Evidence map›Paper›PMID 32671513›Full record

ArticleMolecular and cellular biochemistry2020

OP16 induces deadly autophagy and apoptosis of cells by inhibiting Akt in esophageal squamous cell carcinoma.

Guiqin Hou, Ang Jia, Li Yang, Yu Zhao, Yi Hu, Wuduo Zhao, Wen Zhao, Hong-Min Liu, Zhaoming Lu

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Multi-Components in ModifiedClinical and experimental gastroenterology · 2025
    Article
  2. Review
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  4. Inhibitory Effects ofEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
  5. 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

9 authors at 1 institution in 1 country.

Guiqin HouState Key Laboratory of Esophageal Cancer Prevention & Treatment, School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Ang JiaState Key Laboratory of Esophageal Cancer Prevention & Treatment, School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Li YangState Key Laboratory of Esophageal Cancer Prevention & Treatment, School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Yu ZhaoState Key Laboratory of Esophageal Cancer Prevention & Treatment, School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Yi HuState Key Laboratory of Esophageal Cancer Prevention & Treatment, School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Wuduo ZhaoCenter of Advanced Analysis & Gene Sequencing, Zhengzhou University, Zhengzhou, 450001, China.
Wen ZhaoState Key Laboratory of Esophageal Cancer Prevention & Treatment, School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Hong-Min LiuState Key Laboratory of Esophageal Cancer Prevention & Treatment, School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Zhaoming LuState Key Laboratory of Esophageal Cancer Prevention & Treatment, School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, 450001, China. lzm310@zzu.edu.cn.ORCID http://orcid.org/0000-0001-5190-1528
Zhengzhou University · CN

Funding

Henan Provincial University Science and Technology Innovation Team, Department of Education of Henan Province 19IRTSTHN001Key Research Project of University, Department of Education of Henan Province 20A350019Science and Technology Department of Henan Province 202102310127
6 · The paper itself

Abstract

backgroundOP16, a derivative of the novel ent-kaurene diterpenoid compound separated from Rabdosia rubescens, has been confirmed for its efficacy and safety in the treatment of esophageal squamous cell carcinoma (ESCC) in our previous study. However, the precise mechanisms of tumor lethality mediated by OP16 have not yet been fully characterized.

aimsTo investigate the effects and molecular mechanism of OP16 on autophagy and apoptosis of ESCC cells.

methodsEffects and mechanism of OP16 on autophagy of ESCC cells were first detected by Western blot, immunofluorescence, mRFP-GFP-LC3 adenovirus infection and transmission electron microscope. Next, function of autophagy and apoptosis induced by OP16 on cell death was investigated by flow cytometry and CCK-8 assay. Finally, molecular mechanism of OP16 affecting autophagy and apoptosis of ESCC cells was explored by Western blot.

resultsWe demonstrated that OP16 could induce autophagy by promoting the formation of autophagosome and autolysosome, and promote autophagic cell death in ESCC. Furthermore, we also found that OP16 could promote cell apoptosis by activating mitochondria apoptosis pathway in ESCC. Finally, we demonstrated that OP16 affecting autophagy and mitochondria apoptosis pathway was mediated by phosphorylation of Akt.

conclusionOur data show that OP16 could promote cell death through affecting autophagy and mitochondria apoptosis pathway mediated by Akt in ESCC, which enriches the theoretical mechanism of anti-tumor effects of OP16 and provides a basis for treatment of OP16 on ESCC.

Indexed as

ApoptosisAutophagyCell ProliferationDiterpenes, KauraneEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaGene Expression Regulation, NeoplasticHumansPhosphorylationProto-Oncogene Proteins c-aktTumor Cells, CulturedDiterpenes, KauraneOP16 compoundProto-Oncogene Proteins c-aktAktApoptosisAutophagyEsophageal squamous cell carcinomaOridonin

Identifiers

PMID32671513
OpenAlexW3042940346

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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.