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Targeting a transcription factor NF-κB by green tea catechins using in silico and in vitro studies in pancreatic
Mohd Suhail1,2, Mohd Rehan1,2, Mohammad Tarique3
1King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia.
Abstract:
Pancreatic cancer remains a lethal disease and a major public health problem globally. Nuclear factor-kappa B (NF-κB) has been identified as a therapeutic target in several cancers and plays an important role in inflammatory responses. Many phytochemicals, including catechins, have been reported in the scientific literature with efficient anticancer potential and minimal side effects. This study aims to gain insights into the inhibitory mechanism of catechin derivatives epicatechin (EC), epigallocatechin (EGC), epicatechin gallate (ECG), and epigallocatechin gallate (EGCG) using in silico and in vitro studies especially considering NF-κB targeting. We explored the binding pose, interacting residues and molecular interactions for catechin derivatives with NF-κB. Docking analysis showed that the catechin derivatives acted as covalent inhibitors with the p65 subunit of NF-κB and interacted with other residues through non-bonding interactions and hydrogen bonds. Further, we validated the effect of EGCG on NF-κB activity in pancreatic cancer cell lines MIAPaCa-2 and SU 86.86. Our in vitro data showed EGCG effectively reduced cell growth and proliferation, induced apoptosis, and inhibited NF-κB activity in the studied cell lines. In addition, EGCG repressed the expression of NF-κB target genes including MMP9, MMP2, cMyc, and BCL-2. Thus, targeting NF-κB with EGCG could be a potential therapeutic alternative for pancreatic cancer treatment.
Insights
Epigallocatechin gallate (EGCG) shows potential as a pancreatic cancer treatment by inhibiting nuclear factor-kappa B (NF-κB). This study explored EGCG
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Pancreatic cancer is a deadly disease with limited treatment options.
- Nuclear factor-kappa B (NF-κB) is implicated in cancer development and inflammation.
- Phytochemicals, like catechins, offer potential anticancer effects with fewer side effects.
Purpose of the Study:
- To investigate the inhibitory mechanism of catechin derivatives against NF-κB in pancreatic cancer.
- To evaluate the efficacy of epigallocatechin gallate (EGCG) as a therapeutic agent for pancreatic cancer.
Main Methods:
- In silico molecular docking to analyze catechin derivative interactions with NF-κB.
- In vitro studies using pancreatic cancer cell lines (MIAPaCa-2, SU 86.86).
- Assessment of EGCG's effects on cell growth, apoptosis, NF-κB activity, and target gene expression.
Main Results:
- Catechin derivatives, including EGCG, were identified as covalent inhibitors of the NF-κB p65 subunit.
- EGCG significantly reduced pancreatic cancer cell growth and proliferation.
- EGCG induced apoptosis and inhibited NF-κB activity and its target genes (MMP9, MMP2, cMyc, BCL-2).
Conclusions:
- EGCG demonstrates significant anticancer activity against pancreatic cancer cell lines.
- Targeting NF-κB with EGCG presents a promising therapeutic strategy for pancreatic cancer.
- EGCG's mechanism involves direct inhibition of NF-κB and downregulation of key oncogenes.
