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] |