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Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
Syringin exerts anti-breast cancer effects through PI3K-AKT and EGFR-RAS-RAF pathways
Fei Wang1, Chong Yuan1, Bo Liu2,3
1Faculty of Pharmacy, Hubei University of Chinese Medicine, Wuhan, 430065, China.
Background:
Breast cancer (BC) is one of the most common malignant tumors with the highest mortality in the world. Modern pharmacological studies have shown that Syringin has an inhibitory effect on many tumors, but its anti-BC efficacy and mechanism are still unclear.
Methods:
First, Syringin was isolated from Acanthopanax senticosus (Rupr. & Maxim.) Harms (ASH) by systematic solvent extraction and silica gel chromatography column. The plant name is composed of genus epithet, species additive words and the persons' name who give its name. Then, the hub targets of Syringin against BC were revealed by bioinformatics. To provide a more experimental basis for later research, the hub genes which could be candidate biomarkers of BC and a ceRNA network related to them were obtained. And the potential mechanism of Syringin against BC was proved in vitro experiments.
Results:
Syringin was obtained by liquid chromatography-mass spectrometry (LC-MS), nuclear magnetic resonance (NMR), and high-performance liquid chromatography (HPLC). Bioinformatics results showed that MAP2K1, PIK3CA, HRAS, EGFR, Caspase3, and PTGS2 were the hub targets of Syringin against BC. And PIK3CA and HRAS were related to the survival and prognosis of BC patients, the PIK3CA-hsa-mir-139-5p-LINC01278 and PIK3CA-hsa-mir-375 pathways might be closely related to the mechanism of Syringin against BC. In vitro experiments confirmed that Syringin inhibited the proliferation and migration and promoted apoptosis of BC cells through the above hub targets.
Conclusions:
Syringin against BC via PI3K-AKT-PTGS2 and EGFR-RAS-RAF-MEK-ERK pathways, and PIK3CA and HRAS are hub genes for adjuvant treatment of BC.
Insights
Syringin, a compound from Acanthopanax senticosus, inhibits breast cancer (BC) progression by targeting key genes like PIK3CA and HRAS. This study elucidates its anti-BC mechanisms and potential as an adjuvant therapy.
Area of Science:
- Pharmacology
- Bioinformatics
- Oncology
Background:
- Breast cancer (BC) is a leading cause of cancer mortality worldwide.
- Syringin exhibits anti-tumor properties, but its specific anti-BC effects and mechanisms require elucidation.
Purpose of the Study:
- To investigate the anti-breast cancer efficacy of Syringin.
- To identify the molecular targets and pathways involved in Syringin's anti-BC action.
- To explore Syringin's potential as an adjuvant therapy for breast cancer.
Main Methods:
- Syringin isolation from Acanthopanax senticosus (ASH) using solvent extraction and chromatography.
- Bioinformatic analysis to identify hub targets of Syringin against BC.
- In vitro experiments to validate Syringin's effects on BC cell proliferation, migration, and apoptosis.
Main Results:
- Syringin was isolated and characterized using LC-MS, NMR, and HPLC.
- Bioinformatics identified MAP2K1, PIK3CA, HRAS, EGFR, Caspase3, and PTGS2 as hub targets.
- PIK3CA and HRAS were linked to BC patient survival; specific ceRNA pathways were identified.
- In vitro studies confirmed Syringin's inhibition of BC cell proliferation and migration, and promotion of apoptosis.
Conclusions:
- Syringin exerts anti-breast cancer effects through the PI3K-AKT-PTGS2 and EGFR-RAS-RAF-MEK-ERK pathways.
- PIK3CA and HRAS are identified as crucial hub genes for Syringin's anti-BC activity and potential adjuvant treatment.
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