Lychee Seed Extract Targets Proliferation, Differentiation, and Cell Cycle Proteins to Suppress Human Colorectal Tumor Growth in Xenograft Models

TL;DR

Lychee seed extract shows anti-cancer effects in colorectal tumor models by targeting proteins involved in cell growth and division.

Contribution

LCSE demonstrates in vivo anti-tumor activity in CRC xenografts through non-apoptotic mechanisms.

Findings

LCSE significantly inhibited tumor growth in HT-29 xenografts and reduced key proliferation markers.

In SW480 tumors, LCSE showed inhibitory effects at higher doses with limited impact on p53.

No systemic toxicity was observed in mice treated with LCSE.

Abstract

Colorectal cancer (CRC) remains a leading global health challenge, and natural products are increasingly explored for their multi-targeted therapeutic potential. Litchi chinensis seed extract (LCSE) has shown promising anti-cancer activity in vitro, though its in vivo effects remain underexplored. LCSE was analyzed by colorimetric assays and HPLC to quantify the phytochemical composition. Nude mice bearing HT-29 or SW480 xenografts were orally administered LCSE (0.1 or 0.6 g/kg) daily for 14 days. Tumor volume was measured, and immunohistochemistry was used to assess EGFR, p21, p53, Ki-67, CEA, CK20, CDX2, and Bax expression. Phytochemical profiling demonstrated LCSE contains abundant phenolics and flavonoids, with gallic acid as a predominant constituent, underscoring the potential bioactive properties. LCSE significantly inhibited tumor growth in HT-29 xenografts and dose-dependently reduced EGFR, p21, p53, cell cycle proteins and proliferation/differentiation markers. In SW480 tumors, inhibitory effects were evident primarily at the higher dose, with limited reduction in p53 expression. Bax levels remained unchanged in both models, indicating a non-apoptotic mechanism. No systemic toxicity was observed in treated mice. LCSE exhibits dose-dependent anti-tumor activity in CRC xenografts, likely mediated through suppression of proliferation and modulation of key regulatory proteins rather than apoptosis. These findings support LCSE as a safe, multi-target botanical candidate for CRC intervention and justify further mechanistic and translational studies.

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