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Molecular Effects of Parkia speciosa Hassk. Empty Pod Extract in Colon Cancer: A Transcriptomic and Proteomic
Athit Chaiwichien1, Supawadee Osotprasit1, Tepparit Samrit1,2
1Faculty of Allied Health Sciences, Burapha University, Chonburi 20131, Thailand.
Abstract:
This study elucidates the multi-targeted antineoplastic mechanisms of Parkia speciosa empty pod extract (PSET) against HCT-116 and HT-29 colorectal cancer (CRC) cells through integrated transcriptomic and proteomic analyses. Phytochemical profiling indicates that PSET is rich in bioactive metabolites, notably quercetin, rutin, and pyrogallol, which orchestrate its profound ability to inhibit tumor proliferation, migration, and invasion. Transcriptomic data revealed that PSET profoundly suppresses the oncogenic Wnt/β-catenin signaling axis while simultaneously activating p53-mediated cell cycle arrest. Complementary proteomic profiling uncovered critical metabolic vulnerabilities, demonstrating that PSET abrogates the Warburg effect by disrupting key glycolytic enzymes (e.g., ENO1, GAPDH, LDHA), thereby inducing metabolic starvation. Furthermore, the extract precipitated a catastrophic collapse of the cytoskeletal architecture and downregulated epithelial-mesenchymal transition (EMT) markers, effectively paralyzing the cells' metastatic machinery. The integrated transcriptomic and proteomic signatures also highlighted an irrecoverable state of cellular stress, characterized by an overwhelming unfolded protein response and dysregulated RNA splicing, ultimately driving the cells toward apoptosis. In conclusion, this integrated omics approach provides robust molecular validation that PSET systemically dismantles colorectal cancer survival networks, highlighting its strong potential as a natural, multi-targeted therapeutic agent.
Insights
Parkia speciosa empty pod extract (PSET) exhibits multi-targeted anti-cancer effects against colorectal cancer (CRC) cells. It suppresses tumor growth, migration, and invasion by disrupting key survival pathways and inducing metabolic stress and apoptosis.
Area of Science:
- Molecular Biology
- Cancer Research
- Pharmacology
Background:
- Colorectal cancer (CRC) remains a significant global health challenge.
- There is a growing need for novel, effective, and natural therapeutic agents.
- Parkia speciosa possesses traditional medicinal uses, warranting scientific investigation.
Purpose of the Study:
- To elucidate the multi-targeted antineoplastic mechanisms of Parkia speciosa empty pod extract (PSET).
- To investigate the effects of PSET on colorectal cancer (CRC) cell lines (HCT-116 and HT-29).
- To validate findings using integrated transcriptomic and proteomic analyses.
Main Methods:
- Phytochemical profiling of PSET to identify key bioactive compounds.
- Transcriptomic and proteomic analyses to understand molecular mechanisms.
- Assays to evaluate inhibition of proliferation, migration, invasion, and metabolic pathways.
Main Results:
- PSET, rich in quercetin, rutin, and pyrogallol, inhibits CRC proliferation, migration, and invasion.
- PSET suppresses the Wnt/β-catenin pathway and activates p53-mediated cell cycle arrest.
- PSET abrogates the Warburg effect, disrupts glycolysis, downregulates EMT markers, and induces apoptosis via cellular stress.
Conclusions:
- PSET demonstrates potent, multi-targeted anti-cancer activity against colorectal cancer cells.
- Integrated omics data validates PSET's ability to dismantle cancer survival networks.
- PSET shows significant potential as a natural therapeutic agent for colorectal cancer.
