Evidence map›Paper›PMID 40506557›Full record

ArticleMedical oncology (Northwood, London, England)2025

Polyphyllin I inhibits ovarian cancer growth by inducing G0/G1 phase arrest and inhibiting the c-Myc signaling pathway.

Qing Tang, Kun Huang, Mengjie Li, Ziqiao Zhao, Yuanle Deng, Yueqi Zuo, Ningyu Wang, Yongxia Zhu

Abstract read
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In one paragraph

Article in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
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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

8 authors.

Qing Tang *Department of Pharmacy, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, University of Electronic Science and Technology of China, Chengdu, China.
Kun Huang *School of Life Science and Engineering, Southwest Jiaotong University, Chengdu, China.
Mengjie Li *College of Pharmacy, Qinghai University for Nationalities, Xining, China.
Ziqiao ZhaoDepartment of Pharmacy, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, University of Electronic Science and Technology of China, Chengdu, China.
Yuanle DengDepartment of Pharmacy, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, University of Electronic Science and Technology of China, Chengdu, China.
Yueqi ZuoShaanxi Key Laboratory of Brain Disorders & Institute of Basic and Translational Medicine, Xi'an Medical University, Xi'an, China.
Ningyu WangSchool of Life Science and Engineering, Southwest Jiaotong University, Chengdu, China.
Yongxia ZhuDepartment of Pharmacy, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, University of Electronic Science and Technology of China, Chengdu, China. yongxia_zhu0409@uestc.edu.cn.

Funding

Chengdu Science and Technology Program 2024-YF05-00783-SNNatural Science Basic Research Plan in Shaanxi Province of China 2023-JC-QN-0877Sichuan Science and Technology Program 2025ZNSFSC1858 and 2024NSFSC1742
6 · The paper itself

Abstract

Ovarian cancer is a deadly gynecological malignancy often diagnosed at an advanced stage, with few treatment options available. Polyphyllin I (PPI), the primary active ingredient of Paris polyphylla, has shown excellent anti-cancer activity against various cancers. However, studies on PPI use and ovarian cancer are limited, and the potential mechanisms remain unclear. This study explored the effects of anti-ovarian cancer and the potential mechanisms of action of PPI. Methods such as MTT, colony formation, three-dimensional spheroid formation, flow cytometry, and western blotting were employed to assess the anti-proliferative effects of PPI on different ovarian cancer cell lines. RNA sequencing was used to discover potential mechanisms by evaluating the effects of PPI on transcriptional signatures and identifying differences in gene expression patterns. The results indicate that PPI demonstrated dose- and time-dependent anti-proliferative effects on ovarian cancer cell lines. PPI also up-regulated 1518 genes and down-regulated 800 genes. The genes showed enrichment in the "apoptosis" gene sets, while exhibiting negative enrichment in the "cell cycle" and "Myc signaling pathway" gene sets. PPI caused cell cycle arrest at the G0/G1 phase by increasing the expression of p21 and p27 and inhibiting the activity of the CDK2/cyclin E complex. PPI triggered cell apoptosis, which was associated with elevated cellular reactive oxygen species and mitochondrial membrane potential depolarization. Finally, PPI reduced c-Myc protein levels and affected mRNA levels of c-Myc pathway-related genes. PPI effectively suppressed ovarian cancer cell proliferation, indicating its potential as a treatment option for ovarian cancer.

Indexed as

DiosgeninG1 Phase Cell Cycle CheckpointsOvarian NeoplasmsProto-Oncogene Proteins c-mycApoptosisCell Cycle CheckpointsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansResting Phase, Cell CycleSignal TransductionDiosgeninMYC protein, humanpolyphyllin IProto-Oncogene Proteins c-mycApoptosisCell cyclec-MycOvarian cancerPolyphyllin I

Identifiers

PMID40506557

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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.