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

**Authors:** Jaemoo Chun, Sarah Shin, Jeeyoun Jung

PMC · DOI: 10.3390/molecules31050807 · 2026-02-28

## 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.

## Key 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.

## Linked entities

- **Genes:** Bcl2l1 (BCL2-like 1) [NCBI Gene 12048], STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774], CDK1 (cyclin dependent kinase 1) [NCBI Gene 983], IL2 (interleukin 2) [NCBI Gene 3558], Cdk4 (Cyclin-dependent kinase 4) [NCBI Gene 36854], CDKN1A (cyclin dependent kinase inhibitor 1A) [NCBI Gene 1026], IFI27 (interferon alpha inducible protein 27) [NCBI Gene 3429], BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596]
- **Proteins:** Bcl2l1 (BCL2-like 1), STAT3 (signal transducer and activator of transcription 3), CDK1 (cyclin dependent kinase 1), IL2 (interleukin 2), Cdk4 (Cyclin-dependent kinase 4), CDKN1A (cyclin dependent kinase inhibitor 1A), IFI27 (interferon alpha inducible protein 27), BCL2 (BCL2 apoptosis regulator)
- **Chemicals:** Rb1 (PubChem CID 736494), Rg1 (PubChem CID 441923), Rd (PubChem CID 7009612)
- **Diseases:** Colorectal cancer (MONDO:0005575), CRC (MONDO:0005575)

## Full-text entities

- **Genes:** BCL2L1 (BCL2 like 1) [NCBI Gene 598] {aka BCL-XL/S, BCL2L, BCLX, Bcl-X, PPP1R52}, CDK1 (cyclin dependent kinase 1) [NCBI Gene 983] {aka CDC2, CDC28A, P34CDC2}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}, IL2 (interleukin 2) [NCBI Gene 3558] {aka IL-2, TCGF, lymphokine}, H3P16 (H3 histone pseudogene 16) [NCBI Gene 644914] {aka H3.6, H3F3AP6, p21}, DCTN6 (dynactin subunit 6) [NCBI Gene 10671] {aka WS-3, WS3, p27}, BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596] {aka Bcl-2, PPP1R50}
- **Diseases:** cancer (MESH:D009369), CRC (MESH:D015179)
- **Chemicals:** Rb1, Rg1, and Rd (-), ginsenosides (MESH:D036145)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12986227/full.md

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Source: https://tomesphere.com/paper/PMC12986227