Proteomics-Based Evidence for a Pro-Oncogenic Role of ESRP1 in Human Colorectal Cancer Cells

Ala, Ugo; Manco, Marta; Mandili, Giorgia; Tolosano, Emanuela; Novelli, Francesco; Provero, Paolo; Altruda, Fiorella; Fagoonee, Sharmila

doi:10.3390/ijms21020575

Cited by 13 publications

(14 citation statements)

References 39 publications

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“…There was marked PI3K/AKT pathway activation and SNAI1 protein overexpression, which skewed the cells towards adopting a partially mesenchymal, and more tumorigenic, molecular profile. These data were further supported by proteomics data on ESRP1-modulated CRC cells [12]. The observation that ESRP1 can have pro-tumorigenic and pro-metastatic activities was also shown by other studies [13][14][15].…”

Section: Introductionsupporting

confidence: 75%

“…The CRC cell lines used in this study had been previously characterized, at both the genomic and transcriptomic level, and authenticated [19]. COLO320DM cells were cultured in RPMI (ThermoFisher Scientific, Monza, Italy), 10% FBS and penicillin/streptomycin (PS), while HCA24 and Caco-2 cells were kept in DMEM, 10% FBS and PS as previously described [12]. ESRP1 expression was modulated with shRNA cloned into pLKO.1 lentiviral vector for stable knockdown and with human ESRP1 ORF cloned into pLX304 lentiviral vector for stable overexpression [11].…”

Section: Cell Lines and Esrp1 Expression Modulationmentioning

confidence: 99%

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The RNA-Binding Protein ESRP1 Modulates the Expression of RAC1b in Colorectal Cancer Cells

Manco

Ala

Cantarella

et al. 2021

Cancers

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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 a 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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Section: Introductionsupporting

confidence: 75%

Section: Cell Lines and Esrp1 Expression Modulationmentioning

confidence: 99%

The RNA-Binding Protein ESRP1 Modulates the Expression of RAC1b in Colorectal Cancer Cells

Manco

Ala

Cantarella

et al. 2021

Cancers

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“…Epithelial splicing regulatory protein-1 (ESRP1) that signals through oncogenic MAPK signaling pathway is also differentially dysregulated in EpKS compared to EnKS patients. ESRP1 has been shown to support anchorage-independent growth of colorectal cancer cells and promote metastasis formation in vitro [67,68]. It also supports mesenchymal to epithelial transition in ovarian cancer cells [69].…”

Section: Hiv-1 Indirectly Promotes Ks Development/maintenancementioning

confidence: 99%

Comparative transcriptome analysis of endemic and epidemic Kaposi’s sarcoma (KS) lesions and the secondary role of HIV-1 in KS pathogenesis

et al. 2020

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In sub-Saharan Africa, endemic Kaposi's sarcoma (EnKS) is still prevalent despite high incidence of epidemic Kaposi's sarcoma (EpKS) resulting from the ongoing HIV-1 epidemic. While KSHV is clearly the etiologic agent of KS, the mechanisms underlying KS development are not fully understood. For example, HIV-1 co-infection and concomitant immune dysfunction have been associated with EpKS development. However, the direct or indirect role(s) of HIV-1, and therefore of immune suppression, in EpKS remains unclear. How, or whether, EpKS is mechanistically distinct from EnKS is unknown. Thus, the absence of HIV-1 co-infection in EnKS provides a unique control for investigating and deciphering whether HIV-1 plays a direct or indirect role in the EpKS tumor microenvironment. We hypothesized that HIV-1 co-infection would induce transcriptome changes that differentiate EpKS from EnKS, thereby defining the direct intra-tumor role of HIV-1 in KS. Comparison of ARTtreated and-naïve patients would further define the impact of ART on the KS transcriptome. We utilized RNA-seq followed by multiparameter bioinformatics analysis to compare transcriptomes from KS lesions to uninvolved control skin. We provide the first transcriptomic comparison of EpKS versus EnKS, ART-treated vs-naïve EpKS and male vs female EpKS to define the roles of HIV-1 co-infection, the impact of ART, and gender on KS gene expression profiles. Our findings suggest that ART-use and gender have minimal impact on transcriptome profiles of KS lesions. Gene expression profiles strongly correlated between EpKS and EnKS patients (Spearman r = 0.83, p<10 −10). A subset of genes involved in tumorigenesis and inflammation/immune responses showed higher magnitude, but not unique dysregulation in EnKS compared to EpKS. While gender and ART had no detectable contribution, the trend toward higher magnitude of gene dysregulation in EnKS coupled with

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“… Tan et al (2012) used the colon cancer cell line, HCT-116, to identify Stathmin-1 as a protein biomarker of cancer cell migration. Ala et al (2020) identified the pro-oncogenic role of ERSP1 in the colorectal cell lines HCA24 and COLO320DM. Hu et al (2018) used HCT-116 and RKO, selectively cultured to be highly invasive, to identify the Cdc42-Cdc42BPA signaling pathway as a marker for colon cancer invasion.…”

Section: D Cell Culturementioning

confidence: 99%

Proteomics of Colorectal Cancer: Tumors, Organoids, and Cell Cultures—A Minireview

Lindhorst

Hummon

2020

Front. Mol. Biosci.

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Proteomics, the study of the complete protein composition of a sample, is an important field for cancer research. Changes in the proteome can serve as a biomarker of cancer or lead to the development of a targeted therapy. This minireview will focus on mass spectrometry-based proteomics studies applied specifically to colorectal cancer, particularly the variety of cancer model systems used, including tumor samples, two-dimensional (2D) and three-dimensional (3D) cell cultures such as spheroids and organoids. A thorough discussion of the application of these systems will accompany the review of the literature, as each provides distinct advantages and disadvantages for colorectal cancer research. Finally, we provide conclusions and future perspectives for the application of these model systems to cancer research as a whole.

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Proteomics-Based Evidence for a Pro-Oncogenic Role of ESRP1 in Human Colorectal Cancer Cells

Cited by 13 publications

References 39 publications

The RNA-Binding Protein ESRP1 Modulates the Expression of RAC1b in Colorectal Cancer Cells

The RNA-Binding Protein ESRP1 Modulates the Expression of RAC1b in Colorectal Cancer Cells

Comparative transcriptome analysis of endemic and epidemic Kaposi’s sarcoma (KS) lesions and the secondary role of HIV-1 in KS pathogenesis

Proteomics of Colorectal Cancer: Tumors, Organoids, and Cell Cultures—A Minireview

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