Chunxia Ding, Xiaoying Xu, Lingyun Wei, Yixiao Wang
{"title":"丹酚酸F在调控卵巢癌细胞增殖、迁移、侵袭和凋亡中的潜在作用及其与EP300/PI3K/AKT通路的关联的初步探讨","authors":"Chunxia Ding, Xiaoying Xu, Lingyun Wei, Yixiao Wang","doi":"10.17219/acem/195334","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Salvianolic acid F (SAF), an important water-soluble monomeric component, is derived from the herbal medicine Salvia miltiorrhiza (SM) Bunge. Although SAF has been suggested to suppress various cancers, its role in ovarian cancer (OC) and the underlying mechanisms remain largely unclear.</p><p><strong>Objectives: </strong>This study aimed to investigate the effects of SAF on OC cell growth, invasion, migration, and apoptosis, as well as to elucidate the underlying mechanisms, including those involving the EP300/PI3K/AKT signaling pathway.</p><p><strong>Material and methods: </strong>In vitro cell culture experiments were conducted to assess the effects of SAF on the proliferation, migration, invasion, and apoptosis of OVCAR-3 (Ovarian Cancer Cell Line 3) and SK-OV-3 (Sloan-Kettering Ovarian Cancer 3) cells. Network pharmacology was further employed to explore SAF's impact on OC and to elucidate the potential underlying mechanisms. The EP300-mediated PI3K/AKT signaling pathway was selected for validation to confirm SAF's effects on inducing apoptosis and inhibiting cell proliferation in these OC cell lines.</p><p><strong>Results: </strong>Salvianolic acid F suppressed the growth, invasion and migration of SK-OV-3 and OVCAR-3 cells, and induced apoptosis. A network pharmacology analysis of SAF's effects on OC identified core targets, TP53, EP300, STAT3, MMP9, NFKB1, HIF1A, and PTGS2, through protein-protein interaction (PPI) network analysis using the STRING database. Salvianolic acid F inhibited EP300 expression in SK-OV-3 cells, reduced the p-PI3K/PI3K ratio, and increased both the Bax/Bcl-2 ratio and the cleaved caspase-3/caspase-3 ratio in OVCAR-3 and SK-OV-3 cells. However, the addition of A485, an EP300 inhibitor, did not further enhance the effects of SAF.</p><p><strong>Conclusions: </strong>Salvianolic acid F inhibited OC cell growth, migration and invasion while promoting apoptosis. The EP300/PI3K/AKT pathway is a key mechanism through which SAF regulates OC progression. Additionally, SAF may represent a promising candidate drug for treating OC.</p>","PeriodicalId":7306,"journal":{"name":"Advances in Clinical and Experimental Medicine","volume":" ","pages":""},"PeriodicalIF":1.9000,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Preliminary exploration of the potential role of salvianolic acid F in regulating ovarian cancer cell proliferation, migration, invasion, and apoptosis and its association with the EP300/PI3K/AKT pathway.\",\"authors\":\"Chunxia Ding, Xiaoying Xu, Lingyun Wei, Yixiao Wang\",\"doi\":\"10.17219/acem/195334\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Salvianolic acid F (SAF), an important water-soluble monomeric component, is derived from the herbal medicine Salvia miltiorrhiza (SM) Bunge. Although SAF has been suggested to suppress various cancers, its role in ovarian cancer (OC) and the underlying mechanisms remain largely unclear.</p><p><strong>Objectives: </strong>This study aimed to investigate the effects of SAF on OC cell growth, invasion, migration, and apoptosis, as well as to elucidate the underlying mechanisms, including those involving the EP300/PI3K/AKT signaling pathway.</p><p><strong>Material and methods: </strong>In vitro cell culture experiments were conducted to assess the effects of SAF on the proliferation, migration, invasion, and apoptosis of OVCAR-3 (Ovarian Cancer Cell Line 3) and SK-OV-3 (Sloan-Kettering Ovarian Cancer 3) cells. Network pharmacology was further employed to explore SAF's impact on OC and to elucidate the potential underlying mechanisms. The EP300-mediated PI3K/AKT signaling pathway was selected for validation to confirm SAF's effects on inducing apoptosis and inhibiting cell proliferation in these OC cell lines.</p><p><strong>Results: </strong>Salvianolic acid F suppressed the growth, invasion and migration of SK-OV-3 and OVCAR-3 cells, and induced apoptosis. A network pharmacology analysis of SAF's effects on OC identified core targets, TP53, EP300, STAT3, MMP9, NFKB1, HIF1A, and PTGS2, through protein-protein interaction (PPI) network analysis using the STRING database. Salvianolic acid F inhibited EP300 expression in SK-OV-3 cells, reduced the p-PI3K/PI3K ratio, and increased both the Bax/Bcl-2 ratio and the cleaved caspase-3/caspase-3 ratio in OVCAR-3 and SK-OV-3 cells. However, the addition of A485, an EP300 inhibitor, did not further enhance the effects of SAF.</p><p><strong>Conclusions: </strong>Salvianolic acid F inhibited OC cell growth, migration and invasion while promoting apoptosis. The EP300/PI3K/AKT pathway is a key mechanism through which SAF regulates OC progression. 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引用次数: 0
摘要
背景：丹参酚酸F （Salvianolic acid F， SAF）是一种重要的水溶性单体成分，来源于中药丹参（Salvia miltiorrhiza， SM）。虽然SAF已被认为可以抑制多种癌症，但其在卵巢癌（OC）中的作用及其潜在机制仍不清楚。目的：本研究旨在探讨SAF对OC细胞生长、侵袭、迁移和凋亡的影响，并阐明其潜在机制，包括与EP300/PI3K/AKT信号通路有关的机制。材料与方法：通过体外细胞培养实验，研究SAF对OVCAR-3 （Ovarian Cancer Line 3）和SK-OV-3 （Sloan-Kettering Ovarian Cancer 3）细胞增殖、迁移、侵袭和凋亡的影响。网络药理学进一步探讨了SAF对OC的影响，并阐明了潜在的机制。选择ep300介导的PI3K/AKT信号通路验证SAF在OC细胞系中诱导凋亡和抑制细胞增殖的作用。结果：丹酚酸F抑制SK-OV-3和OVCAR-3细胞的生长、侵袭和迁移，诱导细胞凋亡。通过使用STRING数据库进行蛋白-蛋白相互作用（PPI）网络分析，对SAF对OC的影响进行了网络药理学分析，确定了核心靶点TP53、EP300、STAT3、MMP9、NFKB1、HIF1A和PTGS2。丹酚酸F抑制SK-OV-3细胞中EP300的表达，降低了OVCAR-3和SK-OV-3细胞中p-PI3K/PI3K比值，升高了Bax/Bcl-2比值和cleaved - caspase-3/caspase-3比值。然而，EP300抑制剂A485的加入并没有进一步增强SAF的作用。结论：丹酚酸F抑制OC细胞生长、迁移和侵袭，促进细胞凋亡。EP300/PI3K/AKT通路是SAF调控OC进展的关键机制。此外，SAF可能是一种很有希望的治疗OC的候选药物。
Preliminary exploration of the potential role of salvianolic acid F in regulating ovarian cancer cell proliferation, migration, invasion, and apoptosis and its association with the EP300/PI3K/AKT pathway.
Background: Salvianolic acid F (SAF), an important water-soluble monomeric component, is derived from the herbal medicine Salvia miltiorrhiza (SM) Bunge. Although SAF has been suggested to suppress various cancers, its role in ovarian cancer (OC) and the underlying mechanisms remain largely unclear.
Objectives: This study aimed to investigate the effects of SAF on OC cell growth, invasion, migration, and apoptosis, as well as to elucidate the underlying mechanisms, including those involving the EP300/PI3K/AKT signaling pathway.
Material and methods: In vitro cell culture experiments were conducted to assess the effects of SAF on the proliferation, migration, invasion, and apoptosis of OVCAR-3 (Ovarian Cancer Cell Line 3) and SK-OV-3 (Sloan-Kettering Ovarian Cancer 3) cells. Network pharmacology was further employed to explore SAF's impact on OC and to elucidate the potential underlying mechanisms. The EP300-mediated PI3K/AKT signaling pathway was selected for validation to confirm SAF's effects on inducing apoptosis and inhibiting cell proliferation in these OC cell lines.
Results: Salvianolic acid F suppressed the growth, invasion and migration of SK-OV-3 and OVCAR-3 cells, and induced apoptosis. A network pharmacology analysis of SAF's effects on OC identified core targets, TP53, EP300, STAT3, MMP9, NFKB1, HIF1A, and PTGS2, through protein-protein interaction (PPI) network analysis using the STRING database. Salvianolic acid F inhibited EP300 expression in SK-OV-3 cells, reduced the p-PI3K/PI3K ratio, and increased both the Bax/Bcl-2 ratio and the cleaved caspase-3/caspase-3 ratio in OVCAR-3 and SK-OV-3 cells. However, the addition of A485, an EP300 inhibitor, did not further enhance the effects of SAF.
Conclusions: Salvianolic acid F inhibited OC cell growth, migration and invasion while promoting apoptosis. The EP300/PI3K/AKT pathway is a key mechanism through which SAF regulates OC progression. Additionally, SAF may represent a promising candidate drug for treating OC.
期刊介绍：
Advances in Clinical and Experimental Medicine has been published by the Wroclaw Medical University since 1992. Establishing the medical journal was the idea of Prof. Bogumił Halawa, Chair of the Department of Cardiology, and was fully supported by the Rector of Wroclaw Medical University, Prof. Zbigniew Knapik. Prof. Halawa was also the first editor-in-chief, between 1992-1997. The journal, then entitled "Postępy Medycyny Klinicznej i Doświadczalnej", appeared quarterly.
Prof. Leszek Paradowski was editor-in-chief from 1997-1999. In 1998 he initiated alterations in the profile and cover design of the journal which were accepted by the Editorial Board. The title was changed to Advances in Clinical and Experimental Medicine. Articles in English were welcomed. A number of outstanding representatives of medical science from Poland and abroad were invited to participate in the newly established International Editorial Staff.
Prof. Antonina Harłozińska-Szmyrka was editor-in-chief in years 2000-2005, in years 2006-2007 once again prof. Leszek Paradowski and prof. Maria Podolak-Dawidziak was editor-in-chief in years 2008-2016. Since 2017 the editor-in chief is prof. Maciej Bagłaj.
Since July 2005, original papers have been published only in English. Case reports are no longer accepted. The manuscripts are reviewed by two independent reviewers and a statistical reviewer, and English texts are proofread by a native speaker.
The journal has been indexed in several databases: Scopus, Ulrich’sTM International Periodicals Directory, Index Copernicus and since 2007 in Thomson Reuters databases: Science Citation Index Expanded i Journal Citation Reports/Science Edition.
In 2010 the journal obtained Impact Factor which is now 1.179 pts. Articles published in the journal are worth 15 points among Polish journals according to the Polish Committee for Scientific Research and 169.43 points according to the Index Copernicus.
Since November 7, 2012, Advances in Clinical and Experimental Medicine has been indexed and included in National Library of Medicine’s MEDLINE database. English abstracts printed in the journal are included and searchable using PubMed http://www.ncbi.nlm.nih.gov/pubmed.
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