Evidence map›Paper›PMID 29435821›Full record

ArticleJournal of physiology and biochemistry2018

7,8-Dihydroxycoumarin exerts antitumor potential on DMBA-induced mammary carcinogenesis by inhibiting ERα, PR, EGFR, and IGF1R: involvement of MAPK1/2-JNK1/2-Akt pathway.

Abhishek Kumar, Priyashree Sunita, Shivesh Jha, Shakti P Pattanayak

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Article in Journal of physiology and biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

7 citing papers in PubMed, 24 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Abhishek KumarDivision of Pharmacology, Department of Pharm. Sciences & Technology, Birla Institute of Technology, Mesra, Ranchi, Jharkhand, 835215, India.
Priyashree SunitaGovernment Pharmacy Institute, Department of Health, Family Welfare and Medical Education, Government of Jharkhand, Bariatu, Ranchi, 834009, India.
Shivesh JhaDivision of Pharmacognosy, Department of Pharmaceutical Sciences & Technology, Birla Institute of Technology, Mesra, Ranchi, Jharkhand, 835215, India.
Shakti P PattanayakDivision of Pharmacology, Department of Pharm. Sciences & Technology, Birla Institute of Technology, Mesra, Ranchi, Jharkhand, 835215, India. sppattanayak@bitmesra.ac.in.
Birla Institute of Technology, Mesra · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer (BC) is a persistent and impulsive metabolic disorder with the highest prevalence in women, worldwide. 7,12-Dimethylbenz(a)anthracene (DMBA) is a potent polyaromatic hydrocarbon (PAH)-based carcinogen producing mammary carcinomas in rats resembling the human hormone-dependent BC. 7,8-Dihydroxycoumarin (78DC) is a coumarin derivative that possesses diversified and favorable pharmacology profile to be considered in anticancer research against various malignancies. The present study was intended to investigate the antiproliferative and chemotherapeutic potentials of 78DC (20, 40, and 80 mg/kg BW) against DMBA (20 mg in olive oil)-induced mammary carcinoma Sprague-Dawley rats. We established the in silico approach for evaluation of the effect of 78DC on hormonal (estrogen receptor-α (ERα), progesterone receptor (PR)), growth factor receptors (EGFR and IGFR), 17β-hydroxysteroid dehydrogenase type 1 (17β-HD1), and aromatase. Effect of 78DC on estrogen synthesis, tumor growth, proliferation markers (Ki-67 and PCNA), cytokines (IL-10, IL-1β, IL-12), chemokine (MCP-1), and cellular expressions of ERα, PR, EGFR, IGF1R, p-MAPK1/2, p-JNK1/2, p-Akt, 17β-HD1, and aromatase was evaluated in mammary carcinoma bearing SD rats. DMBA induces large tumor burden and histological alterations in mammary gland with a subsequent increase in ERα, PR, EGFR, IGF1R, Ki-67, proliferating cell nuclear antigen (PCNA ), cytokines, and chemokine expressions. This was also correlated with the changes in rapid cell differentiation and proliferation. In contrast, 78DC treatment to the cancer-bearing animals abbreviated these changes and revealed to possess antitumorigenic and antiproliferative potentials. Further, a significant decrease in expressions of ERα, PR, EGFR, IGFR, p-MAPK1/2, p-JNK1/2, p-Akt, 17β-HD1, and aromatase signifies a reduction in estrogen sensitivity and secondary signaling pathways that may contribute to the prevention of tumor growth. The current findings revealed that 78DC potentially reduce cancer cell proliferation and reverted mammary cancer-induced changes in experimental animals in a dose-dependent manner.

Indexed as

17-Hydroxysteroid Dehydrogenases9,10-Dimethyl-1,2-benzanthraceneAnimalsAntineoplastic AgentsAromataseBiomarkers, TumorCarcinogensCell ProliferationCytokinesDose-Response Relationship, DrugErbB ReceptorsEstrogen Receptor alphaFemaleHumansInflammation MediatorsKi-67 Antigen17-Hydroxysteroid Dehydrogenases3 (or 17)-beta-hydroxysteroid dehydrogenase9,10-Dimethyl-1,2-benzanthraceneAntineoplastic AgentsAromataseBiomarkers, TumorCarcinogensCytokinesdaphnetinErbB ReceptorsEstrogen Receptor alphaInflammation MediatorsKi-67 AntigenProliferating Cell Nuclear AntigenProtein KinasesReceptor, IGF Type 1Receptors, ProgesteroneUmbelliferones7,8-DihydroxycoumarinDMBAEGFRERαIGF1RPRProliferation markersSignaling pathway

Identifiers

PMID29435821
OpenAlexW2790355033

What OpenQuestion holds

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Read underepoch 390

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.