Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human cancer cells treated with unfolded protein response modulators under endoplasmic reticulum stress conditions


ABSTRACT: The unfolded protein response (UPR) is a cellular defense mechanism against glucose deprivation, a cell condition that occurs in solid tumors. A key feature of the UPR is the activation of the transcription program that allows the cell to cope with endoplasmic reticulum (ER) stress. We used micoarrays to show that the UPR transcription program is disrupted by the antitumor macrocyclic compound versipelostatin (VST) and antidiabetic biguanides metformin, buformin and phenformin, depending on cellular glucose availability. Experiment Overall Design: Total 42 samples were prepared for RNA extraction and hybridization on Affymetrix microarrays. Experiment Overall Design: To induce the UPR, we treated cells (HeLa, HT-29, HT1080, MKN74) for 15 or 18 hours under ER stress conditions by replacing the medium with glucose-free medium or by adding either 2-Deoxy-D-glucose (2DG) or Tunicamycin (TM) to glucose-containing medium. UPR modulators (VST, biguanides or pyrvinium pamoate) were added at various final concentrations immediately after cells were placed in glucose-free medium or just before the chemical stressors were added to glucose-containing culture medium.

ORGANISM(S): Homo sapiens

SUBMITTER: Akihiro Tomida 

PROVIDER: E-GEOD-13548 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Chemical genomics identifies the unfolded protein response as a target for selective cancer cell killing during glucose deprivation.

Saito Sakae S   Furuno Aki A   Sakurai Junko J   Sakamoto Asami A   Park Hae-Ryong HR   Shin-Ya Kazuo K   Tsuruo Takashi T   Tomida Akihiro A  

Cancer research 20090512 10


Glucose deprivation, a cell condition that occurs in solid tumors, activates the unfolded protein response (UPR). A key feature of the UPR is the transcription program activation, which allows the cell to survive under stress conditions. Here, we show that the UPR transcription program is disrupted by the antidiabetic biguanides metformin, buformin, and phenformin depending on cellular glucose availability. These drugs inhibit production of the UPR transcription activators XBP1 and ATF4 and indu  ...[more]

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