Evidence map›Paper›PMID 33805467›Full record

ArticleAntioxidants (Basel, Switzerland)2021

Targeting AKT/mTOR and Bcl-2 for Autophagic and Apoptosis Cell Death in Lung Cancer: Novel Activity of a Polyphenol Compound.

Sucharat Tungsukruthai, Onrapak Reamtong, Sittiruk Roytrakul, Suchada Sukrong, Chanida Vinayanwattikun, Pithi Chanvorachote

Abstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. International journal of molecular sciences · 2023
    Article
  6. Article
  7. Review
  8. Pennogenin-3-Pharmaceuticals (Basel, Switzerland) · 2022
    Article
  9. Article
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

6 authors.

Sucharat TungsukruthaiDoctor of Philosophy Program in Interdisciplinary Pharmacology, Graduate School, Chulalongkorn University, Bangkok 10330, Thailand.
Onrapak ReamtongDepartment of Molecular Tropical Medicine and Genetics, Faculty of Tropical Medicine, Mahidol University, Bangkok 10400, Thailand.ORCID 0000-0002-1154-6485
Sittiruk RoytrakulFunctional Ingredients and Food Innovation Research Group, National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathumthani 12120, Thailand.ORCID 0000-0003-3696-8390
Suchada SukrongResearch Unit of DNA Barcoding of Thai Medicinal Plants, Chulalongkorn University, Bangkok 10330, Thailand.ORCID 0000-0003-4062-2632
Chanida VinayanwattikunDivision of Medical Oncology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
Pithi ChanvorachoteCell-Based Drug and Health Products Development Research Unit, Chulalongkorn University, Bangkok 10330, Thailand.

Funding

Chulalongkorn University CU_GR_62_63_33_05
6 · The paper itself

Abstract

Autophagic cell death (ACD) is an alternative death mechanism in resistant malignant cancer cells. In this study, we demonstrated how polyphenol stilbene compound PE5 exhibits potent ACD-promoting activity in lung cancer cells that may offer an opportunity for novel cancer treatment. Cell death caused by PE5 was found to be concomitant with dramatic autophagy induction, as indicated by acidic vesicle staining, autophagosome, and the LC3 conversion. We further confirmed that the main death induction caused by PE5 was via ACD, since the co-treatment with an autophagy inhibitor could reverse PE5-mediated cell death. Furthermore, the defined mechanism of action and upstream regulatory signals were identified using proteomic analysis. Time-dependent proteomic analysis showed that PE5 affected 2142 and 1996 proteins after 12 and 24 h of treatment, respectively. The crosstalk network comprising 128 proteins that control apoptosis and 25 proteins involved in autophagy was identified. Protein-protein interaction analysis further indicated that the induction of ACD was via AKT/mTOR and Bcl-2 suppression. Western blot analysis confirmed that the active forms of AKT, mTOR, and Bcl-2 were decreased in PE5-treated cells. Taken together, we demonstrated the novel mechanism of PE5 in shifting autophagy toward cell death induction by targeting AKT/mTOR and Bcl-2 suppression.

Indexed as

AKT/mTORapoptosisautophagic cell deathautophagyBcl-2lung cancerpolyphenolproteomicsstilbene compounds

Identifiers

PMID33805467
PMCPMC8066183

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.