ESRP1 knockdown in breast cancer cells
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ABSTRACT:
PROVIDER: PRJNA515910 | ENA |
REPOSITORIES: ENA
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Project description:ESRP1 is an epithelial-specific splicing factor. It mainly regulates expressions of genes related to intercellular adhesion, actin cytoskeleton, cell polarity and cell migration at the post-transcriptional level by alternative splicing. It also plays an important role in the development and progression of cancers. This study analyzed the transcriptome changes of ESRP1 stably overexpression SKOV3 cells by high-throughput sequencing, discovered and validated the functional effects of ESRP1 on ovarian cancer cells
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Project description:RNA-binding proteins and their mediated alternative splicing play important roles in tumor cell invasion and migration. Here, we report that ESRP1 is a key regulator of gastric cancer cell metastasis. Overexpression of ESRP1 inhibits the invasion and migration of gastric cancer cells, in vivo and in vitro. Furthermore, we found that ESRP1 causes a wide range of alternative splicing events, and ESRP1-mediated CLSTN1 exon skipping may be a key mechanism for its inhibition of gastric cancer cell invasion and metastasis. Taken together, our data provide a molecular framework for the role of ESRP1 in gastric cancer development.
2023-12-27 | GSE233685 | GEO
Project description:Pnn depletion in developing mouse corneal epithelium led to disrupted alternative splicing of multiple ESRP-regulated epithelial-type exons. In human corneal epithelial cells (HCET), ESRP1 and PNN displayed close localization in and around nuclear speckles and their physical association in protein complexes was identified. In this study, gene expression profiling was performed to identify PNN- and ESRP1-regulated alternative pre-mRNA splicing in human corneal epithelial cells. Immortalized human corneal epithelial cells harboring doxycycline-inducible shRNA against PNN or ESRP1 were created. Whole transcriptome array analysis on ESRP1 or PNN knockdown HCET cells revealed clear alterations in transcript level and splicing pattern of specific subsets of genes with significant overlaps in their candidate targets. Our data suggest that ESRP1 and PNN modulate alternative splicing of a specific subset of exons, but not general splicing events. ESRP1 and PNN may together participate in the regulation of epithelial-specific splicing program in a genome-wide fashion. Parental HCET, shRNA-PNN HCET, and shRNA-ESRP1 HCET cells were cultured for 3 days with/without doxycycline. Total RNA was isolated from four biological replicates of each sample group and then subjected to hGlue3_0 transcriptome array analysis.
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Project description:Colorectal cancer (CRC) ranks third for incidence and second for number of deaths among cancer types worldwide. Poor patient survival, due to inadequate response to currently available treatment regimens, points out to the urgent requirement for personalized therapy in CRC patients. Our aim was to provide mechanistic insights into the pro-tumorigenic role of the RNA-binding protein ESRP1, which is highly expressed in a subset of CRC patients. We show that, in CRC cells, ESRP1 binds to and has the same trend in expression as RAC1b, a well-known tumor promoter. Thus, RAC1b may be a potential therapeutic target in ESRP1-overexpressing CRC. RNA binding proteins are well recognized as critical regulators of tumorigenic processes through their capacity to modulate RNA biogenesis, including alternative splicing, RNA stability and mRNA translation. The RNA binding protein Epithelial Splicing Regulatory Protein 1 (ESRP1) can act as tumor suppressor or promoter in a cell type- and disease context-dependent manner. We have previously shown that elevated expression of ESRP1 in colorectal cancer cells can drive tumor progression. To gain further insights into the pro-tumorigenic mechanism of action of ESRP1, we performed cDNA microarray analysis on two colorectal cells lines modulated for ESRP1 expression. Intriguingly, RAC1b was highly expressed, both at mRNA and protein levels, in ESRP1-overexpressing cells, while the opposite trend was observed in ESRP1-silenced CRC cells. Moreover, RAC1 and RAC1b mRNA co-immunoprecipitate with ESRP1 protein. Silencing of RAC1b expression significantly reduced the number of soft agar colonies formed by ESRP1-overexpressing cells, suggesting that ESRP1 acted, at least partially, through RAC1b in its tumor-promoting activities in CRC cells. Thus, our data provide molecular cues on targetable candidates in CRC cases with high ESRP1 expression.
2021-08-31 | GSE180126 | GEO
Project description:Colorectal cancer (CRC) ranks third for incidence and second for number of deaths among cancer types worldwide. Poor patient survival, due to inadequate response to currently available treatment regimens, points out to the urgent requirement for personalized therapy in CRC patients. Our aim was to provide mechanistic insights into the pro-tumorigenic role of the RNA-binding protein ESRP1, which is highly expressed in a subset of CRC patients. We show that, in CRC cells, ESRP1 binds to and has the same trend in expression as RAC1b, a well-known tumor promoter. Thus, RAC1b may be a potential therapeutic target in ESRP1-overexpressing CRC. RNA binding proteins are well recognized as critical regulators of tumorigenic processes through their capacity to modulate RNA biogenesis, including alternative splicing, RNA stability and mRNA translation. The RNA binding protein Epithelial Splicing Regulatory Protein 1 (ESRP1) can act as tumor suppressor or promoter in a cell type- and disease context-dependent manner. We have previously shown that elevated expression of ESRP1 in colorectal cancer cells can drive tumor progression. To gain further insights into the pro-tumorigenic mechanism of action of ESRP1, we performed cDNA microarray analysis on two colorectal cells lines modulated for ESRP1 expression. Intriguingly, RAC1b was highly expressed, both at mRNA and protein levels, in ESRP1-overexpressing cells, while the opposite trend was observed in ESRP1-silenced CRC cells. Moreover, RAC1 and RAC1b mRNA co-immunoprecipitate with ESRP1 protein. Silencing of RAC1b expression significantly reduced the number of soft agar colonies formed by ESRP1-overexpressing cells, suggesting that ESRP1 acted, at least partially, through RAC1b in its tumor-promoting activities in CRC cells. Thus, our data provide molecular cues on targetable candidates in CRC cases with high ESRP1 expression.
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Project description:Expression data from LncRNA TROJAN knockdown breast cancer cells
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Project description:The transcriptome-wide response of hypoxic breast cancer cells upon MBNL2 knockdown was analyzed. Differential gene expression and alternative splicing were investigated.
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