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Effect of the different isoforms of RPL22L1 protein on the transcriptome of human glioblastoma cells and their interactome

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE180466 | GEO | 2021/12/01

REPOSITORIES: GEO

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Interactome of different isoforms of RPL22L1 protein in human glioblastoma cells

Project description:Glioblastoma multiforme (GBM) is characterized by an exceptionally high intratumoral heterogeneity. However, the molecular mechanisms underlying the origin of different GBM cell populations remain unclear. Here we found that the composition of ribosomes of GBM cells in the tumor core and edge differ due to alternative RNA splicing. The acidic pH in the core switches pre-mRNA splicing of the ribosomal gene RPL22L1 toward the RPL22L1b isoform. This allows cells to survive acidosis, increases stemness and correlates with worse patient outcome. Mechanistically, RPL22L1b promotes RNA splicing by binding to lncMALAT1 in the nucleus, resulting in its degradation. Contrarily, in the tumor edge region, RPL22L1a interacts with ribosomes in cytoplasm and upregulates translation of multiple mRNAs including TP53. We found that RPL22L1 isoform switch is regulated by SRSF4 and identified the compound, that inhibits this process and decreases tumor growth. These findings demonstrate how distinct GBM cell populations arise during tumor growth. Targeting this mechanism may decrease GBM heterogeneity and facilitate therapy.

2021-12-01 | GSE180464 | GEO

Effect of the different isoforms of RPL22L1 protein on the transcriptome of human glioblastoma cells.

2021-12-01 | GSE180465 | GEO

Interactome of different isoforms of RPL22L1 protein in human glioblastoma cells

Project description:Interactome of different isoforms of RPL22L1 protein in human glioblastoma cells

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Effect of the different isoforms of RPL22L1 protein on the transcriptome of human glioblastoma cells and their interactome

Project description:Effect of the different isoforms of RPL22L1 protein on the transcriptome of human glioblastoma cells and their interactome

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Effect of the different isoforms of RPL22L1 protein on the transcriptome of human glioblastoma cells.

Project description:Effect of the different isoforms of RPL22L1 protein on the transcriptome of human glioblastoma cells.

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Mapping the chemotherapy-induced RNA interactome in Glioblastoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-04-24 | GSE98128 | GEO

RPL22L1, a novel candidate oncogene promotes temozolomide resistance by activating STAT3 in glioblastoma.

Project description:Aggressiveness and drug resistance are major challenges in the clinical treatment of glioblastoma (GBM). Our previously research reported a novel candidate oncogene ribosomal protein L22 like 1 (RPL22L1). The aim of this study was to elucidate the potential role and mechanism of RPL22L1 in progression and temozolomide (TMZ) resistance of GBM. Online database, tissue microarrays and clinical tissue specimens were used to evaluate the expression and clinical implication of RPL22L1 in GBM. We performed cell function assays, orthotopic and subcutaneous xenograft tumor models to evaluate the effects and molecular mechanisms of RPL22L1 on GBM. RPL22L1 expression was significantly upregulated in GBM and associated with poorer prognosis. RPL22L1 overexpression enhanced GBM cell proliferation, migration, invasion, TMZ resistance and tumorigenicity, which could be reduced by RPL22L1 knockdown. Further, we found RPL22L1 promoted mesenchymal phenotype of GBM and the impact of these effects was closely related to EGFR/STAT3 pathway. Importantly, we observed that STAT3 specific inhibitor (Stattic) significantly inhibited the malignant functions of RPL22L1, especially on TMZ resistance. RPL22L1 overexpressed increased combination drug sensitive of Stattic and TMZ both in vitro and in vivo. Moreover, Stattic effectively restored the sensitive of RPL22L1 induced TMZ resistance in vitro and in vivo. Our study identified a novel candidate oncogene RPL22L1 which promoted the GBM malignancy through STAT3 pathway. And we highlighted that Stattic combined with TMZ therapy might be an effective treatment strategy in RPL22L1 high-expressed GBM patients.

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SETMAR isoforms in glioblastoma: A matter of protein stability.

Project description:Glioblastomas (GBMs) are the most frequent and the most aggressive brain tumors, known for their chemo- and radio-resistance, making them often incurable. We also know that SETMAR is a protein involved in chromatin dynamics and genome plasticity, of which overexpression confers chemo- and radio-resistance to some tumors. The relationships between SETMAR and GBM have never been explored. To fill this gap, we define the SETMAR status of 44 resected tumors and of GBM derived cells, at both the mRNA and the protein levels. We identify a new, small SETMAR protein (so called SETMAR-1200), enriched in GBMs and GBM stem cells as compared to the regular enzyme (SETMAR-2100). We show that SETMAR-1200 is able to increase DNA repair by non-homologous end-joining, albeit with a lower efficiency than the regular SETMAR protein. Interestingly, the regular/small ratio of SETMAR in GBM cells changes depending on cell type, providing evidence that SETMAR expression is regulated by alternative splicing. We also demonstrate that SETMAR expression can be regulated by the use of an alternative ATG. In conclusion, various SETMAR proteins can be synthesized in human GBM that may each have specific biophysical and/or biochemical properties and characteristics. Among them, the small SETMAR may play a role in GBMs biogenesis. On this basis, we would like to consider SETMAR-1200 as a new potential therapeutic target to investigate, in addition to the regular SETMAR protein already considered by others.

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MYC protein interactome profiling reveals functionally distinct regions that cooperate to drive tumorigenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

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