Anti-tumor function

Cancer types

ginsenosides

cells or tissues

Mechanisms

Ref.

anti-proliferation

breast cancer

Rg3

breast cancer cells

up-regulated tumor-related genes through alteration of epigenetic methylation levels down-regulated hypermethylated TRMT1L, PSMC6 and NOX4, up-regulated methylated ST3GAL4, RNLS and KDM5A

[5]

colorectal cancer

Rg3

SW-480 cells

down-regulating the transcriptional activity of C/EBP beta NF-kappaB

[6]

Lewis lung cancer

Rg3

lung cancer cells

reducing ROS and down-regulating the expression of cyclin and cyclin dependent kinase

[7]

malignant melanoma

Rg3

malignant melanoma cells

inducing G0/G1 cell cycle arrest, reducing histone deacetylase 3 (HDAC3) and up-regulating p53 acetylation

[8]

melanoma

Rg3

melanoma cells

deactivation of EGFR/MAPK pathway mediated by decreased FUT4/LeY expression

[9]

pancreatic cancer

Rg3

pancreatic cancer cells

increased the expression levels of caspase-3, 9 and cleaved PARP, down-regulating the EGFR/PI3K/AKT pathway, reduced the expression levels of p-EGFR, p-PI3K, and p-AKT

[10]

glioma

Rh2

human A172 glioma cell

regulating CDK4/CyclinD complex and AKT, down-regulated CDK4 and cyclin D, reduced the level of phosphorylated AKT

[11]

lung cancer

Rh2

H1299 cells

induced ROS mediated endoplasmic reticulum stress-dependent apoptosis, and up-regulated the expression of activated transcription factor 4 (ATF4), CCAAT/enhanced binding protein homologous protein (CHOP), and caspase-4

[12]

prostate cancer

Rh2

prostate cancer cells

inhibiting microrna-4295, activates the cell cycle inhibitor p21 (CDKN1A)

[14]

colorectal cancer

Rp1

colorectal cancer LoVo cells

up-regulate apolipoprotein apo-a1

[15]

breast cancer

Rp1

breast cancer cells

inhibit the Akt/mTOR/P70S6 kinase signaling pathway.

[16]

Pro-apoptosis

lung cancer

Rg3

Lewis lung cancer (LLC) cells

regulating apoptosis-related proteins, such as Bcl-2, Bax, PARP-1, and lysed caspase-3

[7]

lung cancer

Rg3

non-small cell lung cancer (NSCLC) cells

up-regulated the pro-apoptotic protein Bax, down-regulated the anti-apoptotic protein Bcl-2, thereby activating caspase-3.

[17]

gastric cancer

Rg3

gastric cancer cells

up-regulated the expression of SP1, activated caspase 3, 8, 9 and PARP, down-regulated HSF1

[18]

human osteosarcoma

Rg3

osteosarcoma cell lines

reduced the protein expression of Bcl2, repressed PI3K/AKT/mTOR signaling pathway and increased the expression of lysed caspase3

[19]

ovrian cancer

Rg3

HO-8910 cells

suppression of the PI3K/Akt pathway, reducing the expression of caspase-3 and caspase-9

[20]

breast cancer

Rh4

McF-7 cells

down-regulating Bcl-2, up-regulating Bax, and activating caspase-8, -3 and PARP

[21]

colorectal cancer

Rh4

colorectal cancer cells

activating the ROS/JNK/p53 pathway

[22]

colorectal cancer

Rh2

HCT116 and SW480 cells

induce the caspase-mediated apoptosis, activated the p53 pathway, increasing the level of pro-apoptotic protein Bax and reducing the level of anti-apoptotic protein Bcl-2

[23]

prostate cancer

Rh2

DU145 cells

up-regulating the expression of PPAR-delta and p-STAT3, induction OF ROS/superoxide

[25]

autophagy

breast cancer

Rg3

breast cancer cells

decreased P62 levels, increased generation of LC3-II cleaved from LC3-I

[29]

ovarian cancer

Rg3

SKOV3 cells

increasing the levels of LC3-II, Atg5, and Atg7

[28]

colorectal cancer

Rh4

colorectal cancer cells

activating ROS/JNK/p53 pathway, increased the Beclin 1 levels, increase the expression of Atg-7 and LC3-II, promote the autophagy

[22]

breast cancer

Rg2

MCF-7 cells

Increased p53 levels by transcriptional activation of GR, activated TSC1 and TSC2, phosphorylated AMPK, inhibited the mTOR pathway, and increased autophagy

[32]

breast cancer

Rg5

breast cancer cells

inhibiting P13K/AKT/mTOR pathway, decreased P62 levels, increased Atg5, Atg7, Atg12, accelerated the LC3-I to LC3-II transformation

[33]

non-small-cell cancer

CK

non-small-cell cancer cells

induced generation of LC3-II cleaved from LC3-I, and decreased the P62 levels

[34]

Anti-metasis

breast cancer

Rg3

MDA-MB-231 cells

inhibits CXCR4 expression and

[37]

ovarian cancer

Rg3

SKOV3 cells

down-regulating the expression of VEGF mRNA and protein, reducing microvascular density and blocking angiogenesis

[38]

ovarian cancer

Rg3

SKOV3 cells

reduction of MMP-9 expression, promote the invasion

[39]

breast cancer

Rd

4T1 cells

decreasing miR-18a-mediated Smad2 expression, decaying migration

[56]

hepatocellr cancer

Rd

HepG2 cells

down-regulating the expression of MMP-1, MMP-2, and MMP-7 by inhibiting ERK and MAPK signaling pathways

[57]

melanoma cancer

Rp1

B16F10 Cells

down-regulating the expression of beta1-integrin (CD29), inhibiting the formation of blood vessels

[63]

glioblastoma multiforme

Rh2

U251 cells

inhibit AKT mediated MMP13 activation

[58]

colerectal cancer

20(S)-Rh2

CRC cells

down-regulatingIL-6-induced signal transducer, STAT3, MMPs (MMP-1, -2, and -9)

[60]

colorectal cancer

20(S)-Rg3

SW280 and SW620 cells

inhibited the expression of fatty acid synthetase and histone H4

[10]

colerectal cancer

Rb2

HT29 and SW620 cells

down-regulating stemness and Epithelial-mesenchymal transition (EMT)-related genes via the EGFR/SOX2 signaling axis

[61]

malignant gliomas

Rh1

U87MG and U373MG cells

inhibited mRNA expressions and promoter activity, down-regulating the expression of MMP-1, -3, and -9

[59]

Inhibiting EMT

lung cancer

20(R)-Rg3

A549 cells

suppressing the expression of E-cadherin and vimentin by inhibiting TGF-ß1 activation

[46]

liver cancer

Rg1

HepG2 cells

increased the expression of E-cadherin and inhibited the expression of the mesenchymal phenotype marker vimentin by inhibiting TGF-β1

[54]

ovarian cancer

Rg1

SKOV3 cells

recovered the expression of E-cadherin and attenuated expression of vimentin by regulating NF-κB pathway

[55]

ovarian cancer

Rb1

SKOV3 and 3AO cells

by down-regulating the expression of miR-25, E-cadherin transcriptional activator EP300 is overexpressed, thus increasing E-cadherin level

[62]

breast cancer

CK

MCF-7 cells

decreasing N-cadherin and vimentin, and increase level of E-cadherin through inhibition the activation of PI3K/Akt pathway

[66] [67]

Chemotherapy sensibilization

lung cancer

Rg3

hypoxic lung cancer cell

blocking of NF-κB mediated EMT and stemness, reduced the toxicity induced by cisplatin

[70] [71] [72]

lung cancer

Rg3

lung cancer cells

attenuated cisplatin resistance and increased chemosensitivity by down-regulating PD-L1 and resuming immune

[10]

colon cancer

Rg3

colon cancer cells

enhanced the sensitivity of cisplatin by reducing the basal level of nuclear factor erythroid 2-related factor2-mediated heme oxygenase-1/NAD(P)H quinone oxidoreductase-1

[13]

pancreatic cancer

Rg3

pancreatic cancer cells

enhances the anti-proliferative activity of erlotinib by downregulation of EGFR/PI3K/Akt signaling pathway By downregulation of EGFR/PI3K/Akt signaling pathway

[75]

hepatocellar cancer

Rg3

hepatocellular carcinoma cells

sensitize TRAIL-induced cell death CHOP-mediated DR5 upregulation

[59]

ovarian cancer

Rb1

ovarian cancer cells

promote sensitivity of cisplatin and paclitaxel by suppressing the Wnt/β-catenin signaling and EMT

[76]

lung cancer

Rd

lung cancer cells

significant sensitization was achieved by inhibiting NRF2

[79]

esophageal cancer

Ro

esophageal cancer cells

delayed DNA repair and the accumulation of DNA damage by potentiating 5-Fu cytotoxicity via delaying CHEK1 (checkpoint kinase 1) degradation and downregulating DNA replication process

[28]