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Bioinformatics-based discovery of the involvement of PSAT1 in mediating the anti-lung adenocarcinoma activity of
Zhiwen Cao1,2, Lulu Zhang3, Wenqiang Zhang1
1Jiangxi Provincial Key Laboratory of Molecular Medicine, The Second Affiliated Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Nanchang, China.
Background:
Triptolide (TP) exhibits various pharmacological activities. Our previous studies have confirmed the efficacy of TP against lung adenocarcinoma (LUAD). However, the potent pharmacological activity of TP is underpinned by its complex mechanisms. Exploring its potential mechanisms is of great value for promoting the clinical application of TP and extending its clinical use.
Methods:
Differentially expressed genes (DEGs) associated with LUAD were analyzed and acquired from the TCGA database, while DEGs related to TP were obtained through RNA sequencing. Hub genes were identified through LASSO and random forest models. The efficacy of TP against LUAD was validated using tumor-bearing mouse models and A549 cells. The validation of hub genes was conducted using RT-qPCR. The regulatory effect of hub genes on TP efficacy was validated through overexpression cell models. Furthermore, the potential mechanisms by which TP improves gemcitabine (GEM) resistance were explored using a GEM-resistant cell line in combination with the overexpression model.
Results:
This study validated the therapeutic effect of TP against LUAD in vivo and in vitro. Bioinformatics revealed that the mechanism of TP's effect against LUAD might be associated with amino acid-related biological processes. Five hub genes were screened and identified by combining bioinformatics methods and experiments. The overexpression model validated that PSAT1 plays an effective role in the efficacy of TP and in alleviating GEM resistance.
Conclusion:
This study preliminarily demonstrated that the anti-LUAD effect of TP was associated with the PSAT1-regulated serine biosynthesis pathway, and that TP effectively improves GEM resistance by inhibiting PSAT1 expression.
Insights
Triptolide (TP) effectively treats lung adenocarcinoma (LUAD) by targeting the PSAT1 gene. This mechanism also helps overcome gemcitabine (GEM) resistance in LUAD treatment.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Triptolide (TP) demonstrates significant pharmacological activities, with prior research confirming its efficacy against lung adenocarcinoma (LUAD).
- Understanding the complex mechanisms underlying TP's potent effects is crucial for its clinical application in LUAD treatment.
Purpose of the Study:
- To elucidate the underlying mechanisms of Triptolide (TP) in treating lung adenocarcinoma (LUAD).
- To investigate TP's role in overcoming gemcitabine (GEM) resistance in LUAD.
- To identify key genes and pathways involved in TP's anti-LUAD effects.
Main Methods:
- Bioinformatic analysis of TCGA database for LUAD-associated differentially expressed genes (DEGs).
- RNA sequencing to identify TP-related DEGs.
- LASSO and random forest models for hub gene identification.
- In vivo and in vitro validation of TP efficacy.
- RT-qPCR and overexpression models to validate hub genes and their regulatory effects.
Main Results:
- TP demonstrated validated therapeutic effects against LUAD both in vivo and in vitro.
- Bioinformatics analysis suggested that TP's mechanism involves amino acid-related biological processes.
- Five hub genes were identified, with PSAT1 validated as playing a key role in TP's efficacy and alleviating GEM resistance.
Conclusions:
- TP's anti-LUAD effect is preliminarily linked to the PSAT1-regulated serine biosynthesis pathway.
- TP enhances gemcitabine (GEM) resistance by inhibiting PSAT1 expression, offering a potential therapeutic strategy for LUAD.
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