p53-targeted lncRNA ST7-AS1 acts as a tumour suppressor by interacting with PTBP1 to suppress the Wnt/β-catenin signalling pathway in glioma

Sheng, Jie; He, Xin; Yu, Wei; Chen, Yingxi; Long, Yuxiang; Wang, Kejian; Zhu, Shaojun

doi:10.1016/j.canlet.2020.12.039

Cited by 51 publications

(34 citation statements)

References 44 publications

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“…Our GSEA analysis showed that high S1PR3 expression was associated with cell cycle, DNA replication, JAK-STAT signaling pathway, MAPK signaling pathway, mTOR signaling pathway, p53 signaling pathway, TGF-β signaling pathway, PD-L1 expression and PD-1 checkpoint pathway, and RNA degradation signaling pathway. Aberrant activation of the essential signaling pathways JAK-STAT, MAPK, mTOR, p53, and TGF-β has been shown to be associated with the development of glioma [36][37][38][39][40]. We investigated and validated the relationship between S1PR3 and related genes based on the TCGA dataset and identi ed the ve most positively associated genes as ANO6, ECM2, ELF4, IQGAP and VIM, while the ve most negatively associated genes were CKMT1A, CKMT1B, KCNIP2, RHBDL1 and RUNDC3.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Influence of S1PR3 expression on the glioma microenvironment and prognostic significance in low-grade gliomas

Chen

Zhong

Xie

et al. 2022

Preprint

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Background The S1P/S1PR3 axis has been demonstrated to be associated with the development of multiple human cancers, but the potential role of it in the biological mechanisms of glioma, par-ticularly TME cell infiltration, remains unknown. Methods We analyzed gene expression data of gliomas and corresponding clinicopathological information to assess overall survival by univariate and multivariate Cox regression. We also analyzed the signaling pathways and genes associated with S1PR3 overexpression by Gene Set Enrichment Analysis, and the characteristics of oncogenic pathways, biological pathways, and TME cell infiltration, and validated the results with PCR, cell proliferation, and migration assays. Results Cox regression analysis confirmed that S1PR3 overexpression was significantly correlated with overall survival and clinicopathological features. Nomogram for prognostic prediction was successfully constructed using S1PR3 and related genes, and Gene Set Enrichment Analysis revealed the association of S1PR3 overexpression with cell cycle, DNA replication, MAPK, p53 and TGF-β signaling pathway. Meanwhile, S1PR3 was shown to be significantly associated with many immune checkpoints and immune cell infiltration. Conclusions Our study demon-strated that S1PR3 overexpression is a potential prognostic molecular marker for poor prognosis in glioma, that S1PR3 plays an important role in immune cell infiltration in TME. And identification of S1PR3-regulated signaling pathways and immune checkpoints enhances our understanding of TME infiltration characteristics, contributes to the development of immunotherapeutic strategies.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Influence of S1PR3 expression on the glioma microenvironment and prognostic significance in low-grade gliomas

Chen

Zhong

Xie

et al. 2022

Preprint

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“…ST7-AS1—suppression of tumorigenicity 7 antisense RNA 1 which is derived from the reverse transcription of the chromosome region 7q31.2 is found to be underexpressed in the tissues of patients with GBM. ST7-AS1 binds and inhibits polypyrimidine tract-binding protein 1 (PTBP1), thus suppressing the Wnt/β-catenin signaling and leading to an increase in the tumor progression ( Sheng et al, 2021 ).…”

Section: The Non Coding Rnamentioning

confidence: 99%

Unveiling a Ghost Proteome in the Glioblastoma Non-Coding RNAs

Cardon

Fournier

Salzet

2021

Front. Cell Dev. Biol.

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Glioblastoma is the most common brain cancer in adults. Nevertheless, the median survival time is 15 months, if treated with at least a near total resection and followed by radiotherapy in association with temozolomide. In glioblastoma (GBM), variations of non-coding ribonucleic acid (ncRNA) expression have been demonstrated in tumor processes, especially in the regulation of major signaling pathways. Moreover, many ncRNAs present in their sequences an Open Reading Frame (ORF) allowing their translations into proteins, so-called alternative proteins (AltProt) and constituting the “ghost proteome.” This neglected world in GBM has been shown to be implicated in protein–protein interaction (PPI) with reference proteins (RefProt) reflecting involvement in signaling pathways linked to cellular mobility and transfer RNA regulation. More recently, clinical studies have revealed that AltProt is also involved in the patient’s survival and bad prognosis. We thus propose to review the ncRNAs involved in GBM and highlight their function in the disease.

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“…In contrast, the tumor suppressor p53 negatively impacts the essential genes and co- essential network modules (Fig 1D)(Wainberg et al, 2021). The meta-analysis indicates known p53-regulated tumor-suppressor lncRNAs (e.g., PICART1 (Cao et al, 2017), LINC00475 (Melo et al, 2016), NEAT1 (Mello et al, 2017), LNCTAM34A / GUARDIN (Hu et al, 2018), and ST7 - AS1 (Sheng et al, 2021)) were consistently negatively associated with the proliferation/growth-regulating co-essential modules (Fig 1E). Literature evidence suggests that elevated levels of these lncRNAs upon p53 activation suppress tumorigenesis (Cao et al, 2017; Hu et al, 2018; Mello et al, 2017; Melo et al, 2016; Sheng et al, 2021).…”

Section: Resultsmentioning

confidence: 99%

“…The meta-analysis indicates known p53-regulated tumor-suppressor lncRNAs (e.g., PICART1 (Cao et al, 2017), LINC00475 (Melo et al, 2016), NEAT1 (Mello et al, 2017), LNCTAM34A / GUARDIN (Hu et al, 2018), and ST7 - AS1 (Sheng et al, 2021)) were consistently negatively associated with the proliferation/growth-regulating co-essential modules (Fig 1E). Literature evidence suggests that elevated levels of these lncRNAs upon p53 activation suppress tumorigenesis (Cao et al, 2017; Hu et al, 2018; Mello et al, 2017; Melo et al, 2016; Sheng et al, 2021). Collectively, our approach recapitulates known proliferation/growth-regulating lncRNAs and predicts cancer cell proliferation/growth dependency of a large number (n=289, >77%) of lncRNAs that are functionally poorly or not at all characterized.…”

Section: Resultsmentioning

confidence: 99%

Systematic lncRNA mapping to genome-wide co-essential pathways uncovers cancer dependency on uncharacterized lncRNAs

Mitra

Adams

Eischen

2022

Preprint

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Quantification of gene dependency across hundreds of cell lines using genome-scale CRISPR screens have revealed co-essential pathways/modules and critical functions of uncharacterized genes. In contrast to protein-coding genes, robust CRISPR-based loss-of-function screens are lacking for long non-coding RNAs (lncRNAs), which are key regulators of many cellular process, leaving many essential lncRNAs unidentified and uninvestigated. Integrating copy-number, epigenetic, and transcriptomic data of >800 cancer cell lines with CRISPR-derived co-essential pathways, our method recapitulates known essential lncRNAs and predicts proliferation/growth dependency of 289 poorly characterized lncRNAs. Analyzing lncRNA dependencies across ten cancer types and their expression alteration by diverse growth-inhibitors across cell types, we prioritize 30 high-confidence pan-cancer proliferation/growth-regulating lncRNAs. Further evaluating two previously uncharacterized top proliferation suppressive lncRNAs (PSLR-1, PSLR-2) showed they are transcriptionally regulated by p53, induced by multiple cancer treatments, and significantly correlate to increased cancer patient survival. These lncRNAs modulate G2 cell cycle-regulating genes within the FOXM1 transcriptional network, inducing a G2 arrest and inhibiting proliferation and colony formation. Collectively, our results serve as a powerful resource for exploring lncRNA-mediated regulation of cellular fitness in cancer, circumventing current limitations in lncRNA research.

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p53-targeted lncRNA ST7-AS1 acts as a tumour suppressor by interacting with PTBP1 to suppress the Wnt/β-catenin signalling pathway in glioma

Cited by 51 publications

References 44 publications

RETRACTED: Influence of S1PR3 expression on the glioma microenvironment and prognostic significance in low-grade gliomas

RETRACTED: Influence of S1PR3 expression on the glioma microenvironment and prognostic significance in low-grade gliomas

Unveiling a Ghost Proteome in the Glioblastoma Non-Coding RNAs

Systematic lncRNA mapping to genome-wide co-essential pathways uncovers cancer dependency on uncharacterized lncRNAs

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