Ontology highlight
ABSTRACT:
PROVIDER: PRJNA148691 | ENA |
REPOSITORIES: ENA
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Project description:N-myc downstream-regulated gene 1 (*NDRG1*) is induced by cellular stress such as hypoxia and DNA damage, and in humans, germ line mutations cause Charcot-Marie-Tooth disease. However, the roles of NDRG1 in the cell are not fully understood. Previously, NDRG1 was shown to mediate doxorubicin resistance under hypoxia, suggesting a role for NDRG1 in cell survival under these conditions. We found decreased apoptosis in doxorubicin-treated cells expressing NDRG1 shRNAs under normoxia, demonstrating a requirement for NDRG1 in apoptosis in breast epithelial cells under normal oxygen pressure. We further compared expression profiles in human breast epithelial cells ectopically over-expressing NDRG1 with cells expressing NDRG1 shRNAs in order to identify biological pathways where NDRG1 is involved. The results suggest that NDRG1 may have roles connected to vesicle transport. The previously reported roles of NDRG1 in apoptosis, myelin sheet maintenance, enhanced exocytosis in mast cells and in cellular responses to hypoxia, heavy metals, and androgen may all converge by NDRG1 having a role linked to vesicle transport.
2011-11-04 | GSE33438 | GEO
Project description:N-myc downstream-regulated gene 1 (*NDRG1*) is induced by cellular stress such as hypoxia and DNA damage, and in humans, germ line mutations cause Charcot-Marie-Tooth disease. However, the roles of NDRG1 in the cell are not fully understood. Previously, NDRG1 was shown to mediate doxorubicin resistance under hypoxia, suggesting a role for NDRG1 in cell survival under these conditions. We found decreased apoptosis in doxorubicin-treated cells expressing NDRG1 shRNAs under normoxia, demonstrating a requirement for NDRG1 in apoptosis in breast epithelial cells under normal oxygen pressure. We further compared expression profiles in human breast epithelial cells ectopically over-expressing NDRG1 with cells expressing NDRG1 shRNAs in order to identify biological pathways where NDRG1 is involved. The results suggest that NDRG1 may have roles connected to vesicle transport. The previously reported roles of NDRG1 in apoptosis, myelin sheet maintenance, enhanced exocytosis in mast cells and in cellular responses to hypoxia, heavy metals, and androgen may all converge by NDRG1 having a role linked to vesicle transport.
2011-11-04 | GSE33437 | GEO
Project description:N-myc downstream-regulated gene 1 (*NDRG1*) is induced by cellular stress such as hypoxia and DNA damage, and in humans, germ line mutations cause Charcot-Marie-Tooth disease. However, the roles of NDRG1 in the cell are not fully understood. Previously, NDRG1 was shown to mediate doxorubicin resistance under hypoxia, suggesting a role for NDRG1 in cell survival under these conditions. We found decreased apoptosis in doxorubicin-treated cells expressing NDRG1 shRNAs under normoxia, demonstrating a requirement for NDRG1 in apoptosis in breast epithelial cells under normal oxygen pressure. We further compared expression profiles in human breast epithelial cells ectopically over-expressing NDRG1 with cells expressing NDRG1 shRNAs in order to identify biological pathways where NDRG1 is involved. The results suggest that NDRG1 may have roles connected to vesicle transport. The previously reported roles of NDRG1 in apoptosis, myelin sheet maintenance, enhanced exocytosis in mast cells and in cellular responses to hypoxia, heavy metals, and androgen may all converge by NDRG1 having a role linked to vesicle transport. Two condition design, MCF-7 and ZR-75-1 cell lines grown in hypoxia compared to cells grown at normoxia.
2011-11-04 | E-GEOD-33438 | biostudies-arrayexpress
Project description:N-myc downstream-regulated gene 1 (*NDRG1*) is induced by cellular stress such as hypoxia and DNA damage, and in humans, germ line mutations cause Charcot-Marie-Tooth disease. However, the roles of NDRG1 in the cell are not fully understood. Previously, NDRG1 was shown to mediate doxorubicin resistance under hypoxia, suggesting a role for NDRG1 in cell survival under these conditions. We found decreased apoptosis in doxorubicin-treated cells expressing NDRG1 shRNAs under normoxia, demonstrating a requirement for NDRG1 in apoptosis in breast epithelial cells under normal oxygen pressure. We further compared expression profiles in human breast epithelial cells ectopically over-expressing NDRG1 with cells expressing NDRG1 shRNAs in order to identify biological pathways where NDRG1 is involved. The results suggest that NDRG1 may have roles connected to vesicle transport. The previously reported roles of NDRG1 in apoptosis, myelin sheet maintenance, enhanced exocytosis in mast cells and in cellular responses to hypoxia, heavy metals, and androgen may all converge by NDRG1 having a role linked to vesicle transport. SUM102 and ME16C2 stably transduced with siRNA against NDRG1 compared with empty vector control ZR-75-1 stably transduced with NDRG1 overexpression construct compared with empty vector control Two condition design
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