Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The G1 arrest and maintenance mechanism between the long-term G1-arrested and the G1-arrested cells.

ABSTRACT: Non mitotic tumor cells are resistant to conventional chemotherapeutic drugs. However, the mechanisms underlying this phenomenon remain unclear. Here, we found a population that is viable but remains in the G1 phase for an extended period of time (up to 48 h) by Long-term time-lapse observations in Fucci-HCT116 cells and then we conducted DNA microarray-based comparative analyses between the RR (the long-term G1-arrested cells) and R (the G1-arrested cells) fractions, to determine the molecular basis of the G1 arrest/maintenance mechanism. This study is related to GSE34940. The labeled cRNAs were hybridized on 4X44K v2 Agilent Whole Human Genome dual color Microarrays (G4845A) in two dye swap experiments, resulting in four individual microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Daisuke Okuzaki 

PROVIDER: E-GEOD-61088 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Cell cycle-arrested cancer cells are resistant to conventional chemotherapy that acts on the mitotic phases of the cell cycle, although the molecular mechanisms involved in halting cell cycle progression remain unclear. Here, we demonstrated that RFPL4A, an uncharacterized ubiquitin ligase, induced G1 retention and thus conferred decreased sensitivity to chemotherapy in the human colorectal cancer cell line, HCT116. Long term time lapse observations in HCT116 cells bearing a "fluorescence ubiqui  ...[more]

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