Evidence map›Paper›PMID 38415456›Full record

ArticleCombinatorial chemistry & high throughput screening2025

Pharmacological Mechanisms of Kirenol against Ovarian Carcinoma: A Network Pharmacology and Experimental Validation Study

Xiaoling Mao, Hong Zhu, Jun Gao, Shixin Lin, Yin Bao, Mingyue Zhang, Huan Yang

Open access · hybridAbstract read
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Article in Combinatorial chemistry & high throughput screening, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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3 · Its place in the literature

Who cites it

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4 · The record

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5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Xiaoling MaoJiangxi University of Chinese Medicine, Nanchang, Jiangxi 330006, P.R. China.ORCID 0009-0001-1722-6415
Hong ZhuDepartment of Gynecologic Oncology, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029, P.R. China.ORCID 0000-0001-7289-083X
Jun GaoDepartment of Gynecologic Oncology, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029, P.R. China.
Shixin LinDepartment of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu 610041, P.R. China.
Yin BaoJiangxi University of Chinese Medicine, Nanchang, Jiangxi 330006, P.R. China.
Mingyue ZhangJiangxi University of Chinese Medicine, Nanchang, Jiangxi 330006, P.R. China.
Huan YangDepartment of Third Clinical Medical College of Nanchang University, Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330008, P.R. China.
Jiangxi University of Traditional Chinese Medicine · CNJiangxi Provincial Cancer Hospital · CNNanchang University · CNSichuan University · CN

Funding

Chinese National Natural Science Foundation of China 82060477Jiangxi Provincial Natural Science Foundation 2020BAB206054Nanchang Advantage Science and Technology Innovation Team Project 2019-15-3Nanchang Key Laboratory for Precision Therapy of Gynecological Tumors 2020NCZDSY-003Nan chang Science and Technology Support Plan Key Project Hongkezi2019-258-3Science and Technology Project of Health Commission of Jiangxi 202120073
6 · The paper itself

Abstract

backgroundOvarian carcinoma is an aggressive gynecological malignancy. Kirenol, a diterpene compound, has recently gained attention for its potential anticancer properties. However, its exact anti-tumor mechanism remains largely unexplored.

objectiveIn this study, we explored the inhibitory effects of Kirenol on ovarian cancer using network pharmacology and in vitro experiments and elucidated its underlying mechanisms.

methodsThrough the utilization of molecular docking, we established a network of proteinprotein interactions (PPI), which unveiled CDK4 as an essential target. Additionally, gene enrichment and pathway analysis highlighted the significance of the PI3K/AKT pathway. The viability of ovarian cancer cells and normal ovarian epithelial cells was evaluated using CCK8 assays to determine the effect of Kirenol. Following

resultsKirenol significantly reduced the viability of ovarian cancer cells (SKOV3 and A2780) compared to normal ovarian epithelial cells (IOSE-80). Moreover, Kirenol efficiently suppressed the growth and movement, caused a cell cycle halt, and stimulated programmed cell death in SKOV3 and A2780 cells. Through molecular analysis, it was observed that Kirenol increased the expression of Bax while decreasing the expression of MMP2, MMP9, and Bcl-2. It also attenuated the phosphorylation of PI3K, AKT, and RB and downregulated CDK4 and CCND1 expression. Notably, co-treatment with the PI3K pathway inhibitor LY294002 enhanced the inhibitory effect of Kirenol on ovarian cancer cells.

conclusionIn summary, the combined results of our network pharmacology analysis and in vitro tests emphasized that Kirenol hinders the growth of ovarian cancer cells, causes cell cycle arrest, enhances apoptosis, and hampers migration, possibly by regulating the PI3K/AKT/CDK4 signaling pathway.

Indexed as

Antineoplastic AgentsDiterpenesNetwork PharmacologyOvarian NeoplasmsApoptosisCell Line, TumorCell ProliferationCell SurvivalCyclin-Dependent Kinase 4Dose-Response Relationship, DrugDrug Screening Assays, AntitumorFemaleHumansMolecular Docking SimulationMolecular StructurePhosphatidylinositol 3-KinasesAntineoplastic AgentsCDK4 protein, humanCyclin-Dependent Kinase 4DiterpenesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktapoptosiscell cycleKirenmetastasis.ovarian carcinomaPI3K/AKT/CDK4

Identifiers

PMID38415456
PMCPMC12246733
OpenAlexW4392365302

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LicenceCC BY
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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.