Evidence map›Paper›PMID 32840738›Full record

ArticleMolecular and cellular biochemistry2021

Targeting STAT proteins via computational analysis in colorectal cancer.

Begum Dariya, Santoshi Muppala, Gowru Srivani, Saimila Momin, Afroz Alam, Madhu Sudhana Saddala

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Trial
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  3. Molecules (Basel, Switzerland) · 2026
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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

6 authors at 4 institutions in 2 countries.

Begum DariyaDepartment of Bioscience and Biotechnology, Banasthali University, Vanasthali, Rajasthan, 304022, India.
Santoshi MuppalaDepartment of Cardiovascular & Metabolic Sciences, Cleveland Clinic, Cleveland, OH, USA.
Gowru SrivaniDepartment of Bioscience and Biotechnology, Banasthali University, Vanasthali, Rajasthan, 304022, India.
Saimila MominDepartment of Biology, Emory University, Atlanta, GA, 30322, USA.
Afroz AlamDepartment of Bioscience and Biotechnology, Banasthali University, Vanasthali, Rajasthan, 304022, India.
Madhu Sudhana SaddalaSchool of Medicine, University of Missouri-Columbia, Columbia, MO, 65212, USA. saddalam@missouri.edu.ORCID http://orcid.org/0000-0002-6373-7080
Banasthali University · INCleveland Clinic · USEmory University · USUniversity of Missouri · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is the third most common cancer diagnosed worldwide making it a serious global challenge. CRC progression results from dysregulated cytoplasmic transcription factors, including signal transducer and activator of transcription (STAT) proteins that are involved in JAK-STAT pathway. The STAT proteins contain a conserved SH2 domain that facilitates the initiation of STAT activation via binding to tyrosine motifs followed by STAT dimerization. The STAT proteins include STAT1, STAT2 and STAT3 which all facilitate therapeutic targets for many drugs, since they are associated with pathogenesis in various cancers such as CRC. Genistein is an efficient chemopreventive phytochemical drug against CRC. The current investigation presents a computational study performed to investigate the molecular interaction between STAT1, STAT2 and STAT3 proteins with genistein. The molecular dynamic simulation was conducted for STAT2 protein. The studies from molecular docking revealed that the interaction of STAT proteins and genistein is predicted to be effective with better binding energies. Furthermore, targeting STAT3 could be an efficient therapeutic target and understanding the interaction between STAT3 and genistein can help to contribute to a better inhibition process for CRC progression. Treatment with genistein led to significant suppression of cell proliferation and STAT3 protein expression in both CRC (HCT 116 and HT-29) cell lines. This further provides development of efficient STAT inhibitors with better potency and bioavailability.

Indexed as

Binding SitesCell ProliferationColorectal NeoplasmsComputational BiologyGenisteinHCT116 CellsHT29 CellsHumansInflammationMagnetic Resonance SpectroscopyMolecular Docking SimulationMutagenesis, Site-DirectedProtein DomainsProtein Processing, Post-TranslationalSignal TransductionSTAT1 Transcription FactorGenisteinSTAT1 protein, humanSTAT1 Transcription FactorSTAT2 protein, humanSTAT2 Transcription FactorSTAT3 protein, humanSTAT3 Transcription FactorColorectal cancerGenisteinPhytochemicalSTATTranscription factor

Identifiers

PMID32840738
OpenAlexW3080448062

What OpenQuestion holds

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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.