Evidence map›Paper›PMID 35836889›Full record

ArticleAmerican journal of translational research2022

Decoding signal transducer and activator of transcription 1 across various cancers through data mining and integrative analysis.

Hadia Munir, Ayesha Tassaduque Rana, Muhammad Faheem, Saeedah Musaed Almutairi, Tehmina Siddique, Samra Asghar, Mostafa A Abdel-Maksoud, Ayman Mubarak, Fatma Alzahraa A Elkhamisy, Christian R Studenik and 1 more

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2022. 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
0.3field-weighted citation impact, top 42% 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, 2 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

11 authors at 1 institution in 1 country.

Hadia MunirAkhtar Saeed Medical and Dental College Pakistan.
Ayesha Tassaduque RanaAllama Iqbal Medical College Lahore, Pakistan.
Muhammad FaheemDistrict Head Quarter Hospital Faisalabad Faisalabad, Pakistan.
Saeedah Musaed AlmutairiDepartment of Botany and Microbiology, College of Science, King Saud University Riyadh, P.O. 2455, Riyadh 11451, Saudi Arabia.
Tehmina SiddiqueDepartment of Biotechnology, Faculty of Life Sciences, University of Okara Okara, Pakistan.
Samra AsgharDepartment of Medical Laboratory Technology, Faculty of Rehablitation and Allied Health Sciences, Riphah International University Faisalabad, Pakistan.
Mostafa A Abdel-MaksoudDepartment of Botany and Microbiology, College of Science, King Saud University Riyadh, P.O. 2455, Riyadh 11451, Saudi Arabia.
Ayman MubarakDepartment of Botany and Microbiology, College of Science, King Saud University Riyadh, P.O. 2455, Riyadh 11451, Saudi Arabia.
Fatma Alzahraa A ElkhamisyPathology Department, Faculty of Medicine, Helwan University Cairo, Egypt.
Christian R StudenikDepartment of Pharmaceutical Sciences, Division of Pharmacology and Toxicology, University of Vienna Vienna, Austria.
Hamid YazDepartment of Botany and Microbiology, College of Science, King Saud University Riyadh, P.O. 2455, Riyadh 11451, Saudi Arabia.
Allama Iqbal Medical College · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesUsing different online available databases and Bioinformatics tools, we extensively studied the role STAT1 across different cancers.

methodsSTAT1 mRNA, protein expression, and promoter methylation were analyzed and validated using UALCAN, GENT2, Human Protein Atlas (HPA), and MEXPRESS. Furthermore, the potential prognostic values were evaluated through KM plotter. Then, cBioPortal was utilized to examine the STAT1-related genetic mutations, while pathway enrichment analysis was performed using DAVID. To identify STAT1 targeted microRNAs (miRNAs) and transcription factors (TFs) we used Enricher. Moreover, a correlational analysis between STAT1 expression tumor purity and CD8+ T immune cells and a gene-drug interaction network analysis was performed using TIMER, CTD, and Cytoscape.

resultsIn 23 major human cancers, STAT1 expression was notably up-regulated relative to corresponding controls. As well, the elevated expression of STAT1 was exclusively found to be associated with the reduced overall survival (OS) of Esophageal Carcinoma (ESCA), Kidney Renal Clear Cell Carcinoma (KIRC), and Lung adenocarcinoma (LUAD) patients. This implies that STAT1 plays a significant role in the development and progression of these three cancers. Further pathway analysis indicated that STAT1 enriched genes were involved in six critical pathways, while a few interesting correlations were also documented between STAT1 expression and promoter methylation level, tumor purity, CD8+ T immune cells infiltration, and genetic alteration. In addition, we have also predicted a few miRNAs, TFs, and chemotherapeutic drugs that could regulate the STAT1 expression.

conclusionThe current study revealed the shared oncogenic, diagnostic, and prognostic role of STAT1 in ESCA, KIRC, and LUAD.

Indexed as

CancerCD8+ T immune cellsdiagnosticOS analysisprognosticSTAT1

Identifiers

PMID35836889
PMCPMC9274611
OpenAlexW4285613267

What Socratic holds

Textmetadata
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Registered trials

None linked

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 Socratic graph.