Evidence map›Paper›PMID 35127176›Full record

ArticleJournal of advanced research2022

Targeting PLA2G16, a lipid metabolism gene, by Ginsenoside Compound K to suppress the malignant progression of colorectal cancer.

Li Yang, Lingjie Zheng, Xiaonv Xie, Junjia Luo, Jing Yu, Lihua Zhang, Wenhui Meng, Yingen Zhou, Ling Chen, Dongsheng Ouyang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. PLA2G16-Mediated Tetracosatetraenoic Acid Rewires Fatty Acid Oxidation to Impair CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  15. Aging · 2023
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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

12 authors at 4 institutions in 2 countries.

Li YangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China.
Lingjie ZhengDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China.
Xiaonv XieDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China.
Junjia LuoDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China.
Jing YuDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China.
Lihua ZhangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China.
Wenhui MengDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China.
Yingen ZhouDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China.
Ling ChenDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha 410008, PR China.
Dongsheng OuyangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China.
Honghao ZhouDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China.
Zhirong TanDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, PR China.
National Clinical Research Center for Digestive Diseases · CNXiangya Hospital Central South University · CNCentral South University · CNUniversity of Macau · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Colorectal cancer (CRC) is a common malignant tumor with a high global incidence, metastasis rate and low cure rate. Changes in lipid metabolism-related genes can affect the occurrence and development of CRC, and may be a potential therapeutic target for CRC. Therefore, starting from lipid metabolism-related genes to find natural medicines for tumor treatment may become a new direction in CRC research. Objectives: This study aimed to investigate the effect of PLA2G16, a key gene involved in lipid metabolism, on the biological function of CRC, and whether the anti-CRC effect of GCK is related to PLA2G16. Methods: To explore the role of PLA2G16 in CRC Results: We showed that PLA2G16 was significantly higher in CRC tissues than the adjacent normal appearing tissues, and high PLA2G16 expression correlates with unfavorable prognosis of CRC patients. Further, PLA2G16 promoted the malignant progression of CRC by inhibiting the Hippo signaling pathway determined by RNA-seq analysis, and GCK exerted anti-CRC effects by inhibiting the protein expression of PLA2G16 Conclusion: Our results suggested that PLA2G16 promote the malignant progression of CRC by inhibiting the Hippo signaling pathway and the anti-CRC effect of GCK is through inhibiting the protein expression of PLA2G16.

Indexed as

Colorectal NeoplasmsLipid MetabolismAnimalsCell Line, TumorGinsenosidesHumansMiceMice, Nudeginsenoside compound KGinsenosidesColorectal cancerGinsenoside Compound KHippo signaling pathwayLipid metabolism geneLipidomicsPLA2G16

Identifiers

PMID35127176
PMCPMC8799872
OpenAlexW3167409484

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.