Evidence map›Paper›PMID 28060722›Full record

ArticleOncotarget2017

Polyphyllin I induces mitophagic and apoptotic cell death in human breast cancer cells by increasing mitochondrial PINK1 levels.

Guo-Bing Li, Ruo-Qiu Fu, Han-Ming Shen, Jing Zhou, Xiao-Ye Hu, Yan-Xia Liu, Yu-Nong Li, Hong-Wei Zhang, Xin Liu, Yan-Hao Zhang and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

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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

13 authors at 2 institutions in 2 countries.

Guo-Bing LiDepartment of Pharmacognosy, College of Pharmacy, 3rd Military Medical University, Chongqing, China.
Ruo-Qiu FuDepartment of Pharmacognosy, College of Pharmacy, 3rd Military Medical University, Chongqing, China.
Han-Ming ShenDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Republic of Singapore.
Jing ZhouDepartment of Pharmacognosy, College of Pharmacy, 3rd Military Medical University, Chongqing, China.
Xiao-Ye HuDepartment of Pharmacognosy, College of Pharmacy, 3rd Military Medical University, Chongqing, China.
Yan-Xia LiuDepartment of Pharmacognosy, College of Pharmacy, 3rd Military Medical University, Chongqing, China.
Yu-Nong LiDepartment of Pharmacognosy, College of Pharmacy, 3rd Military Medical University, Chongqing, China.
Hong-Wei ZhangDepartment of Pharmacognosy, College of Pharmacy, 3rd Military Medical University, Chongqing, China.
Xin LiuDepartment of Pharmacognosy, College of Pharmacy, 3rd Military Medical University, Chongqing, China.
Yan-Hao ZhangDepartment of Pharmacognosy, College of Pharmacy, 3rd Military Medical University, Chongqing, China.
Cheng HuangDrug Discovery Lab, School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Rong ZhangDepartment of Pharmacy, The Second Affiliated Hospital of Third Military Medical University, Chongqing, China.
Ning GaoDepartment of Pharmacognosy, College of Pharmacy, 3rd Military Medical University, Chongqing, China.
Army Medical University · CNNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular mechanisms underlying the anti-breast cancer effects of polyphyllin I, a natural compound extracted from Paris polyphylla rhizomes, are not fully understood. In the present study, we found that polyphyllin I induces mitochondrial translocation of DRP1 by dephosphorylating DRP1 at Ser637, leading to mitochondrial fission, cytochrome c release from mitochondria into the cytosol and, ultimately apoptosis. Polyphyllin I also increased the stabilization of full-length PINK1 at the mitochondrial surface, leading to the recruitment of PARK2, P62, ubiquitin, and LC3B-II to mitochondria and culminating in mitophagy. PINK1 knockdown markedly suppressed polyphyllin I-induced mitophagy and enhanced polyphyllin I-induced, DRP1-dependent mitochondrial fission and apoptosis. Furthermore, suppression of DRP1 by mdivi-1 or shRNA inhibited PINK1 knockdown/polyphyllin I-induced mitochondrial fragmentation and apoptosis, suggesting that PINK1 depletion leads to excessive fission and, subsequently, mitochondrial fragmentation. An in vivo study confirmed that polyphyllin I greatly inhibited tumor growth and induced apoptosis in MDA-MB-231 xenografts, and these effects were enhanced by PINK1 knockdown. These data describe the mechanism by which PINK1 contributes to polyphyllin I-induced mitophagy and apoptosis and suggest that polyphyllin I may be an effective drug for breast cancer treatment.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicApoptosis Regulatory ProteinsAutophagyBreast NeoplasmsDiosgeninDose-Response Relationship, DrugDynaminsFemaleGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticGTP PhosphohydrolasesHumansMCF-7 CellsMice, NudeMicrotubule-Associated ProteinsAntineoplastic Agents, PhytogenicApoptosis Regulatory ProteinsDiosgeninDNM1L protein, humanDynaminsGTP PhosphohydrolasesMicrotubule-Associated ProteinsMitochondrial Proteinsparkin proteinpolyphyllin IProtein KinasesPTEN-Induced Putative KinaseUbiquitin-Protein LigasesDRP1mitochondrial fissionmitophagyPINK1polyphyllin I

Identifiers

PMID28060722
PMCPMC5354664
OpenAlexW2565065604

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.