The telomerase enzyme is itself a marker for tumor cells, but the genetic alterations that activate the enzyme during neoplastic transformation have remained a mystery. Here, we show that Myc induces telomerase in both normal human mammary epithelial cells (HMECs) and normal human diploid fibroblasts Gut charakterisiert ist die aus Tetrahymena thermophila (Hymenostomata) isolierte Telomerase, ein Ribonucleoprotein-Komplex (Ribonucleoproteine), bei dem sowohl der Protein- als auch der RNA-Anteil für die enzymatische Aktivität essentiell ist Myc induces telomerase activity in primary mouse embryonic fibroblasts and myeloid cells. A, primary MEFs were infected with either a control (CD8) vector or the Myc-expressing retrovirus, and after 48 h cell extracts were prepared. 0.03 μg of cell extracts were assayed for telomerase activity using telomerase PCR ELISA The ability of telomerase to rescue cells from the adverse consequences of telomere dysfunction is likely critical for its role in facilitating malignant transformation of primary human cells and in maintaining the viability and proliferation of established cancer cells
MYC reguliert die Expression von etwa 15 % aller menschlichen Gene durch die Bindung von Enhancer Box Sequenzen (E-boxes) und durch die Rekrutierung von Histon-Acetyltransferasen. MYC wird durch eine große Anzahl von Teilungssignalen wie Wnt, Shh und EGF durch den MAPK /ERK-Signalweg aktiviert we show that Myc induces telomerase in both normal human mammary epithelial cells (HMECs) and normal human diploid fibroblasts. Myc increases expression of hEST2 (hTRT/TP2), the limiting subunit of telomerase, and both Myc and hEST2 can extend the life span of HMECs. The ability of Myc to activate telomerase ma Myc is a transcription factor with pleiotropic effects on tumorigenesis which are likely to be mediated by its target genes. A known Myc transcriptional target is the catalytic subunit of telomerase, Tert. However, the contribution of Tert activation to Myc-induced tumorigenesis in vivo remains unknown. In this study, we addressed the role of telomerase in Myc-induced skin papillomatosis by using compound mice with a switchable Myc gene, Inv-MycERTAM mice, in combination with either. c-Myc enhances telomerase activity IMR90 cultures do not possess detectable telomerase activity or TERT gene expression (Nakamura et al., 1997; Meyerson et al., 1997) Lower levels of telomerase activity were obtained with td10H v-Myc than with MC29-v-Myc , suggesting that the ability of v-Myc proteins to induce telomerase was related to the extent to which they.
. Erfahrt mehr darüber - wir freuen uns auf eure Bewerbung Telomerase is an RNA-dependent DNA polymerase responsible for synthesizing telomeric DNA at chromosome ends [ 13, 14 ]. The core telomerase complex consists of two components: the rate-limiting, catalytic subunit telomerase reverse transcriptase (hTERT) and the ubiquitously expressed RNA template hTERC [ 13] [ 14, 15 ]
Telomerase consists of at least two essential elements, a catalytic protein component (TERT) for adding telomeric DNA repeats onto chromosome ends and an RNA subunit (hTR or TERC) that serves as the template for telomere repeat addition 3, 4. In most normal cells, telomerase activity (TA) is undetectable Die Telomerase ist ein Enzym des Zellkerns, welches aus einem Protein- (TERT) und einem langen RNA-Anteil (TR) besteht und somit ein Ribonukleoprotein ist. Dieses Enzym stellt die Endstücke der Chromosomen, die sogenannten Telomere, wieder her.Die Enzymaktivität der Telomerase lässt sich durch die TRAP-Methode feststellen
The Myc-expressing cells contained levels of telomerase activity comparable to those seen in a telomerase-positive fibrosarcoma cell line, HT1080 (Fig. (Fig.1 1 B). Although c-Myc expression elevates telomerase in both normal epithelial cells and in normal fibroblasts, the HPV-16 E6 protein has been shown to affect telomerase only in epithelial cells ( Klingelhutz et al. 1996 ) MYC-dependent downregulation of telomerase by FLT3 inhibitors is required for their therapeutic efficacy on acute myeloid leukemia Zeitschrift: Annals of Hematology > Ausgabe 1/2018 Autoren: Xiaolu Zhang, Bingnan Li, Jingya Yu, Jenny Dahlström, Anh Nhi Tran, Magnus Björkhom, Dawei Xu » Zum Volltext PDF-Version jetzt herunterladen Wichtige Hinweise. Xiaolu Zhang and Bingnan Li contributed. Endogenous expression of the cellular c-MYC oncogene may result in dissociation of the Mad1/Max repressor from the E-box complex, leading to de-repression of the TERT gene and telomerase activation . Epigenetic factors responsible for DNA methylation, histone acetylation, methylation, and phosphorylation are another group of factors modulating TERT transcription Background. Telomerase is activated in the majority of cancer tissues and immortalized cell lines. The hTERT (human telomerase reverse transcriptase—major component of telomerase) gene promoter has been cloned and contains many c-myc binding sites that mediate hTERT transcriptional activation. Thus far, the role of hTERT in tumorigenesis in hepatocellular carcinoma (HCC) has been little.
1 MYC-driven neuroblastomas are addicted to a telomerase- independent function of dyskerin Rosemary O'Brien1#, Sieu L. Tran1#, Michelle Maritz1, Bing Liu1, Cheng Fei Kong1, Stefania Purgato2. telomerase, is transcriptionally regulated by c-MYC, and we have found that TMPyP4 also causes a decrease in human telomerase reverse transcriptase transcripts, suggesting two possible mechanisms for the effect of TMPyP4 on telomerase activity. We also show that TMPyP4, but not TMPyP2, is able to prolong survival and decrease tumor growth rates in tw c-Myc-mediated Regulation of Telomerase Activity Is Disabled in Immortalized Cells* Received for publication, March 1, 2001 Published, JBC Papers in Press, June 11, 2001, DOI 10.1074/jbc.M101899200 Rachid Drissi‡, Frederique Zindy§, Martine F. Roussel§, and John L. Cleveland ‡¶ From the Departments of ‡Biochemistry and §Tumor Cell Biology, St. Jude Children's Research Hospital. MYC drives overexpression of telomerase RNA (hTR/TERC) in prostate cancer Levels of TERC correlate with levels of MYC (a known driver of prostate cancer) in clinical samples and we also show the following: forced reductions of MYC result in decreased TERC levels in eight cancer cell lines (prostate, lung, breast, and colorectal); forced overexpression of MYC in PCa cell lines, and in the.
The RNA-binding protein dyskerin, encoded by the DKC1 gene, functions as a core component of the telomerase holoenzyme as well as ribonuclear protein complexes involved in RNA processing and ribosome biogenesis. The diverse roles of dyskerin across many facets of RNA biology implicate its potential contribution to malignancy. In this study, we examined the expression and function of dyskerin. Tumor and Stem Cell Biology MYC-Driven Neuroblastomas Are Addicted to a Telomerase-Independent Function of Dyskerin Rosemary O'Brien1, Sieu L.Tran1, Michelle F. Maritz1, Bing Liu1, Cheng Fei Kong1, Stefania Purgato2, Chen Yang1, Jayne Murray1, Amanda J. Russell1, Claudia L. Flemming1, Georg von Jonquieres1, Hilda A. Pickett3,Wendy B. London4, Michelle Haber1 (2009). Telomerase activation by c-Myc in human mammary epithelial cells requires additional genomic changes. Cell Cycle: Vol. 8, No. 20, pp. 3373-3378 High c-MYC and telomerase activity in regenerating liver, the rapidly regenerating cyclical phase of endometrium and lymphoid germinal centers represent examples in which c-MYC may drive rapid.
Telomerase, also called terminal transferase, is a ribonucleoprotein that adds a species-dependent telomere repeat sequence to the 3' end of telomeres.A telomere is a region of repetitive sequences at each end of the chromosomes of most eukaryotes.Telomeres protect the end of the chromosome from DNA damage or from fusion with neighbouring chromosomes Key words: Epstein‑Barr virus, triptolide, human telomerase 1, c‑Myc. 2 LONG et al: hTERT, SP1 AND c‑Myc ARE INHIBITED BY TRIPTOLIDE Triptolide (TP), a diterpenoid triepoxide, is extracted from the root of the Chinese herb Tripterygium wilfordii (15). TP possesses a broad‑spectrum of bioactivity and cytotoxic func‑ tions, including antitumor, anti‑inflammatory, anti‑fertility and. . We have found that the cationic porphyrin TMPyP4 is not only able to down-regulate the expression and activity of both of these gene products but also has significant antitumor activity. Several proto-oncogenes and tumor suppressor genes have been implicated in the regulation of hTERT gene expression including c-myc, a proto-oncogene product that activates telomerase by direct.
telomerase, is transcriptionally regulated by c-MYC, and we have found that TMPyP4 also causes a decrease in human telomerase reverse transcriptase transcripts, suggesting two possible mechanisms for the effect of TMPyP4 on telomerase activity. We also show that TMPyP4, but not TMPyP2, is able to prolong survival and decrease tumor growth rates. Telomere maintenance has been proposed as an essential prerequisite to human tumor development. The telomerase enzyme is itself a marker for tumor cells, but the genetic alterations that activate the enzyme during neoplastic transformation have remained a mystery. Here, we show that Myc induces telomerase in both normal human mammary epithelial cells (HMECs) and normal human diploid fibroblasts A decrease in telomerase activity was obtained when Myc was deactivated by stopping 4-OHT administration in previously treated Inv-MycER TAM skin (Fig. (Fig.1c); 1c); in particular, telomerase activity decreased 2 days after Myc was switched off, reaching undetectable levels at day 6 after deactivation. All together, these results indicate that Myc directly or indirectly regulates telomerase. MYC-dependent downregulation of telomerase by FLT3 inhibitors is required for their therapeutic efficacy on acute myeloid leukemia Xiaolu Zhang1 & Bingnan Li1 & Jingya Yu1 & Jenny Dahlström1 & Anh Nhi Tran2 & Magnus Björkhom1 & Dawei Xu1 Received: 12 July 2017/Accepted: 10 October 2017/Published online: 27 October 2017 # The Author(s) 2017. This article is an open access publication Abstract. A known Myc transcriptional target is the catalytic subunit of telomerase, Tert. However, the contribution of Tert activation to Myc-induced tumorigenesis in vivo remains unknown. In this study, we addressed the role of telomerase in Myc-induced skin papillomatosis by using compound mice with a switchable Myc gene, Inv-MycERTAM mice, in combination with either telomerase deficiency (Terc.
c-Myc and its network proteins are known to be oncoproteins. How are these proteins involved in telomerase activation during carcinogenesis? Overexpression of Myc is frequently observed in a wide variety of tumor types, and is usually caused by chromosomal translocation involving the c-myc gene as well as by gene amplification (30, 31) Telomerase regulates MYC-driven oncogenesis independent of its reverse transcriptase activity Cheryl M. Koh, 1 Ekta Khattar, 2 Shi Chi Leow, Chia Yi Liu, Julius Muller, Wei Xia Ang, Yinghui Li,2 Guido Franzoso,3 Shang Li,4,5 Ernesto Guccione,1,6 and Vinay Tergaonkar2,6 1Division of Cancer Genetics and Therapeutics, Laboratory of Methyltransferases in Development and Disease, and 2Division of. The continuous advancements in cancer research have contributed to the overwhelming evidence of the presence of telomerase in primary and secondary tumours together with hsp90 and c-Myc. This review will discuss the important role of telomerase together with hsp90 and c-Myc within the initiation and progression of gliomas. Also it will review the differential expression of these genes in the.
Download Citation | c-Myc and telomerase activation | Comment on: Telomerase activation by c-Myc in human mammary epithelial cells requires additional genomic changes.Alexey V. Bazarov, William C. A parallel G-quadruplex structure was recently identified in the NHE III 1 element of the c-myc gene promoter that functioned as a transcriptional repressor. Different series of telomeric G-quadruplex interacting ligands reported to block telomerase activity were evaluated in a new PCR stop assay on the c-myc quadruplex (Pu22myc). Results indicated that the cationic porphyrin TMPyP4 previously.
Results. HPV-16 E6 Induction of the Telomerase hTERT Promoter Requires Myc Activity. Recent studies have demonstrated that E6 transactivation of the hTERT promoter does not involve increased Myc protein expression (22, 23).However, to evaluate whether Myc protein might be necessary for E6-mediated transactivation, we coexpressed E6 and Mad expression vectors in telomerasenegative HFKs This study examined telomerase activity and gene expression profiles for three genes in Gallus gallus domesticus: telomerase reverse transcriptase (chTERT), telomerase RNA (chTR), and c‐myc. Expression of these genes was studied in chicken embryonic stem (chES) cells, chicken embryo fibroblasts (CEFs), and DT40 cells using quantitative real‐time polymerase chain reaction Therefore, by expressing c-Myc, we express telomerase to extend telomeres. We want to maintain the length of telomeres, not to constantly increase it. Therefore, we have designed a two component oscillatory system in order to express doses of c-Myc, and thus doses of telomerase. This system is less affected by differences in promoter strengths, repressor half lives, and repressor dissociation. Recent evidence suggests that the Myc and Mad1 proteins are implicated in the regulation of the gene encoding the human telomerase reverse transcriptase (hTERT), the catalytic subunit of telomerase. We have analyzed the in vivo interaction between endogenous c-Myc and Mad1 proteins and the hTERT promoter in HL60 cells with the use of the chromatin immunoprecipitation assay
c-Myc overexpression has been implicated in several malignancies including gastric cancer. Here, we report that acidified bile acids enhance tumor progres-sion and telomerase activity in gastric cancer via c-Myc activation both in vivo and in vitro. c-Myc mRNA and protein levels were assessed in ten primary an Myc activates telomerase. Wang J., Xie L.Y., Allan S., Beach D., Hannon G.J. Telomere maintenance has been proposed as an essential prerequisite to human tumor development. The telomerase enzyme is itself a marker for tumor cells, but the genetic alterations that activate the enzyme during neoplastic transformation have remained a mystery Human telomerase is a ribonucleoprotein composed of human telomerase RNA component (hTR), human telomerase catalytic subunit (hTERT), and a PinX1 Inhibits Telomerase Activity in Gastric Cancer Cells Through Mad1/c-Myc Pathway | springermedizin.d A known Myc transcriptional target is the catalytic subunit of telomerase, Tert. However, the However, the contribution of Tert activation to Myc-induced tumorigenesis in vivo remains unknown
human telomerase reverse transcriptase (TERT) protein (1132 amino acids, 127 kDa)  and the telomerase RNA component (TERC), where both components are required for telomerase activity . A telomerase-associated protein example, DNA repair protein Ku (a heterodimer of Ku70 and Ku80 subunits), interacts with telomerase through interac Retraction Note: siRNA directed against c-Myc inhibits proliferation and downregulates human telomerase reverse transcriptase in human colon cancer Colo 320 cells | springermedizin.de Skip to main conten Mit jeder Zellteilung werden die Telomere kürzer, da die (normale) DNA-Polymerase am Folgestrang nicht mehr ansetzen kann. Die Telomerase gleicht die Verkürzung der DNA-Enden wieder aus. Dieses Enzym ist ein RNA-Protein-Komplex, der als spezialisierte Reverse Transkriptase funktioniert. Dazu fügt sie an das 3'-OH-Ende G-reiche Wiederholungseinheiten an, deren RNA-Vorlage sich in der. Telomerase Reverse Transcriptase and p53 Regulate Mammalian Peripheral Nervous System and CNS Axon Regeneration Downstream of c-Myc Jin-Jin Ma , Xin Ju , Ren-Jie Xu , Wei-Hua Wang , Zong-Ping Luo , Chang-Mei Liu , Lei Yang , Bin Li , Jian-Quan Chen , Bin Meng , Hui-Lin Yang , Feng-Quan Zhou and Saijilaf Interaction of c-Myc promoter G-quadruplex with NM23H2 was shown to regulate c-Myc in cancer cells in 2009 Regulation of c-myc through Human telomerase reverse transcriptase (hTERT) is also directly regulated through promoter G-quadruplex by interaction with the transcription factor NM23H2 where epigenetic modifications were dependent on NM23H2-G-quadruplex association. [41
Free Shipping Worldwide. Lengthen Telomere Recently, it has been reported that telomerase regulates Myc-dependent oncogenesis by stabilizing Myc levels on chromatin (Koh et al., 2016). Taken together, these findings suggest that telomerase contributes to activation of growth-promoting genes through multiple signaling pathways in cancer. In this work, we show that telomerase interacts with NOL1 and promotes transcription of the cyclin D1 gene in the absence of Wnt or NF-κB signaling. Whereas NOL1 alone is sufficient to bind the.
Now, however, scientists report that using telomerase to extend the life-span of human tissue culture cells is associated with activation of the c-myc oncogene and thus may present some level of. Reptin and its cooperation with c-MYC. Thus, Reptin regulates telomerase at two different levels. This finding, together with the requirementof Reptin for the cl onogenic potential of cancer cells and its over-expression in gastriccancer and other solid tumors, suggests that Reptin may be a putative therapeutic target. Background Telomerase, an RNA-dependent DNA polymerase responsible for. A more recently discovered approach to cell immortalization is through the expression of Telomerase Reverse Transcriptase protein (TERT), particularly for cells that are most affected by telomere length (e.g., human). This protein is inactive in most somatic cells, but when hTERT is exogenously expressed, the cells are able to maintain sufficient telomere lengths to avoid replicative senescence. Analysis of several telomerase-immortalized cell lines has verified that the cells maintain a. that negatively regulates telomerase activity in HaCaTcells (Cerezo et al, 2002). In addition, we examined the role of c-Myc, because, similarly to other models (Wang et al,1998;Wuet al,1999), c-Myc also proved to regulate positively hTERT transcription in the Ha-CaT keratinocytes. The HaCaT-myc cells therefore represented THE JOURNAL † RESEARCH † www.fasebj.org HMGB2 is a negative regulator of telomerase activity in human embryonic stem and progenitor cells Martin Kuˇc´ırek,* Alireza J. Bagherpoor,* Josef Jaroˇs, †,‡Aleˇs Hampl, and Michal Stros*ˇ,1 *Laboratory of Analysis of Chromosomal Proteins, Department of Cell Biology and Radiobiology, Institute of Biophysics of the Czec
The promoter of the telomerase component hTERT was constitutively activated in GSE24-2 cells in a c-myc expression-dependent manner. Deletion analyses and mutagenesis of the human c-myc promoter demonstrated that the target sequence for activation was the nuclease hypersensitive element-III (NHEIII) site located upstream to the P1 region of the promoter. Further, expression of GSE24-2 in cell lines derived from patients with X-DC and in VA13 cells induced increased hTERT RNA and hTR levels. Telomerase, which comprises both TERT and the telomerase RNA (TERC), adds telomere repeats to chromosome ends to offset the loss of telomere sequences that occurs due to the end-replication problem, the inability of DNA polymerase to replicate fully the lagging DNA strand of telomerase is also upregulated by the MYC oncoprotein. The upregulation of telomerase by MYC might also help elucidate the pathway of telomerase activation in human lymphocytes. Telomerase activity is induced in some early hematopoietic precursor cells and also in mature, fully differentiated T and B cells upon antigen recepto . 4 Telomerase, the enzyme that allows telomeres to maintain their length, is normally present at low levels in untransformed cells, but its activity increases with cell cycle entry, peaking in the S phase. Telomerase consists of an RNA template (TERC) and the catalytic component (TERT). TERT activity is controlled, in part, by.
It has been suggested that LMP1 can be used to aid myc control telomerase. In addition, we also found that C-terminus of LMP1, including CTAR1 and CTAR2 domains participated in telomerase activation. Together, these findings suggested that LMP1 activated telomerase via c-myc. KW - C-myc. KW - Epstein-Barr virus latent membrane protein Some studies favored the view that MYC drove initial proliferation and subsequent differentiation, concomitant with the activation of the p53 G2 checkpoint and also demonstrated that inactivation of the p53-Rb pathway is required for immortalization through overepression of MYC [13, 14]. Thus, some cases of intestinal metaplasia may carry short telomeres and due to this telomere dysfunction, MYC stimulates hTERT expression. However, in the absence of genome checkpoint functions (i.
c-Myc, b-catenin, NF-jB STAT, and Pax proteins), some of which can even have dual functions (including AP-1 and HIF-2) [for detailed review see 1]. Further-more, there are epigenetic mechanisms and genetic alter- ations that can cause activation of hTERT expression. The latter are mainly hTERT promoter mutations, of which the two most common ones - C288T and C250T - have been identiﬁed. Telomerase is an enzyme that adds specific DNA sequence repeats (TTAGGG in all vertebrates) to the 3' (three prime) end of DNA strands in the telomere regions, which are found at the ends of eukaryotic chromosomes. The telomeres contain condensed DNA material, giving stability to the chromosomes. The enzyme is a reverse transcriptase that carries its own RNA molecule, which is used as a. Die Telomerase wird ansonsten nur in Stammzellen und in der Embryonalentwicklung aktiv. Eine Forschergruppe Neben dieser Telomerregulation konnte auch gezeigt werden, das Line-1 auch Stammzell-assoziierte Gene wie KLF-4 und c-myc induziert. Beide Mechanismen, die Induktion von humaner Telomerase sowie die Induktion von Stammzellfaktoren, erklären nun auch den negativen prognostischen. Recent studies have reported that, in addition to TL maintenance, telomerase is also involved in gene expression regulation, cell proliferation, apoptosis, WNT/β-catenin signaling, NF-kB signaling, MYC-driven oncogenesis, DDR, cell adhesion and migration, and epithelial-mesenchymal transition [32-35]. All these activities of telomerase are thought to contribute significantly to the. MYC; MYC proto-oncogene, bHLH transcription factor: Aliases: MRTL, MYCC, c-Myc, bHLHe39 : Location: 8q24.21: Summary: This gene is a proto-oncogene and encodes a nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. The encoded protein forms a heterodimer with the related transcription factor MAX. This complex binds to the E box DNA.
Telomerase is a specialized RNA template-containing reverse transcriptase able to compensate for telomeric loss occurring at each cell replication, which is reactivated in tumor cells [ 13 ]. In previous studies we found that saquinavir was able to increase telomerase in T cells [ 8, 9 ] It has been shown that c-Myc induces hTERT expression and telomerase activity in normal human mammary epithelial cell and primary fibroblasts . Sequence analysis indicates that the hTERT promoter bears two E-boxes in its core region −34 and −242 nucleotides upstream of the ATG (37, 110, 224, 246). The presence of E-boxes is compatible with a direct effect of c-Myc on hTERT activation. Zusammenfassung Die Telomerase ist ein Ribonukleoproteinkomplex, der für die vollständige Verdoppelung der chromosomalen Enden, der Telomer-DNA, verantwortlich ist. Somit wirkt die Telomerase der Verkürzung der Telomere-DNA bei der Replikation entgegen und verhindert dadurch genetische Instabilität. Die Regulation der Enzymaktivität ist in erster Linie abhängig von der Expression ihrer.
Stabilization of c-myc G-Quadruplex DNA, inhibition of telomerase activity, disruption of mitochondrial functions and tumor cell apoptosis by platinum(II) complex with 9-amino-oxoisoaporphine. European Journal of Medicinal Chemistry 2016, 124, 417-427. DOI: 10.1016/j.ejmech.2016.08.054 Telomerase is composed of an RNA component, telomerase RNA (TR), and a protein component, telomerase reverse transcriptase (TERT) . #3676), anti-phospho acetyl-CoA carboxylase (p-ACC) (Cell Signaling Technology, #3661), anti-c-Myc (Santa Cruz Biotechnology, Santa Cruz, CA, USA, sc788) and anti-actin (ABM, Richmond, BC, Canada, G043). Quantitative real-time PCR. Total RNA from each sample. Read Telomerase activity and differential expression of telomerase genes and c‐myc in chicken cells in vitro, Developmental Dynamics on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips As both telomerase inhibition and Myc inhibition are cancer-specific targets for cancer therapy, ginger extract might prove to be beneficial as a complementary agent in cancer prevention and maintenance therapy. Figures; References; Related; Details; Cited By. Telomerase Inhibitors from Natural Products and Their Anticancer Potential . 21 December 2017 | International Journal of Molecular. Recent advances in telomerase inhibition have been achieved by using antisense oligonucleotides and ribozymes to target the telomerase mRNA or the telomerase RNA template. Also, small molecules are potent catalytic inhibitors of telomerase. However, therapeutic regimes incorporating these agents will be challenging to implement in the clinic because of their delayed effectiveness. Drugs that.
Telomerase is required for the complete replication of chromosomal ends. In tumors, the human telomerase reverse transcriptase subunit (hTERT) is up-regulated, thereby removing a critical barrier for unlimited cell proliferation. To understand more about hTERT regulation, we measured hTERT RNA levels by quantitative reverse transcription (RT)-PCR Telomerase is a ribonucleoprotein complex that maintains the length and integrity of telomeres, and thereby enables cellular proliferation. Understanding the regulation of telomerase in hematopoietic cells is relevant to the pathogenesis of leukemia, in which telomerase is constitutively activated, as well as bone marrow failure syndromes that feature telomerase insufficiency
Telomerase reverse transcriptase promoter mutations in hepatocellular carcinogenesis (CACGTG), located at -242 bp and -34 bp to the translational start site, for c-Myc binding . The binding of c-Myc to the E-box activates TERT transcription, suggesting a role of c-Myc in regulation of the expression of TERT [19,20]. GC-boxes (GGGCGG), the binding sites for zinc finger transcription factor. B: Schema der Regulation der humanen Telomerase (Kyo et al. 2002) Noch bevor der hTERT-Promotor charakterisiert wurde, konnte Wang et al. 1998 zeigen, dass durch retrovirale Überexpression des c-myc Onkogens in Telomerase-negativen Zellen Telomerase induziert werden kann (Wang et al. 1998). Mit de Here we show that the ethyl acetate fraction of ginger extract can inhibit the expression of the two prominent molecular targets of cancer, the human telomerase reverse transcriptase (hTERT) and c-Myc, in A549 lung cancer cells in a time- and concentration-dependent manner. The treated cells exhibited diminished telomerase activity because of reduced protein production rather than direct.
Telomerase defers the onset of telomere shortening and cellular senescence by adding telomeric repeat DNA to chromosome ends, and its activation contributes to carcinogenesis. Telomerase minimally consists of the telomerase reverse transcriptase (TERT) and the telomerase RNA (TR). However, how telomerase assembles is largely unknown. Here, we demonstrate that PES1 (Pescadillo), a protein. SiRNA directed against c-Myc inhibits proliferation and downregulates human telomerase reverse transcriptase in human colon cancer Colo 320 cells-3 . By Huang Hao (95580), Yu Nancai (95581), Fu Lei (95582), Wei Xiong (58411), Su Wen (95583), Huang Guofu (95584), Wu yanxia (95585), Huang Hanju (95586), Liu Qian (95587) and Xiao Hong (95588) Cite . BibTex; Full citation; Abstract. Ts colony. The c-Myc protein level was also determined in SKBR-3 and HBL-100 cells. Our results show that the cucurbitacin B inhibits growth and telomerase activity in the three breast cancer cell lines and exerts an obvious inhibitory effect in the estrogen receptor (ER)-negative breast cancer SKBR-3 cells. The expression of hTERT and c-Myc were also inhibited by cucurbitacin B, In addition, a clear. XPC, Oct-4, Sox2, and c-Myc were downregulated at P7 compared with P3 in DPCs with long-term culture. XPC genes were upregulated in DPCs at P2 after transfection and maintained high expression level at P3 and P7. Cell proliferation, PI value, and telomerase activity were enhanced, whereas apoptosis was suppressed in transfected DPCs. Oct-4/Sox2.