Project description:The goal of this study was to determine what the effect of modulating Cnot7 expression levels would have on the steady state transcription program of the 4T1 mammary tumor cell line.
Project description:The goal of this study was to determine what the effect of modulating Cnot7 expression levels would have on the steady state transcription program of the 4T1 mammary tumor cell line. Three biological replicates for over expression compared to vector control. Three biological replicates for two different shRNAs versus shScramble control
Project description:4T1 is a mammary tumor cell line to which the NFAT1 transcription factor is essential for tumorigenesis and metastasis. control or shRNA transduced 4T1 cells growing in culture were collected and RNA was extracted from each sample and processed for hybridization to Affymetrix arrays.
Project description:Previous findings demonstrated that HHT treatment alters cell morphology and MET marker protein levels without affecting the transcriptome in the 4T1 breast cancer cell line. The present study therefore examines the effect of HHT on the proteome.
Project description:Native RNA immunoprecipitation of Cnot7-bound transcripts. Abstract: Accumulating evidence supports the role of an aberrant transcriptome as a driver of tumor cell metastatic potential. Deadenylation is a general regulatory node for post-transcriptional control by microRNAs and other determinants of RNA stability. We show here that CCR4-NOT subunit CNOT7 is a deadenylase-dependent driver of tumor cell autonomous metastatic potential. Metastasis promotion by CNOT7 is dependent on contact with CNOT1 and TOB1. We further show TOB1 independently drives metastasis. RNA-immunoprecipitation and integrated transcriptome wide analyses reveal that CNOT7-regulated transcripts are enriched for a tripartite 3’UTR motif bound by RNA-binding proteins known to complex with CNOT7, TOB1, and CNOT1. Collectively, our data support a model of CNOT7, TOB1, CNOT1, and RNA-binding proteins collectively exerting post-transcriptional control on a metastasis suppressive transcriptional program to drive tumor cell metastasis. 48 total samples, 4-5 biological replicates, two forms of control: input samples and vector controls
