour adjacent tissues to identify differentially expressed genes (DEGs), followed by performing systematic review on common identified DEGs. Fifty-eight common DEGs were identified from the analysis of 82 tumour tissue samples obtained from four gene expression datasets (NCBI GEO). These DEGS were then systematically searched for their roles in modulating EMT in CRC based on previously published studies. Following this, 10 common DEGs (CXCL1, CXCL8, MMP1, MMP3, MMP7, TACSTD2, VIP, HPGD, ABCG2, CLCA4) were included in this study and subsequently subjected to further bioinformatic analysis. Their roles and functions in modulating EMT in CRC were discussed in this review. This study enhances our understanding of the molecular mechanisms underlying EMT and uncovers potential candidate genes and pathways that could be targeted in CRC.
    Matched MeSH terms: Signal Transduction/genetics
  20. Targeting genes in insulin-associated signalling pathway, DNA damage, cell proliferation and cell differentiation pathways by tocotrienol-rich fraction in preventing cellular senescence of human diploid fibroblasts
    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: Signal Transduction
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