Evidence map›Paper›PMID 25786122›Full record

ArticlePloS one2015

Curcumin and emodin down-regulate TGF-β signaling pathway in human cervical cancer cells.

Pooja Chandrakant Thacker, Devarajan Karunagaran

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 100 citations in OpenAlex.

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  19. Phosphate Toxicity and Epithelial to Mesenchymal Transition.Advances in experimental medicine and biology · 2022
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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

2 authors at 1 institution in 1 country.

Pooja Chandrakant ThackerDepartment of Biotechnology, Bhupat and Jyoti Mehta School of Biosciences, Indian Institute of Technology Madras, Chennai 600036, India.
Devarajan KarunagaranDepartment of Biotechnology, Bhupat and Jyoti Mehta School of Biosciences, Indian Institute of Technology Madras, Chennai 600036, India.
Indian Institute of Technology Madras · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cervical cancer is the major cause of cancer related deaths in women, especially in developing countries and Human Papilloma Virus infection in conjunction with multiple deregulated signaling pathways leads to cervical carcinogenesis. TGF-β signaling in later stages of cancer is known to induce epithelial to mesenchymal transition promoting tumor growth. Phytochemicals, curcumin and emodin, are effective as chemopreventive and chemotherapeutic compounds against several cancers including cervical cancer. The main objective of this work was to study the effect of curcumin and emodin on TGF-β signaling pathway and its functional relevance to growth, migration and invasion in two cervical cancer cell lines, SiHa and HeLa. Since TGF-β and Wnt/β-catenin signaling pathways are known to cross talk having common downstream targets, we analyzed the effect of TGF-β on β-catenin (an important player in Wnt/β-catenin signaling) and also studied whether curcumin and emodin modulate them. We observed that curcumin and emodin effectively down regulate TGF-β signaling pathway by decreasing the expression of TGF-β Receptor II, P-Smad3 and Smad4, and also counterbalance the tumorigenic effects of TGF-β by inhibiting the TGF-β-induced migration and invasion. Expression of downstream effectors of TGF-β signaling pathway, cyclinD1, p21 and Pin1, was inhibited along with the down regulation of key mesenchymal markers (Snail and Slug) upon curcumin and emodin treatment. Curcumin and emodin were also found to synergistically inhibit cell population and migration in SiHa and HeLa cells. Moreover, we found that TGF-β activates Wnt/β-catenin signaling pathway in HeLa cells, and curcumin and emodin down regulate the pathway by inhibiting β-catenin. Taken together our data provide a mechanistic basis for the use of curcumin and emodin in the treatment of cervical cancer.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic Agents, Phytogenicbeta CateninCell Line, TumorCell MovementCell ProliferationCollagenCurcuminCyclin D1Cyclin-Dependent Kinase Inhibitor p21Drug CombinationsDrug SynergismEmodinEpithelial-Mesenchymal TransitionFemaleHeLa CellsAntineoplastic Agents, Phytogenicbeta CateninCCND1 protein, humanCollagenCTNNB1 protein, humanCurcuminCyclin D1Cyclin-Dependent Kinase Inhibitor p21Drug CombinationsEmodinLamininmatrigelNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomerasePIN1 protein, humanProtein Serine-Threonine KinasesProteoglycansReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IISmad3 ProteinSMAD3 protein, humanSmad4 ProteinSMAD4 protein, humanSNAI1 protein, humanSnail Family Transcription FactorsTranscription FactorsTransforming Growth Factor betaWnt Proteins

Identifiers

PMID25786122
PMCPMC4365016
OpenAlexW2014436209

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.