Evidence mapPaperPMID 41329427Full record

ArticleMolecular biology reports2025

Effects of atranorin on the proliferation, apoptosis and metastasis of two different gastric cancer cell lines and exploring underlying mechanisms.

Nihal Almuraikhi, Saleh Hussain A Almasabi, Abdulfattah Y Alhazmi, Abdulrahman Almohammed, Jameel Barnawi, Salah Alghamdi, Khalid Alhazmi

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Article in Molecular biology reports, 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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5 · Who and what money

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7 authors.

Nihal AlmuraikhiStem Cell Unit, Department of Anatomy, College of Medicine, King Saud University, Riyadh, 11461, Saudi Arabia.
Saleh Hussain A AlmasabiDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Najran University, Najran, 61441, Saudi Arabia. Shahmad@nu.edu.sa.
Abdulfattah Y AlhazmiPharmaceutical Practices Department, College of Pharmacy, Umm Al-Qura University, Makkah, Saudi Arabia.
Abdulrahman AlmohammedDepartment of Pathology, College of Medicine, Imam Muhammad Ibn Saud Islamic University (IMSIU), Riyadh, 13317, Saudi Arabia.
Jameel BarnawiDepartment of Medical Lab Technology, Faculty of Applied Medical Sciences, University of Tabuk, Tabuk 71491, Saudi Arabia.
Salah AlghamdiDepartment of Surgery, Faculty of Medicine, University of Tabuk, Tabuk, Saudi Arabia.
Khalid AlhazmiDepartment of Pathology, Faculty of Medicine, University of Tabuk, Tabuk, Saudi Arabia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGastric cancer is the fifth most prevalent malignancy worldwide. Atranorin is a polyphenol with significant anti-tumor activities. This study was conducted to evaluate the effect of atranorin on proliferation, apoptosis, and metastasis in two different human gastric cancer cell lines, AGS and HGC-27.

methodsThe anti-proliferative and anti-migration effects of atranorin were evaluated using the MTT and scratch assays, respectively. The expression of apoptosis-related markers, including caspase 3, caspase 9, caspase 8, Bax, and Bcl2, and metastasis markers, including E-cadherin, N-cadherin, vimentin, fibronectin 1, and VEGFA, was quantified at the mRNA and protein levels via quantitative real-time PCR (qRT-PCR) and Western blotting, respectively.

resultsFollowing exposure to varying concentrations of atranorin for 48 and 72 h, both cell lines exhibited a significant, dose-dependent decrease in cell proliferation compared with control groups. Atranorin treatment significantly increased the expression of caspase 3, caspase 9, and Bax in the HGC-27 cell line; conversely, no significant alterations were observed in the expression of caspase 8 and BCL2. In the AGS cell line, atranorin treatment did not significantly affect the expression of apoptosis markers. Atranorin induced apoptosis and inhibited migration in HGC-27 cells. Moreover, atranorin significantly upregulated E-cadherin and downregulated N-cadherin, vimentin, fibronectin 1, and VEGFA.

conclusionAtranorin inhibits proliferation in HGC-27 and AGS cells, induces intrinsic apoptosis, and inhibits metastasis in HGC-27 cells, suggesting its potential as a drug candidate, particularly for targeting metastasis and inducing apoptosis in highly metastatic HGC-27 cells.

Indexed as

ApoptosisStomach NeoplasmsCadherinsCell Line, TumorCell MovementCell ProliferationFibronectinsGene Expression Regulation, NeoplasticHumansNeoplasm MetastasisVascular Endothelial Growth Factor ACadherinsFibronectinsVascular Endothelial Growth Factor AApoptosisAtranorinGastric cancerMetastasisProliferation

Identifiers

PMID41329427

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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 Socratic graph.