NDRG1/2 expression is inhibited in primary acute myeloid leukemia

Tschan, Mario P.; Shan, Deborah; Laedrach, Judith; Eyholzer, Marianne; Leibundgut, Elisabeth Oppliger; Baerlocher, Gabriela M.; Tobler, Andreas; Stroka, Deborah; Fey, Martin F.

doi:10.1016/j.leukres.2009.08.037

Cited by 41 publications

(32 citation statements)

References 21 publications

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“…As a downstream regulated gene of Myc, it has been confirmed that the expression of NDRG2 was reduced in many types of tumors. Our previous data and other reports showed that NDRG2 expression was decreased in a variety of malignancy such as breast cancer, lung cancer, hepatocellular cancer, glioma, oral squamous cell carcinoma, thyroid cancer, and myeloid leukemia, which suggested that it might serve as an important role in the modulation of the aggressive behavior of malignant tumor progression (7)(8)(9)(10)(11)(12)(13)(14)(15)(16). We have previously shown that NDRG2 expression was significantly decreased in colorectal cancer (CRC) and associated with tumor differentiation status by real-time PCR, Western blot, and immunohistochemical assay (14,17).…”

Section: Introductionmentioning

confidence: 75%

Prediction of Colorectal Cancer Relapse and Prognosis by Tissue mRNA Levels of NDRG2

Chu

Zhang

et al. 2011

Molecular Cancer Therapeutics

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NDRG2 (N-Myc downstream-regulated gene 2) is aberrantly expressed in colorectal cancer (CRC) and related to tumor differentiation status. In the present study, we investigated the association between NDRG2 mRNA levels in primary CRC to determine whether levels of NDRG2 mRNA could predict relapse and survival. A hospital-based study cohort of 226 CRC patients was involved in the study. NDRG2 mRNA levels were determined by real-time PCR. Correlations of NDRG2 mRNA expression with tumor clinicopathologic features, disease-free survival, and overall survival of the patients were studied. Significant decreased expression of NDRG2 mRNA was detected in tumor specimens. NDRG2 mRNA expression significantly correlated with differentiation status (P < 0.001), lymph node metastasis (P < 0.001), and tumor node metastasis stage (P < 0.001). Patients with reduced level of NDRG2 mRNA had a statistically significantly shorter disease-free survival and overall survival duration than patients with preserved expression of NDRG2 mRNA. In multivariate analysis, NDRG2 mRNA level was found to be an independent prognostic factor for both disease-free survival and overall survival of CRC patients. The present research provided the first evidence that decreased NDRG2 mRNA expression in primary human CRC might be a powerful, independent predictor of recurrence and outcome.

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Section: Introductionmentioning

confidence: 75%

Prediction of Colorectal Cancer Relapse and Prognosis by Tissue mRNA Levels of NDRG2

Chu

Zhang

et al. 2011

Molecular Cancer Therapeutics

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“…For example, NDRG1 is identified as a tumor suppressor-its expression could reduce the invasion and metastasis of breast, colon, prostate, and pancreatic cancers by modulating proliferation, differentiation, and angiogenesis of cancer cells (Kehlen et al, 2003;Kovacevic et al, 2008;Liu et al, 2011;Malette et al, 2003;Tschan et al, 2010). NDRG2 is also described as a tumor suppressor.…”

Section: Discussionmentioning

confidence: 99%

NDRG4 is Downregulated in Glioblastoma and Inhibits Cell Proliferation

Ding

Zhang

Yoon

et al. 2012

OMICS: A Journal of Integrative Biology

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NDRG4 is a member of the N-myc downregulated gene family (NDRG) belonging to the alpha/beta hydrolase superfamily. We have previously documented discrepancy between our analysis of the expression and function of NDRG4 in glioblastoma multiforme (GBM) and a recent publication by Schilling et al., who reported that NDRG4 is upregulated in GBM compared to human cortex tissues and knock down of NDRG4 reduced the viability of GBM cells. In the present study, we found that NDRG4 is indeed downregulated, at both RNA and protein levels, by quantitative RT-PCR and Western blot analysis, in GBM compared to normal tissues, and that over expression of NDRG4 inhibited proliferation of GBM cells. These new observations can inform the selection of lead molecular compounds for drug discovery as well as novel diagnostics for GBM. They also lend evidence to NDRG4 a role of tumor suppressor.

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“…Gene expression assays for ATG2A, ATG2B, and ATG14L used in a 96-well format on the StepOnePlus Sequence detection system were Hs00390076_m1, Hs00216083_m1, and Hs00208732_m1, respectively (Life Technologies, Zug, Switzerland). Hydroxymethylbilane synthase (HMBS) primers and probes have been described previously ( 54 ), and data analysis was performed as described ( 55 ).…”

Section: Quantitative Real-time Rt-pcrmentioning

confidence: 99%

Lipid droplet and early autophagosomal membrane targeting of Atg2A and Atg14L in human tumor cells

Pfisterer

Bakula²,

Frickey

et al. 2014

Journal of Lipid Research

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Cellular autophagy is an evolutionarily highly conserved degradation pathway for both stochastic and selective degradation of cytoplasmic cargo within the lysosomal compartment. As such, this process of self-eating secures cellular homeostasis and survival, while malfunction contributes to the initiation and development of many agerelated human diseases including diabetes, tumorigenesis, and neurodegeneration ( 1-4 ). Autophagy is constitutively active on a low basal level resulting in constant cytoplasmic turnover and the specifi c elimination of macromolecule aggregates and damaged organelles. Following a great variety of cellular insults such as nutrient starvation, autophagy is induced above basal level and produces monomers and energy for subsequent recycling processes.Autophagy is hallmarked by the formation of doublemembrane vesicles called autophagosomes that are generated from initial preautophagosomal membrane precursors or phagophores. Elongation of the phagophore and subsequent vesicle closure complete the formation of autophagosomes that sequester the cytoplasmic cargo and communicate with the lysosomal compartment to acquire acidic hydrolases for cargo breakdown ( 5-7 ).Abstract Autophagy is a lysosomal bulk degradation pathway for cytoplasmic cargo, such as long-lived proteins, lipids, and organelles. Induced upon nutrient starvation, autophagic degradation is accomplished by the concerted actions of autophagy-related (ATG) proteins. Here we demonstrate that two ATGs, human Atg2A and Atg14L, colocalize at cytoplasmic lipid droplets (LDs) and are functionally involved in controlling the number and size of LDs in human tumor cell lines. We show that Atg2A is targeted to cytoplasmic ADRP-positive LDs that migrate bidirectionally along microtubules. The LD localization of Atg2A was found to be independent of the autophagic status. Further, Atg2A colocalized with Atg14L under nutrient-rich conditions when autophagy was not induced. Upon nutrient starvation and dependent on phosphatidylinositol 3-phosphate [PtdIns(3)P] generation, both Atg2A and Atg14L were also specifically targeted to endoplasmic reticulum-associated early autophagosomal membranes, marked by the PtdIns(3)P effectors double-FYVE containing protein 1 (DFCP1) and WD-repeat protein interacting with phosphoinositides 1 (WIPI-1) , both of which function at the onset of autophagy. These data provide evidence for additional roles of Atg2A and Atg14L in the formation of early autophagosomal membranes and also in lipid metabolism. -Pfi sterer, S. G., D. Bakula, T. Frickey, A. Cezanne, D. Brigger, M. P. Tschan, H. Robenek, and T. ProikasCezanne. Lipid droplet and early autophagosomal membrane targeting of Atg2A and Atg14L in human tumor cells.

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NDRG1/2 expression is inhibited in primary acute myeloid leukemia

Cited by 41 publications

References 21 publications

Prediction of Colorectal Cancer Relapse and Prognosis by Tissue mRNA Levels of NDRG2

Prediction of Colorectal Cancer Relapse and Prognosis by Tissue mRNA Levels of NDRG2

NDRG4 is Downregulated in Glioblastoma and Inhibits Cell Proliferation

Lipid droplet and early autophagosomal membrane targeting of Atg2A and Atg14L in human tumor cells

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