Evidence map›Paper›PMID 34715855›Full record

ArticleCancer cell international2021

Proteo-transcriptomics meta-analysis identifies SUMO2 as a promising target in glioblastoma multiforme therapeutics.

Aswani P Krishna, Sebastian John, Puja Laxmanrao Shinde, Rashmi Mishra

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 55% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Aswani P KrishnaBrain and Cerebro-Vascular Mechanobiology Research, Laboratory of Translational Mechanobiology, Department of Neurobiology, Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram, 695014, Kerala, India.
Sebastian John *Brain and Cerebro-Vascular Mechanobiology Research, Laboratory of Translational Mechanobiology, Department of Neurobiology, Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram, 695014, Kerala, India.
Puja Laxmanrao Shinde *Brain and Cerebro-Vascular Mechanobiology Research, Laboratory of Translational Mechanobiology, Department of Neurobiology, Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram, 695014, Kerala, India.
Rashmi MishraBrain and Cerebro-Vascular Mechanobiology Research, Laboratory of Translational Mechanobiology, Department of Neurobiology, Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram, 695014, Kerala, India. rashmimishra@rgcb.res.in.ORCID http://orcid.org/0000-0001-6729-2528
Rajiv Gandhi Centre for Biotechnology · INManipal Academy of Higher Education · IN

Funding

department of biotechnology , ministry of science and technology BT/PR26735/MED/31/378/2017department of biotechnology , ministry of science and technology BT/PR4959/MED/30/770/2012department of biotechnology , ministry of science and technology BT/PR6331/GBD/27/403/2012department of biotechnology , ministry of science and technology BT/RLF/Re-entry/16/2011
6 · The paper itself

Abstract

backgroundGlioblastoma multiforme (GBM) is a deadly brain tumour with minimal survival rates due to the ever-expanding heterogeneity, chemo and radioresistance. Kinases are known to crucially drive GBM pathology; however, a rationale therapeutic combination that can simultaneously inhibit multiple kinases has not yet emerged successfully.

resultsHere, we analyzed the GBM patient data from several publicly available repositories and deduced hub GBM kinases, most of which were identified to be SUMOylated by SUMO2/3 isoforms. Not only the hub kinases but a significant proportion of GBM upregulated genes involved in proliferation, metastasis, invasion, epithelial-mesenchymal transition, stemness, DNA repair, stromal and macrophages maintenance were also identified to be the targets of SUMO2 isoform. Correlatively, high expression of SUMO2 isoform was found to be significantly associated with poor patient survival.

conclusionsAlthough many natural products and drugs are evidenced to target general SUMOylation, however, our meta-analysis strongly calls for the need to design SUMO2/3 or even better SUMO2 specific inhibitors and also explore the SUMO2 transcription inhibitors for universally potential, physiologically non-toxic anti-GBM drug therapy.

Indexed as

Cancer drug target discoveryGlioblastoma multiformeKinases and cancerSUMO2TCGA

Identifiers

PMID34715855
PMCPMC8555349
OpenAlexW3208968924

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.