Molecular analysis of transferrin receptor mRNA expression in acute myeloid leukaemia

Κollia, Panagoula; Stavroyianni, Niki; Stamatopoulos, Kostas; Zoi, Katerina; Viniou, Nora‐Athina; Mantzourani, Marina; Noguchi, Constance Tom; Paterakis, George; Abazis, Danai; Pangalos, Constantinos; Loukopoulos, Dimitris; Yataganas, Xenophon

doi:10.1046/j.1365-2141.2001.03065.x

Cited by 19 publications

(16 citation statements)

References 26 publications

(32 reference statements)

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“…The sequences of oligonucleotides were 5 s: 5Ј-CAG TGG CCA ATT TCT TCT CG-3Ј and 11as: 5Ј-CTG CCT CTG GTG TAT CCT CAC A-3Ј. 22 …”

Section: Detection Of Transferrin Receptor Mrna By Rt-pcrmentioning

confidence: 99%

“…The sequences of oligonucleotides were 5 s: 5Ј-CAG TGG CCA ATT TCT TCT CG-3Ј and 11as: 5Ј-CTG CCT CTG GTG TAT CCT CAC A-3Ј. 22 RNA was first converted to cDNA by Superscript reverse transcriptase and then amplified by Platinum Taq polymerase using Superscript One Step reverse-transcription-polymerase chain reaction (RT-PCR) kit (Invitrogen). The relative expression of TfR1 was analyzed using quantitative RT-PCR with GAPDH as an internal control.…”

mentioning

confidence: 99%

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Gambogic acid, a novel ligand for transferrin receptor, potentiates TNF-induced apoptosis through modulation of the nuclear factor-κB signaling pathway

Pandey

Sung

Ahn

et al. 2007

Blood

235

176

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IntroductionAlthough plant-derived products have served humankind as treatments of various ailments for centuries, neither their active components nor their molecular targets are fully understood. Identifying the active chemical entities and their molecular targets can lead to discovering new clinical uses of such products, as in the cases of vincristine, vinblastine, paclitaxel, camptothecin, roscovitin, and homoharringtonine. 1 Between 1980 and 2000, as many as 70% of all drugs approved by the US Food and Drug Administration to treat cancer were based on natural sources. 1,2 Gambogic acid (GA) is a naturally occurring brownish-toorange resin called gamboge, which is derived from Garcinia hanburyi. It has a long history of medicinal use in Southeast Asia, and it is used as a folk medicine and coloring agent in China. Recent studies showed that GA can inhibit the growth of a wide variety of tumor cells, including cells of human hepatoma, 3 breast cancer, 4 gastric carcinoma, 5-8 and lung carcinoma. 9 Using cell-and caspase-based high-throughput screening assays, Zhang et al identified GA as a potent inducer of apoptosis. 4 Studies have also indicated that GA suppresses the growth of human tumors (eg, lung carcinoma, 9 and hepatoma). 3 How GA mediates these effects is not fully understood, but it has been shown to inhibit telomerase and telomerase reverse transcriptase mRNA expression, 3,8,9 inhibit human telomerase reverse transcriptase (hTERT) promoter, 8 suppress cyclin-dependent kinase 7 (CDK7)-mediated phosphorylation of CDC2/34, 7 down-regulate Bcl-2, 5 and interact with c-Myc. 3 A recent report suggests that GA mediates its apoptotic effects through its interaction with the transferrin receptor (TfR1). 10 Because hTERT, c-Myc, and Bcl-2 gene expression modulated by GA is regulated by NF-B activation, it is possible that GA mediates its effects by modulating the NF-B pathway.NF-B is a transcription factor that consists of 5 proteins: c-Rel, RelA (p65), RelB, NF-B1 (p50 and p105), and NF-B2 (p52). 11 They are regulated by inhibitors of the inhibitory subunit of NF-B (IB) family of anchorin domain-containing proteins, which includes IB␣, IB␤, IB␥, IB⑀, Bcl-3, p105, and p100. 11 When inactive, NF-B is sequestered in the cytoplasm as a heterotrimer consisting of p50, p65, and IB subunits. Most carcinogens, inflammatory agents, and tumor promoters, including cigarette smoke, phorbol ester, okadaic acid, H 2 O 2 , and tumor necrosis factor (TNF), have been shown to activate NF-B. In response to an activation signal, the IB␣ subunit is phosphorylated at serine residues 32 and 36, ubiquitinated at lysine residues 21 and 22, and degraded through the proteasomal pathway, thus exposing the nuclear localization signals on the p50-p65 heterodimer. The p65 is then phosphorylated, leading to nuclear translocation and binding to a specific sequence in DNA, which in turn results in gene transcription. The phosphorylation of IB␣ is catalyzed by IB␣ kinase (IKK), which is essential for NF-B activation. IKK consists of 3 subun...

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“…The sequences of oligonucleotides were 5 s: 5Ј-CAG TGG CCA ATT TCT TCT CG-3Ј and 11as: 5Ј-CTG CCT CTG GTG TAT CCT CAC A-3Ј. 22 …”

Section: Detection Of Transferrin Receptor Mrna By Rt-pcrmentioning

confidence: 99%

mentioning

confidence: 99%

Gambogic acid, a novel ligand for transferrin receptor, potentiates TNF-induced apoptosis through modulation of the nuclear factor-κB signaling pathway

Pandey

Sung

Ahn

et al. 2007

Blood

235

176

View full text Add to dashboard Cite

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“…The TfR (CD71) is a well-known substrate for clathrin-dependent endocytosis (19)(20)(21)(22), and its endocytosis and trafficking are critically important for its essential role in cellular uptake of iron in the form of holo-transferrin. Intriguingly, transferrin and TfR have both been implicated in thymocyte development (23)(24)(25) and TfR has been found to be elevated on immature cycling thymocytes (26) and leukemias (27,28). Therefore, we asked whether Hrb might participate in regulation of CD71 in the context of oncogenic Notch signaling.…”

Section: Hrb Loss Increases Surface Cd71 and Is Required For Efficienmentioning

confidence: 99%

HIV-1 Rev–binding protein accelerates cellular uptake of iron to drive Notch-induced T cell leukemogenesis in mice

Khwaja¹,

Liu²,

Tong³

et al. 2010

J. Clin. Invest.

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Somatic activating mutations in Notch1 contribute to the pathogenesis of T cell acute lymphoblastic lymphoma (T-ALL), but how activated Notch1 signaling exerts this oncogenic effect is not completely understood. Here we identify HIV-1 Rev-binding protein (Hrb), a component of the clathrin-mediated endocytosis machinery, as a critical mediator of Notch-induced T-ALL development in mice. Hrb was found to be a direct transcriptional target of Notch1, and Hrb loss reduced the incidence or delayed the onset of T-ALL in mouse models in which activated Notch1 signaling either contributes to or drives leukemogenesis. Consistent with this observation, Hrb supported survival and proliferation of hematopoietic and T cell precursor cells in vitro. We demonstrated that Hrb accelerated the uptake of transferrin, which was required for upregulation of the T cell protooncogene p21. Indeed, iron-deficient mice developed Notch1-induced T-ALL substantially more slowly than control mice, further supporting a critical role for iron uptake during leukemogenesis. Taken together, these results reveal that Hrb is a critical Notch target gene that mediates lymphoblast transformation and disease progression via its ability to satisfy the enhanced demands of transformed lymphoblasts for iron. Further, our data suggest that Hrb may be targeted to improve current treatment or design novel therapies for human T-ALL patients.

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“…Among the five remaining CGs with medium expression on ABI plate, three were discarded due to minor reasons: HPRT and PGK (X-chromosomal location) and TFRC (variable expression in hematopoietic cells). 33,34 Among the six additional primer and probe sets, covering four CGs, in-house B2M RQ-PCR set appeared to be suitable since no statistically significant difference between PB and BM was observed. Comparison between normal and leukemic samples was not possible since only four normal samples were tested (see Material and methods).…”

Section: Control Genes For Diagnosis and Mrd Detection By Rq-pcr E Bementioning

confidence: 99%

Evaluation of candidate control genes for diagnosis and residual disease detection in leukemic patients using ‘real-time’ quantitative reverse-transcriptase polymerase chain reaction (RQ-PCR) – a Europe against cancer program

et al. 2003

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Real-time quantitative RT-PCR (RQ-PCR) is a sensitive tool to monitor minimal residual disease (MRD) in leukemic patients through the amplification of a fusion gene (FG) transcript. In order to correct variations in RNA quality and quantity and to calculate the sensitivity of each measurement, a control gene (CG) transcript should be amplified in parallel to the FG transcript. To identify suitable CGs, a study group within the Europe Against Cancer (EAC) program initially focused on 14 potential CGs using a standardized RQ-PCR protocol. Based on the absence of pseudogenes and the level and stability of the CG expression, three genes were finally selected: Abelson (ABL), beta-2-microglobulin (B2M), and beta-glucuronidase (GUS). A multicenter prospective study on normal (n ¼ 126) and diagnostic leukemic (n ¼ 184) samples processed the same day has established reference values for the CG expression. A multicenter retrospective study on over 250 acute and chronic leukemia samples obtained at diagnosis and with an identified FG transcript confirmed that the three CGs had a stable expression in the different types of samples. However, only ABL gene transcript expression did not differ significantly between normal and leukemic samples at diagnosis. We therefore propose to use the ABL gene as CG for RQ-PCRbased diagnosis and MRD detection in leukemic patients. Overall, these data are not only eligible for quantification of fusion gene transcripts, but also for the quantification of aberrantly expressed genes.

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Molecular analysis of transferrin receptor mRNA expression in acute myeloid leukaemia

Cited by 19 publications

References 26 publications

Gambogic acid, a novel ligand for transferrin receptor, potentiates TNF-induced apoptosis through modulation of the nuclear factor-κB signaling pathway

Gambogic acid, a novel ligand for transferrin receptor, potentiates TNF-induced apoptosis through modulation of the nuclear factor-κB signaling pathway

HIV-1 Rev–binding protein accelerates cellular uptake of iron to drive Notch-induced T cell leukemogenesis in mice

Evaluation of candidate control genes for diagnosis and residual disease detection in leukemic patients using ‘real-time’ quantitative reverse-transcriptase polymerase chain reaction (RQ-PCR) – a Europe against cancer program

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