Evidence map›Paper›PMID 32824273›Full record

ArticleNutrients2020

Sinensetin Induces Autophagic Cell Death through p53-Related AMPK/mTOR Signaling in Hepatocellular Carcinoma HepG2 Cells.

Seong Min Kim, Sang Eun Ha, Ho Jeong Lee, Shailima Rampogu, Preethi Vetrivel, Hun Hwan Kim, Venu Venkatarame Gowda Saralamma, Keun Woo Lee, Gon Sup Kim

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

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  12. Total Flavonoids inInternational journal of molecular sciences · 2023
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  16. Review
  17. Function and Application of Flavonoids in the Breast Cancer.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Alternative autophagy: mechanisms and roles in different diseases.Cell communication and signaling : CCS · 2022
    Review
  20. 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

9 authors at 3 institutions in 1 country.

Seong Min KimResearch Institute of Life science and College of Veterinary Medicine, Gyeongsang National University, 501 Jinju-daero, Jinju 52828, Korea.ORCID 0000-0003-3359-7504
Sang Eun HaResearch Institute of Life science and College of Veterinary Medicine, Gyeongsang National University, 501 Jinju-daero, Jinju 52828, Korea.
Ho Jeong LeeBiological Resources Research Group, Bioenvironmental Science & Toxicology Division, Gyeongnam Branch Institute, Korea Institute of Toxicology (KIT), 17 Jeigok-gil, Jinju 52834, Korea.ORCID 0000-0001-9646-195X
Shailima RampoguDivision of Life Sciences, Division of Applied Life Science (BK21 Plus), Plant Molecular Biology and Biotechnology Research Center (PMBBRC), Research Institute of Natural Science (RINS), Gyeongsang National University (GNU), 501 Jinju-daero, Jinju 52828, Korea.
Preethi VetrivelResearch Institute of Life science and College of Veterinary Medicine, Gyeongsang National University, 501 Jinju-daero, Jinju 52828, Korea.
Hun Hwan KimResearch Institute of Life science and College of Veterinary Medicine, Gyeongsang National University, 501 Jinju-daero, Jinju 52828, Korea.
Venu Venkatarame Gowda SaralammaCollege of Pharmacy, Yonsei University, Incheon 21983, Korea.
Keun Woo LeeDivision of Life Sciences, Division of Applied Life Science (BK21 Plus), Plant Molecular Biology and Biotechnology Research Center (PMBBRC), Research Institute of Natural Science (RINS), Gyeongsang National University (GNU), 501 Jinju-daero, Jinju 52828, Korea.
Gon Sup KimResearch Institute of Life science and College of Veterinary Medicine, Gyeongsang National University, 501 Jinju-daero, Jinju 52828, Korea.ORCID 0000-0002-0844-1009
Gyeongsang National University · KRKorea Institute of Toxicology · KRYonsei University · KR

Funding

National Research Foundation of Korea 2012M3A9B8019303National Research Foundation of Korea 2020R1A2B5B01001807
6 · The paper itself

Abstract

Sinensetin (SIN) has been reported to exhibit anti-inflammatory and anti-cancer activity. However, the cellular and molecular mechanism by which SIN promotes hepatocellular carcinoma (HCC) cell death remains unclear. In the present study, we investigated the induction of cell death by SIN and its underlying mechanism in HepG2 cells, an HCC cell line. We found that SIN significantly induced cell death in HepG2 cells, whereas the proliferation rate of Thle2, human liver epithelial cells, was unaffected by SIN. SIN-treated HepG2 cells were not affected by apoptotic cell death; instead, autophagic cell death was induced through the p53-mediated AMPK/mTOR signaling pathway. Inhibition of p53 degradation led to both autophagy and apoptosis in HepG2 cells. p53 translocation led to SIN-induced autophagy, whereas p53 translocation inhibited SIN-induced apoptosis. However, SIN showed apoptosis in the p53-mutant Hep3B cell line. Molecular docking simulation of the p53 core domain showed effective binding with SIN, which was found significant compared with the known p53 activator, RITA. Collectively, these data suggest that SIN may be a potential anti-cancer agent targeting autophagic cell death in human liver cancer.

Indexed as

AMP-Activated Protein KinasesAntineoplastic AgentsApoptosisAutophagic Cell DeathCarcinoma, HepatocellularCell SurvivalFlavonoidsHep G2 CellsHumansLiver NeoplasmsMolecular Docking SimulationSignal TransductionTOR Serine-Threonine KinasesTumor Suppressor Protein p53AMP-Activated Protein KinasesAntineoplastic AgentsFlavonoidsMTOR protein, humansinensetinTOR Serine-Threonine KinasesTumor Suppressor Protein p53AMPKautophagyhepatocellular carcinomap53sinensetin

Identifiers

PMID32824273
PMCPMC7468969
OpenAlexW3049408622

What OpenQuestion 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 OpenQuestion graph.