Evidence map›Paper›PMID 35462210›Full record

ArticleTranslational oncology2022

Eriodictyol mediated selective targeting of the TNFR1/FADD/TRADD axis in cancer cells induce apoptosis and inhibit tumor progression and metastasis.

Shibjyoti Debnath, Abhisek Sarkar, Dipanwita Das Mukherjee, Subha Ray, Barun Mahata, Tarun Mahata, Pravat K Parida, Troyee Das, Rupak Mukhopadhyay, Zhumur Ghosh and 1 more

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  8. Review
  9. Review
  10. Article
  11. Article
  12. Optimized De Novo Eriodictyol Biosynthesis inInternational journal of molecular sciences · 2023
    Article
  13. FADD as a key molecular player in cancer progression.Molecular medicine (Cambridge, Mass.) · 2022
    Review
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 2 institutions in 1 country.

Shibjyoti DebnathDivision of Molecular Medicine, Bose Institute, Kolkata, West Bengal, 700054, India.
Abhisek SarkarDivision of Molecular Medicine, Bose Institute, Kolkata, West Bengal, 700054, India.
Dipanwita Das MukherjeeDivision of Molecular Medicine, Bose Institute, Kolkata, West Bengal, 700054, India.
Subha RayDivision of Molecular Medicine, Bose Institute, Kolkata, West Bengal, 700054, India.
Barun MahataDivision of Molecular Medicine, Bose Institute, Kolkata, West Bengal, 700054, India.
Tarun MahataDivision of Molecular Medicine, Bose Institute, Kolkata, West Bengal, 700054, India.
Pravat K ParidaDivision of Molecular Medicine, Bose Institute, Kolkata, West Bengal, 700054, India.
Troyee DasThe Bioinformatics Center, Bose Institute, Kolkata, West Bengal, 700054, India.
Rupak MukhopadhyayDepartment of Molecular Biology & Biotechnology, Tezpur University, Assam 784028.
Zhumur GhoshThe Bioinformatics Center, Bose Institute, Kolkata, West Bengal, 700054, India.
Kaushik BiswasDivision of Molecular Medicine, Bose Institute, Kolkata, West Bengal, 700054, India. Electronic address: kbiswas_1@yahoo.com.
Bose Institute · INTezpur University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While the anti-inflammatory activities of Eriodictyol, a plant-derived flavonoid is well-known, reports on its anti-cancer efficacy and selective cytotoxicity in cancer cells are still emerging. However, little is known regarding its mechanism of selective anti-cancer activities. Here, we show the mechanism of selective cytotoxicity of Eriodictyol towards cancer cells compared to normal cells. Investigation reveals that Eriodictyol significantly upregulates TNFR1 expression in tumor cells (HeLa and SK-RC-45) while sparing the normal cells (HEK, NKE and WI-38), which display negligible TNFR1 expression, irrespective of the absence or presence of Eriodictyol. Further investigation of the molecular events reveal that Eriodictyol induces apoptosis through expression of the pro-apoptotic DISC components leading to activation of the caspase cascade. In addition, CRISPR-Cas9 mediated knockout of TNFR1 completely blocks apoptosis in HeLa cells in response to Eriodictyol, confirming that Eriodictyol induced cancer cell apoptosis is indeed TNFR1-dependent. Finally, in vivo data demonstrates that Eriodictyol not only impedes tumor growth and progression, but also inhibits metastasis in mice implanted with 4T1 breast cancer cells. Thus, our study has identified Eriodictyol as a compound with high selectivity towards cancer cells through TNFR1 and suggests that it can be further explored for its prospect in cancer therapeutics.

Indexed as

Cell deathCRISPR-Cas9FlavonoidsSelective cytotoxicityTumorigenesis

Identifiers

PMID35462210
PMCPMC9046888
OpenAlexW4224286615

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.