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A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in human breast cancer cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE59058 | GEO | 2014/09/01

SECONDARY ACCESSION(S): PRJNA254220

REPOSITORIES: GEO

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A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MCF-7 breast cancer cells

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A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MDA-MB-231 breast cancer cells

Project description:The current study analyzed the metadherin (MTDH)-mediated altered gene expression profiles in ER negative MDA-MB-231 cells. Some of these altered gene expressions were further inter connected to various pathways which may eventually be recognized as drug targets or biomarkers in those breast cancers where MTDH plays a role in cancer progression/metastasis. To understand the global differential gene expression profile in MTDH-wild type and a newly identified MTDH-isoform knock down in metastatic breast cancer cells. This data was compared to untreated breast cancer cells.

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A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in human breast cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-09-01 | E-GEOD-59058 | biostudies-arrayexpress

A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MCF-7 breast cancer cells

2014-09-01 | GSE59055 | GEO

A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MCF-7 breast cancer cells

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A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MDA-MB-231 breast cancer cells

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Prognostic value of a newly identified MALAT1 alternatively spliced transcript in breast cancer.

Project description:Epigenetic deregulation is considered as a new hallmark of cancer. The long non-coding RNA MALAT1 has been implicated in several cancers; however, its role in breast cancer is still little known.We used RT-PCR, in situ hybridisation, and RPPA methods to quantify (i) the full-length (FL) and an alternatively spliced variant (?sv) of MALAT1, and (ii) a panel of transcripts and proteins involved in MALAT1 pathways, in a large series of breast tumours from patients with known clinical/pathological status and long-term outcome.MALAT1 was overexpressed in 14% (63/446) of the breast tumours. MALAT1-overexpressed tumour epithelial cells showed marked diffuse nuclear signals and numerous huge nuclear speckles. Screening of the dbEST database led to the identification of ?sv-MALAT1, a major alternatively spliced MALAT1 transcript, with a very different expression pattern compared with FL-MALAT1. This alternative ?sv-MALAT1 transcript was mainly underexpressed (18.8%) in our breast tumour series. Multivariate analysis showed that alternative ?sv-MALAT1 transcript is an independent prognostic factor. ?sv-MALAT1 expression was associated with alterations of the pre-mRNAs alternative splicing machinery, and of the Drosha-DGCR8 complex required for non-coding RNA biogenesis. Alternative ?sv-MALAT1 transcript expression was associated to YAP protein status and with an activation of the PI3K-AKT pathway.Our results reveal a complex expression pattern of various MALAT1 transcript variants in breast tumours, and suggest that this pattern of expressions should be taken into account to evaluate MALAT1 as predictive biomarker and therapeutic target.

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An alternatively spliced p62 isoform promotes breast cancer chemoresistance

Project description:Chemoresistance remains a major obstacle to the successful treatment of breast cancer. Especially, more than 80% of cases cannot achieve pathological complete response (pCR) in patients who received neoadjuvant chemotherapy (NAC). Understanding the mechanisms involved in chemoresistance can guide the development of efficient therapies in patients with breast cancer. Herein, we identified a novel p62 isoform with a short 3′UTR (p62-SU, 662-nt) that is associated with chemoresistance by RNA-sequence and verified by qRT-PCR, 3′RACE, and northern blot in breast cancer cells and tissue specimens. Furthermore, enforced expression of p62-SU dramatically promoted the ability of proliferation, migration, invasion, and chemoresistance compared with p62 isoform with a long/full-length 3′UTR (p62-LU, 1485-nt) in vivo and in vitro. Mechanistically, we revealed that CPSF1 could regulate the 3′UTR shorting of p62 by alternative polyadenylation and then enhanced chemoresistance in breast cancer cells. In addition, we found that p62-SU escaped the repression of miR-124-3p and promoted the ability of p62-SU to produce more protein and, subsequently, p62-dependent chemoresistance. Together, our data suggest the p62-SU, generated by CPSF1, plays an essential role in the regulation of breast cancer chemoresistance through CPSF1-p62-miR-124-3p signaling.

2022-03-06 | GSE197894 | GEO

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