Table 4 Cluster analysis of molecular pathways and proteins in different cancers

Proliferation(apoptosis)

Breast cancer: ↑ caspase-9/cytochrome c-mediated apoptosis [11]; TRAIL(TNF-related apoptosis-inducing ligand)-mediated apoptosis [12]

Liver cancer: ↑ Fas-mediated apoptosis [17]; ↓ arachidonic acid metabolic pathway [18]

Lung cancer: ↑ P53-Induced growth inhibition and apoptosis [26]

Gastric cancer: ↑ apoptosis via inhibiting EGFR signaling [27]

Esophageal cancer: ↑ cell growth inhibition and apoptosis [32]

↑ caspase-3 [11, 12, 17, 26, 32]; P53 [12, 17, 25, 26, 32]; Bax [11, 26, 32]; caspase-9 [11, 17]; PARP [12, 32]; ClvC-3, Ligase4 [11]; Fas [17]; caspase-8 [17]; Bak [26]; P21, P27 [32]

↓ Bcl-2 [11, 26, 32]; Mcl-1 [12, 32]; Bcl-xl [26, 28]; pERK [27, 28]; pSTAT3 [28, 32]; P65 [12]; PGE2, cPLA2, COX-2 [18]; pAKT, pNFκB, NFκB [28]; PI3K, Rac, p-JAK2, Wnt3a, β-catenin, XIAP, Ki-67 [32]

No effect: caspase-3, caspase-9 [18]

Proliferation(autophagy)

Neuroepithelial cancer: ↑ ERK1/2-mediated impairment of mitochondrial aerobic respiration and autophagy [30]

↑ C-parp-1, LC3II [30]

↓ Ki-67, p-ERK1/2 [30]

Proliferation(cell cycle arrest)

Colon cancer: ↓ cell proliferation by inducing the G2/M phase arrest and down-regulated the expression of the related cyclins [22]

Lung cancer: ↑ G1 cell cycle arrest [25]

Gastric cancer: ↑ cell cycle arrest via inhibiting EGFR signaling [27]

Esophageal cancer: ↑ cell cycle arrest at G2/M phase [32]

Cholangiocarcinoma: ↑ G1 cell cycle arrest [34]

↓ cyclin B1 [22, 25, 32]; cyclin D1 [27, 32, 34]; cyclin E [32, 34]; Cdc2 [22]; cdc25c [22]; CDK1, CDK2, CDK4, CDK6 [32]

Proliferation(others)

Breast cancer: ↓ cell proliferation [14]

Liver cancer: ↓ Id-1-induced cell proliferation [19]

Colon cancer: ↓ β-catenin - induced proliferation by binding RXR [21]

Nasopharyngeal carcinoma: ↓ cell proliferation via an Epstein-Barr virus nuclear antigen 1(EBNA1)-dependent mechanism [23]; ↓ cell proliferation by inhibiting STAT3 activation [24]

Lung cancer: ↓cell proliferation via MAPK pathways [25]

Gastric cancer: ↓ cell proliferation via MAPK pathways [28]

Neuroepithelial cancer: ↓cancer growth by suppressing Hedgehog signaling pathway [29]

Endometrial carcinoma: ↓ cell growth via miR-101/COX-2 [31]

Cholangiocarcinoma: ↓ cell proliferation [34]

↑ c-Cbl, p21^WAF1/CIP1 [21]; Cleaved PARP [24]

↓ PCNA [14, 21, 34]; Mcl-1, p-STAT3 [23, 24]; p-MAPK [25, 28]; Id-1 [19]; β-catenin, Ki-67, c-myc, RXRα [21]; EBNA1 [23]; p-Akt, p-CREB [25]; p-JNK, IL-8 [28]; Gli1, PTCH1 [29]; COX-2, PGE2 [31]

Intracellular oxidative stress

Breast cancer: ↑ intracellular reactive oxygen species (ROS) levels [14]

↑ MDA [14]

↓ SOD, CAT, GSH, Vit-C [14]

Inflammation

Breast cancer: ↓ inflammation [14]

↓ IL-1β, IL-6, TNF-α, NF-kB [14]

Angiogenesis

Liver cancer: ↓ Id-1-induced angiogenesis [19]

↓ Id-1, VEGF, HIF-1α [19]

Migration

Breast cancer: ↓ TGF-β1-induced cell migration [13]; vasodilator-stimulated phosphoprotein (VASP)-induced cell migration [16]

Liver cancer: ↓ Id-1-induced migration [19]

Endometrial carcinoma: ↓ cell metastasis via miR-101/COX-2 [31]

↓TGF-β1, MMP-2, MMP-9 [13]; Id-1 [19]; COX-2, PGE2 [31]

No effect: VASP [16]