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Updated: Jan 20, 2026
Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes
Published on: April 13, 2018
Falcarindiol induces apoptosis, ROS accumulation, and cell cycle arrest via EGFR/mTOR pathway modulation: an
Ganesh Timalsina1, Bishnu Prasad Parida2,3, Megha Radhakrishnan1
1Molecular and Human Genetics, Banaras Hindu University, Varanasi, India.
Background:
Falcarindiol, a bioactive polyacetylene, has shown cytotoxic effects in several cancers including breast, colorectal, and oral squamous carcinoma, but its pharmacological actions in cervical cancer are not well defined.
Objectives:
This study aims to integrate in silico approaches to define the multi-target pharmacological mechanisms of falcarindiol in cervical cancer, including ADMET profiling, network pharmacology, target prioritization, and molecular docking especially of EGFR/mTOR associated signaling pathways. Simultaneously, the study aims to experimentally verify the anticancer activity of falcarindiol in cervical cancer cells by examining its impacts on cell viability, apoptosis, mitochondrial dysfunction, reactive oxygen species generation, senescence induction, and cell cycle regulation.
Methods:
Pharmacokinetic and toxicity properties were evaluated using in silico ADMET profiling. Potential molecular targets and signaling pathways were identified from integrated databases, with hub genes prioritized by protein-protein interaction analysis. Protein-ligand binding was assessed through docking. Gene expression and prognostic significance were analyzed using public cancer datasets. Functional effects of falcarindiol were validated in HeLa and SiHa cervical cancer cells by MTT assay, Annexin V/PI, and AO/PI staining, mitotracker intensity, H2DCFDA fluorescence, β-galactosidase staining, and cell cycle analysis.
Results:
Falcarindiol demonstrated favorable ADMET properties and low predicted toxicity. Target prioritization identified EGFR, ERBB2, mTOR, MMP9, and CASP3 as central nodes, with strong interactions confirmed for EGFR and mTOR. Expression analyses revealed upregulation and hypomethylation of these genes in cervical cancer. Falcarindiol reduced viability (IC50 ~ 125-150µM), induced apoptosis, disrupted mitochondrial membrane potential, increased ROS production, and caused G0/G1 arrest in vitro. Senescence was also enhanced in treated cells.
Conclusion:
Falcarindiol exerts multi-targeted pharmacological actions in cervical cancer by modulating EGFR/mTOR signaling and apoptotic pathways, supporting its potential as a therapeutic lead compound.
Insights
Falcarindiol shows promise as a cervical cancer treatment by targeting EGFR/mTOR pathways and inducing apoptosis. This study confirms its anticancer effects and favorable safety profile.
Area of Science:
- Biochemistry and Molecular Biology
- Pharmacology
- Oncology
Background:
- Falcarindiol, a polyacetylene, exhibits cytotoxicity in various cancers.
- Its specific mechanisms in cervical cancer remain underexplored.
Purpose of the Study:
- To elucidate the multi-target pharmacological mechanisms of falcarindiol in cervical cancer using in silico and in vitro methods.
- To investigate its effects on EGFR/mTOR signaling, cell viability, apoptosis, and cell cycle regulation.
Main Methods:
- In silico ADMET profiling and network pharmacology for target identification.
- Molecular docking to assess protein-ligand interactions, focusing on EGFR and mTOR.
- In vitro validation in HeLa and SiHa cells using assays for viability, apoptosis, ROS, and cell cycle.
Main Results:
- Falcarindiol possesses favorable ADMET properties and low predicted toxicity.
- Key targets identified include EGFR, ERBB2, mTOR, MMP9, and CASP3, with strong EGFR/mTOR interactions.
- In vitro studies showed reduced cell viability, induced apoptosis, increased ROS, and G0/G1 cell cycle arrest.
Conclusions:
- Falcarindiol demonstrates multi-targeted action against cervical cancer via EGFR/mTOR and apoptotic pathways.
- It holds potential as a novel therapeutic lead compound for cervical cancer treatment.
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