Evidence map›Paper›PMID 28566733›Full record

ArticleScientific reports2017

A Benzothiazole Derivative (5g) Induces DNA Damage And Potent G2/M Arrest In Cancer Cells.

Mahesh Hegde, Supriya V Vartak, Chandagirikoppal V Kavitha, Hanumappa Ananda, Doddakunche S Prasanna, Vidya Gopalakrishnan, Bibha Choudhary, Kanchugarakoppal S Rangappa, Sathees C Raghavan

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 31 citations in OpenAlex.

  1. Mutations atMolecular and cellular biology · 2024
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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

9 authors at 4 institutions in 1 country.

Mahesh HegdeDepartment of Biochemistry, Indian Institute of Science, Bangalore, 560012, India.
Supriya V VartakDepartment of Biochemistry, Indian Institute of Science, Bangalore, 560012, India.
Chandagirikoppal V KavithaDepartment of Biochemistry, Indian Institute of Science, Bangalore, 560012, India.
Hanumappa AnandaDepartment of Biochemistry, Indian Institute of Science, Bangalore, 560012, India.
Doddakunche S PrasannaDepartment of Nanotechnology, Visvesvaraya Technological University, Center for Postgraduate Studies, Bengaluru Region, Muddenahalli, Chikkaballapur, Bangalore, 562101, India.
Vidya GopalakrishnanDepartment of Biochemistry, Indian Institute of Science, Bangalore, 560012, India.
Bibha ChoudharyInstitute of Bioinformatics and Applied Biotechnology, Electronics City, Bangalore, 560100, India.
Kanchugarakoppal S RangappaDepartment of Studies in Chemistry, University of Mysore, Mysuru, 570006, India.
Sathees C RaghavanDepartment of Biochemistry, Indian Institute of Science, Bangalore, 560012, India. sathees@biochem.iisc.ernet.in.
Indian Institute of Science Bangalore · INInstitute of Bioinformatics and Applied Biotechnology · INUniversity of Mysore · INVisvesvaraya Technological University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemically synthesized small molecules play important role in anticancer therapy. Several chemical compounds have been reported to damage the DNA, either directly or indirectly slowing down the cancer cell progression by causing a cell cycle arrest. Direct or indirect reactive oxygen species formation causes DNA damage leading to cell cycle arrest and subsequent cell death. Therefore, identification of chemically synthesized compounds with anticancer potential is important. Here we investigate the effect of benzothiazole derivative (5g) for its ability to inhibit cell proliferation in different cancer models. Interestingly, 5g interfered with cell proliferation in both, cell lines and tumor cells leading to significant G2/M arrest. 5g treatment resulted in elevated levels of ROS and subsequently, DNA double-strand breaks (DSBs) explaining observed G2/M arrest. Consistently, we observed deregulation of many cell cycle associated proteins such as CDK1, BCL2 and their phosphorylated form, CyclinB1, CDC25c etc. Besides, 5g treatment led to decreased levels of mitochondrial membrane potential and activation of apoptosis. Interestingly, 5g administration inhibited tumor growth in mice without significant side effects. Thus, our study identifies 5g as a potent biochemical inhibitor to induce G2/M phase arrest of the cell cycle, and demonstrates its anticancer properties both ex vivo and in vivo.

Indexed as

AnimalsApoptosisBenzothiazolesCell Cycle CheckpointsCell Cycle ProteinsCell ProliferationDNA Breaks, Double-StrandedDNA DamageGene Expression Regulation, NeoplasticHeLa CellsHumansMiceNeoplasmsReactive Oxygen SpeciesXenograft Model Antitumor AssaysbenzothiazoleBenzothiazolesCell Cycle ProteinsReactive Oxygen Species

Identifiers

PMID28566733
PMCPMC5451441
OpenAlexW2618479889

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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.