ArticleOncology letters2022
Effects of 2,2',4'-trihydroxychalcone on the proliferation, metastasis and apoptosis of A549 human lung cancer cells.
Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Monotropein represses the proliferation and angiogenesis via the AKT/NF-κB pathway in lung cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to evaluate the antitumor effects of 2,2',4'-trihydroxychalcone (7a) on the A549 human lung cancer cell line. A549 cells were treated with different concentrations of 7a for different time periods. Cells without 7a were used as the negative control group. Cell proliferation, invasion, vasculogenic mimicry (VM) formation, heterogeneous adhesion and apoptosis were measured using Cell Counting Kit-8, Transwell invasion, VM, adhesion and flow cytometric assays, respectively. In addition, the expression of related proteins was determined using western blot analysis or ELISA. The present study found that 7a had a significant inhibitory effect on the survival rate of the A549 lung cancer cells but almost no effect on BEAS-2B human lung epithelial cells or human venous endothelial cells. The migration rate, VM length, invasion rate and heterogeneous adhesion number of cells treated with 7a significantly decreased as the concentration increased, while the apoptosis rate increased. Western blot analysis showed that 7a treatment significantly increased the expression levels of E-cadherin, cleaved poly (ADP-ribose) polymerase, Bax and caspase-3 and simultaneously decreased the expression levels of metalloproteinase-2/9, Bcl-2, phosphorylated (p)-PI3K, p-AKT, p-mTOR, vascular endothelial growth factor (VEGF), E-selectin and N-cadherin. At the same time, the ELISA results showed that the level of the pro-angiogenic factor VEGF in the culture media was reduced in the presence of 7a. In addition, 7a could also reduce the nuclear NF-κB protein expression, which could inhibit the gene transcription of tumor apoptosis and metastasis-related proteins. Therefore, 7a may exert inhibitory effects on A549 cells by inhibiting cell proliferation, migration, VM formation and heterogeneous adhesion, as well as by inducing apoptosis through the suppression of the PI3K/AKT/NF-κB signaling pathway; these findings suggested that 7a may be a promising agent for the treatment of lung cancer.
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