Integrative Mechanistic Investigation of the Anticancer Effects of Panax notoginseng in Colorectal Cancer

TL;DR

This study explores how Panax notoginseng extract fights colorectal cancer through multiple biological pathways, showing promise as a new treatment.

Contribution

The novel contribution is the integrative use of network pharmacology and experimental validation to uncover PNE's multi-target anticancer mechanisms.

Findings

PNE inhibits CRC cell proliferation and induces G0/G1 phase arrest via CDK4/6 and p21/p27 modulation.

PNE promotes apoptosis by regulating BCL2 family proteins in CRC cells.

PNE suppresses tumor growth in a syngeneic mouse model of colorectal cancer.

Abstract

Colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide, necessitating the development of novel multi-targeted therapeutic agents. This study investigates the anticancer effects of Panax notoginseng extract (PNE) against CRC using an integrative approach of network pharmacology and experimental validation. Phytochemical profiling via LC–MS identified major ginsenosides, including Rb1, Rg1, and Rd. Network pharmacology analysis revealed potential targets such as Bcl-xL, STAT3/CDK1, and IL-2, which are associated with apoptosis, cell cycle regulation, and immune modulation, respectively. Experimental results demonstrated that PNE significantly inhibited the proliferation of HCT 116 and HT-29 CRC cells, induced G0/G1 phase arrest by modulating CDK4/6 and p21/p27, and promoted apoptosis by regulating BCL2 family proteins. Furthermore, PNE treatment suppressed tumor growth in a CT26-bearing syngeneic mouse model. These findings highlight that PNE exerts potent anticancer effects through multi-pathway modulation, suggesting its potential as a therapeutic candidate for CRC.

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