Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Identification of MAX signature on MAX deficient SCLC cell lines

ABSTRACT: To development our gene expression approach, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentialy regulated by the transcription factor MAX.Human SCLC cell lines waere analyzed for mutations at the MAX locus. Those cell lines that were found mutated in MAX and showed no MAX protein expression were used as a models to restore the expression of MAX transcription factor, and Identify MAX signature on Human SCLC. Human SCLC cell lines were hybridyzed in the following manner according for different conditions (Mock -Ø, MAX, shBRG1, MAX-shBRG1): 3 different biological samples for Mock, 3 different biological samples for MAX, 3 different samples for shBRG1 and 3 replicates of the same sample for MAX-shBRG1.

ORGANISM(S): Homo sapiens

SUBMITTER: Antonio Gómez 

PROVIDER: E-GEOD-48559 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

MAX inactivation in small cell lung cancer disrupts MYC-SWI/SNF programs and is synthetic lethal with BRG1.

Romero Octavio A OA   Torres-Diz Manuel M   Pros Eva E   Savola Suvi S   Gomez Antonio A   Moran Sebastian S   Saez Carmen C   Iwakawa Reika R   Villanueva Alberto A   Montuenga Luis M LM   Kohno Takashi T   Yokota Jun J   Sanchez-Cespedes Montse M  

Cancer discovery 20131220 3

Our knowledge of small cell lung cancer (SCLC) genetics is still very limited, amplification of L-MYC, N-MYC, and C-MYC being some of the well-established gene alterations. Here, we report our discovery of tumor-specific inactivation of the MYC-associated factor X gene, MAX, in SCLC. MAX inactivation is mutually exclusive with alterations of MYC and BRG1, the latter coding for an ATPase of the switch/sucrose nonfermentable (SWI/SNF) complex. We demonstrate that BRG1 regulates the expression of M  ...[more]

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