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Ginsenosides in Cancer

Ginsenosides are the main bioactive ingredients of Panax and other types of ginsengs. In recent years, the regulation of cancer cell metabolism by ginsenosides has received extensive attention. For example, ginsenoside Rg3 effectively inhibits the proliferation of human colorectal cancer (CRC) cells by inhibiting the transactivation of CCAAT/enhancer-binding protein (C/EBP) and nuclear factor κ b (NF-κB) and the interaction of C/EBPβ with p65. Ginsenoside Rk1 and ginsenoside Rg5 inhibit transforming growth factor β (TGF-β)-induced EMT through promotion of E-cadherin expression and inhibition of vimentin. Ginsenoside Rh1 suppresses activator protein-1 (AP-1) dimer, c-fos, and c-fos through inhibition of the transcriptional activity of matrix metalloproteinase-1 (MMP-1) in HepG2 cells. (AP-1) dimer, c-fos and c-Jun, thus exerting anti-metastatic activity. Figure 1 summarizes detailed information on the antitumor effects of ginsenosides ^[1].

Fig. 1 The antitumor mechanisms of ginsenosides

Many other ginsenosides also have anticancer effects. Table 1 ^[1] summarizes the detailed mechanisms of ginsenosides in the regulation of metabolic reprogramming through unique or crosslinked pathways.

Table 1 The detailed mechanisms of ginsenosides in the regulation of metabolic reprogramming

Ginsenosides	Cancer type	Effect	Mechanism
20S-Rg3	Gliomas	Reverse warburg effect and angiogenesis	Glycolysis pathway↓ HIF-1α↓ NKILA↓
20(S)-Rg3	Ovarian cancer	Reverse warburg effect Reduce DNA methylation	MiR-519a-5p↑ HIF-1α↓
Rg3	Gastric precancerous lesions	Reverse Warburg effect	MiRNA-21↓ PI3K/Akt pathway↓
Rh4	Esophageal cancer	Reverse Warburg effect	PD-L1↓ Akt/mTOR pathway↓
20(S)-Rh2E2	Lewis lung cancer	Inhibit mitochondrial respiration and glycolysis Inhibit tumor growth	α-enolase↓ Glycolytic enzymes↓ AMPK signaling↑ MAPK signaling↑
CK	Liver cancer	Reverse warburg effect Inhibit tumor growth	HIF-1α↓ Bclaf1↓
G-Rh2	Non-small cell lung cancer	Regulate FA metabolism Improve immune deficiency Synergistically inhibit tumor growth	PI3K/AKT pathway↓ SREBP↓ FASN↓
g-PPT	Non-small cell lung cancer	Inhibit lipid metabolism Reverse the resistance to TKIs	LDs↓ SCD1↓
CK	Hepatocellular Carcinoma	Suppress lipid accumulation	AMPK↑ PPAR-α↑ CD36↑ FASN↓ SREBP1c↓ SCD1↓
PPD	Colorectal cancer	Modulate the metabolism of amino acids and lipids	AMPK↑ Sesn2↑ Autophagy↑
Rk1	Hepatocellular carcinoma	Inhibit glutamine metabolism Induce apoptosis Inhibit tumor growth	ERK/c-myc pathway↓
CK	Breast cancer	Exert antitumor activity and trigger apoptosis Suppress glutamine consumption	Amino acids associated with glutamine metabolism↓ GSH↓ ROS↑
Rb1, Rg1	Colorectal cancer	Inhibit colorectal cancer cell growth Induce apoptosis	Inhibit cellular3H-thymidine incorporation
Rg3	Breast cancer	Inhibit proliferation of breast cancer cells	NF-κB↓ Regulate protein synthesis and cell division
G-Rh2	Hepatocellular carcinoma	Induce apoptosis	Mitochondrial release of cytochrome c Activation of caspase-3
Rd, Re	Human neuroblastoma	Inhibit apoptosis	Reduce oxidative stress Improve mitochondrial integrity and functions
GF2	Glioblastoma	Induce cancer cell death	Reduce mitochondrial membrane potential Inhibit cellular oxygen consumption Activate AMPK signaling
CK	Lung cancer	Improve antitumor effect	Increase ROS level Induce mitochondrial apoptosis
Rh1	Breast cancer	Favor mitophagy Regulate ROS and mitochondrial autophagy	PINK↑ Parkin↑ PGC-1α↓
Rg2	Breast cancer	Exert anti-cancer effects	Cell cycle arrest↑ ROS production↑
Rh4	Colorectal cancer	Exert anti-cancer effects Induce apoptosis and autophagic cell death	ROS/JNK/P53↑
Rh4	Colorectal cancer	Inhibit tumor growth Induce ferroptosis and autophagy	ROS/p53 signaling pathway↑
Rg3	Lung cancer	Suppress lung cancer cell invasion	ROS↓ AKT/ERK↓ NF-κB↓ HIF1-α↓
Rg5	Gastric cancer	Induce G2/M phase arrest, apoptosis and autophagy Inhibit gastric cancer cells	ROS↑ MAPK pathway↑
Re	Neuroblastoma	Reduce oxidative stress Alleviate 6-OHDA-induced neuronal damage	GPX4↑
Re	Lung cancer	Sensitize cancer cells to therapeutic drugs	NRF2 pathway↓
Rg3	Colorectal cancer	Enhance the inhibition of colon cancer cell proliferation, migration and invasion Promote apoptosis of colon cancer cells Arrest the cells in the G0/G1 phase	PI3K/AKT pathway↓
Rh1	Breast cancer	Inhibit migration, invasion, and angiogenesis	STAT3 and NF-κB signaling↓ ROS production↑
Rh2	Cervical cancer	Inhibit cell viability Induce apoptosis of cancer cells	ROS production↑ ATP synthesis↓ OXPHOS and glycolysis↓
Rh2	Breast cancer	Reduce the toxic effect of senescent cells Sustain the anti-tumor capacity of normal human breast epithelial cells	NF-κB↓ Mitophagy↑ ROS↓

Alfa Chemistry specializes in providing high-quality ginseng extracts, ginsenosides and multicomponent rare ginsenosides, and we are always available to answer the questions you may have during the R&D and production process. Please do not hesitate to contact us if you are in need of assistance.

Reference

Yao W, Guan Y. Ginsenosides in cancer: A focus on the regulation of cell metabolism. Biomed Pharmacother. 2022 Dec;156:113756.

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