Evidence map›Paper›PMID 28258023›Full record

ArticleRedox biology2017

Importance of ROS-mediated autophagy in determining apoptotic cell death induced by physapubescin B.

Jian Xu, Yihua Wu, Guang Lu, Shujun Xie, Zhongjun Ma, Zhe Chen, Han-Ming Shen, Dajing Xia

Abstract read
In one paragraph

Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–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

29 citing papers in PubMed.

  1. Article
  2. International journal of molecular sciences · 2025
    Article
  3. Article
  4. Review
  5. Review
  6. Frontiers in pharmacology · 2023
    Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Identification of HRSC advances · 2019
    Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors.

Jian XuDepartment of Toxicology, School of Public Health, Zhejiang University, 866 Yu-Hang-Tang Road, Hangzhou 310058, PR China.
Yihua WuDepartment of Toxicology, School of Public Health, Zhejiang University, 866 Yu-Hang-Tang Road, Hangzhou 310058, PR China.
Guang LuDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Shujun XieDepartment of Toxicology, School of Public Health, Zhejiang University, 866 Yu-Hang-Tang Road, Hangzhou 310058, PR China.
Zhongjun MaSchool of Pharmaceutical Sciences, Zhejiang University, 866 Yu-Hang-Tang Road, Hangzhou 310058, PR China.
Zhe ChenChinese Traditional Medicine Hospital of Zhejiang Province, No. 54 You-Dian Road, Hangzhou 310006, PR China.
Han-Ming ShenDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore. Electronic address: han-ming_shen@nuhs.edu.sg.
Dajing XiaDepartment of Toxicology, School of Public Health, Zhejiang University, 866 Yu-Hang-Tang Road, Hangzhou 310058, PR China. Electronic address: dxia@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Physapubescin B, a steroidal compound extracted from the plant Physalis pubescens L. (Solanaceae), has been reported to possess anti-cancer potential, whereas the molecular mechanism remains elusive. In this study, we first demonstrated that physapubescin B induced autophagy in human cancer cells based on the evidence that physapubescin B increased lipidation of microtubule-associated protein 1 light chain 3 (LC3) as well as number of GFP-LC3 puncta. We further examined the molecular mechanisms and found that physapubescin B enhanced the autophagic flux through promotion of reactive oxygen species (ROS)-mediated suppression of mammalian target of rapamycin complex I (mTORC1), the key negative regulator of autophagy. Additionally, excessive ROS caused by physapubescin B also induced p53-dependent apoptotic cell death. Furthermore, we provided evidence that inhibition of autophagy either by a chemical inhibitor or gene silencing promoted physapubescin B-induced apoptotic cell death, indicating that autophagy serves as a cell survival mechanism to protect cell death. Thus, our data provide a clue that inhibition of autophagy would serve as a novel strategy for enhancing the anti-cancer potential of physapubescin B.

Indexed as

AutophagyAntineoplastic Agents, PhytogenicCell SurvivalHCT116 CellsHeLa CellsHumansMechanistic Target of Rapamycin Complex 1Microtubule-Associated ProteinsNeoplasmsReactive Oxygen SpeciesTumor Suppressor Protein p53WithanolidesAntineoplastic Agents, PhytogenicMAP1LC3A protein, humanMechanistic Target of Rapamycin Complex 1Microtubule-Associated Proteinsphysapubescin BReactive Oxygen SpeciesTP53 protein, humanTumor Suppressor Protein p53WithanolidesApoptotic cell deathAutophagyMTORC1Physapubescin BROS

Identifiers

PMID28258023
PMCPMC5333534

What OpenQuestion holds

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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.