ArticleHeliyon2022
Allicin promotes autophagy and ferroptosis in esophageal squamous cell carcinoma by activating AMPK/mTOR signaling.
Article in Heliyon, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.
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.
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.
Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Allicin Overcomes Doxorubicin Resistance of Breast Cancer Cells by Targeting the Nrf2 Pathway.Cell biochemistry and biophysics · 2024Article
- International consensus guidelines for the definition, detection, and interpretation of autophagy-dependent ferroptosis.Autophagy · 2024Review
- Article
- Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases.Signal transduction and targeted therapy · 2023Review
- Mechanisms of radiotherapy resistance and radiosensitization strategies for esophageal squamous cell carcinoma.Molecular cancer · 2023Review
- Pungency Perception and the Interaction with Basic Taste Sensations: An Overview.Foods (Basel, Switzerland) · 2023Review
Corrections and comments
- Retraction · 2023-07-06Author Unresponsive · Euphemisms for Plagiarism · Plagiarism of Image · · see also: https://pubpeer.com/publications/C729D0E3F5F34F05C0CF21DB56493A
- Retracted
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The antitumor effects of allicin have been demonstrated in various cancers. However, whether allicin improves esophageal squamous cell carcinoma (ESCC) has not yet been explored. The present study aimed to explore the function and underlying mechanism of action of allicin in ESCC treatment. Our data showed that allicin significantly suppressed ESCC cell proliferation in a dose- and time-dependent manner. A green fluorescent protein-light chain 3 (LC3) transfection assay showed that autophagosomes were elevated in ESCC cells treated with allicin compared with control ESCC cells and that 3-methyladenine (an autophagy inhibitor) reversed allicin-induced LC3 puncta. Furthermore, allicin significantly elevated the ratio of LC3II/LC3I but decreased p62 expression in ESCC cells. Allicin also increased adenosine monophosphate-activated protein kinase (AMPK) phosphorylation but decreased that of the mechanistic target of rapamycin kinase (mTOR), which then induced the elevation of autophagy-related 5 and autophagy-related 7 proteins in ESCC cells. Furthermore, allicin treatment increased the expression of nuclear receptor coactivator 4 (a selective cargo receptor) but suppressed the expression of ferritin heavy chain 1 (the major intracellular iron-storage protein) in ESCC cells and elevated malondialdehyde and Fe
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.