Evidence map›Paper›PMID 35509820›Full record

ArticleJournal of ginseng research2022

The involvement of Parkin-dependent mitophagy in the anti-cancer activity of Ginsenoside.

Xin Sun, Yeting Hong, Yuhan Shu, Caixia Wu, Guiqin Ye, Hanxiao Chen, Hongying Zhou, Ruilan Gao, Jianbin Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of ginseng research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 32 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

9 authors at 5 institutions in 1 country.

Xin SunDepartment of Oncology, Cancer Center of Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, China.
Yeting HongHangzhou Medical College, Hangzhou, China.
Yuhan ShuCollege of Biomedical Engineering & Instrument Science, Zhejiang University, Hangzhou, China.
Caixia WuClinical Research Institute, Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, People's Hospital of Hangzhou Medical College, Hangzhou, China.
Guiqin YeHangzhou Medical College, Hangzhou, China.
Hanxiao ChenWenzhou Medical University, Wenzhou, China.
Hongying ZhouDepartment of Oncology, Cancer Center of Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, China.
Ruilan GaoInstitution of Hematology Research, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
Jianbin ZhangClinical Research Institute, Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, People's Hospital of Hangzhou Medical College, Hangzhou, China.
Hangzhou Medical College · CNZhejiang Provincial People's Hospital · CNWenzhou Medical University · CNZhejiang Chinese Medical University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colon cancer, the third most frequent occurred cancer, has high mortality and extremely poor prognosis. Ginsenoside, the active components of traditional Chinese herbal medicine Panax ginseng, exerts antitumor effect in various cancers, including colon cancer. However, the detailed molecular mechanism of Ginsenoside in the tumor suppression have not been fully elucidated. Here, we chose the representative ginsenoside Rg3 and reported for the first time that Rg3 induces mitophagy in human colon cancer cells, which is responsible for its anticancer effect. Rg3 treatment leads to mitochondria damage and the formation of mitophagosome; when autophagy is inhibited, the clearance of damaged mitochondria can be reversed. Next, our results showed that Rg3 treatment activates the PINK1-Parkin signaling pathway and recruits Parkin and ubiquitin proteins to mitochondria to induce mitophagy. GO analysis of Parkin targets showed that Parkin interacts with a large number of mitochondrial proteins and regulates the molecular function of mitochondria. The cellular energy metabolism enzyme GAPDH is validated as a novel substrate of Parkin, which is ubiquitinated by Parkin. Moreover, GAPDH participates in the Rg3-induced mitophagy and regulates the translocation of Parkin to mitochondria. Functionally, Rg3 exerts the inhibitory effect through regulating the nonglycolytic activity of GAPDH, which could be associated with the cellular oxidative stress. Thus, our results revealed GAPDH ubiquitination by Parkin as a crucial mechanism for mitophagy induction that contributes to the tumor-suppressive function of ginsenoside, which could be a novel treatment strategy for colon cancer.

Indexed as

BNIP3, BCL2 interacting protein 3COX Ⅳ, cytochrome c oxidase ⅣGAPDHGAPDH, glyceraldehyde-3-phosphate dehydrogenaseGensinosideGSH, glutathioneHSP60, heat shock protein 60 KDaLC3, microtubule-associated proteins 1A/1B light chain 3MFN2, mitofusion 2MitophagyPARK2, ParkinParkinPHGDH, phosphoglycerate dehydrogenasePINK1, PTEN induced putative kinase 1ROSSQSTM1, sequestosome 1TIM23, translocase of the inner membrane 23TOMM20, translocase of outer mitochondrial membrane 20UbiquitinationVDAC1, voltage-dependent anion-selective channel protein 1

Identifiers

PMID35509820
PMCPMC9058836
OpenAlexW3180401434

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.