Evidence map›Paper›PMID 36209343›Full record

ReviewMedical oncology (Northwood, London, England)2022

Myricetin-induced apoptosis in triple-negative breast cancer cells through inhibition of the PI3K/Akt/mTOR pathway.

Preeti Sharma, Mohammad Ahmed Khan, Abul Kalam Najmi, Shubhra Chaturvedi, Mohd Akhtar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  13. Anti-proliferative effect ofBiocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2023
    Article
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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

5 authors at 2 institutions in 1 country.

Preeti SharmaDepartment of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard (Hamdard University), Delhi, 110062, India.
Mohammad Ahmed KhanDepartment of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard (Hamdard University), Delhi, 110062, India.
Abul Kalam NajmiDepartment of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard (Hamdard University), Delhi, 110062, India.
Shubhra ChaturvediDivision of Cyclotron and Radiopharmaceutical Sciences, INMAS, DRDO, Timarpur, Delhi, 110054, India.
Mohd AkhtarDepartment of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard (Hamdard University), Delhi, 110062, India. makhtar_ph@jamiahamdard.ac.in.ORCID http://orcid.org/0000-0002-3333-2672
Jamia Hamdard · INInstitute of Nuclear Medicine & Allied Sciences · IN

Funding

ICMR 45/24/2020-Nan-BMS]
6 · The paper itself

Abstract

Breast cancer is still a severe origin of malignant demise in females, and its prevalence is rising worldwide. Triple-negative breast cancer (TNBC) is a diversified aggressive breast tumor distinguished by inadequate prognosis, early recurrence, high invasion, and extremely metastasized disease. Chemotherapy is being used to treat it; however, it has low efficacy. On the other hand, with the growing number of corroborations on subtypes of TNBC and molecular biology of tumors, significant advancement in TNBC targeted treatment has been made. Myricetin (MYR), a polyhydroxyflavonol compound widely found in nature, has been shown to possess anticancer effects in various cancers. Though, the mechanisms and impacts of MYR on metastasis of TNBC remain unclear. Early and late apoptotic cell death and cell proliferation inhibition were observed in MYR-treated TNBC cells. MYR modulated cell cycle, pro-angiogenic, and invasion effects via the mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/Protein kinase B (PKB/also known as AKT) signaling pathways. Moreover, it regulates the expression of MAPK, PI3K/AKT/mTOR, IκB/NF-κB, Hippo, STAT3, GSK-3β, Nrf2/HO-1, TLR, eNOS / NO, ACE, and AChE. Here, we review the anticancer effects of MYR for TNBC and target the PI3K/AKT/mTOR pathway as a therapeutic target for the fruitful treatment of TNBC to summarize MYR's therapeutic potential.

Indexed as

Proto-Oncogene Proteins c-aktTriple Negative Breast NeoplasmsApoptosisCell Line, TumorCell ProliferationFemaleFlavonoidsGlycogen Synthase Kinase 3 betaHumansMitogen-Activated Protein KinasesNF-E2-Related Factor 2NF-kappa BPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesTOR Serine-Threonine KinasesFlavonoidsGlycogen Synthase Kinase 3 betaMitogen-Activated Protein KinasesMTOR protein, humanmyricetinNF-E2-Related Factor 2NF-kappa BPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesApoptosisMAPKMyricetinPI3K/AKT/mTORProliferationTriple-negative breast cancer

Identifiers

PMID36209343
OpenAlexW4303684502

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.