Cancer type | GLP dose | Study model | Effects | Mechanism | References |
---|---|---|---|---|---|
Breast | In vitro: 0–0.4 μM, 0–72 h | In vitro: MCF-7 cell lines | Decreased cell viability, arrested the cell cycle at the sub-G1 phase, induced apoptosis | ↑: cytochrome C, activated caspase-3, -9, and PARP ↓: – | [95] |
 | In vivo: GLP: 200–400 mg/kg/day paclitaxel: 12.5 mg/kg, twice a week | In vivo: xenograft mice | Reduced tumor growth and size, restored the anti-cancer immune cells, and recovered gut microbiota dysbiosis stimulated by paclitaxel | ↑: – ↓: GLUT3, LDHA, PDK | [109] |
 | In vitro: 0–160 μg/mL, 24 h In vivo: 8 mg/kg | In vitro: 4T1 cell lines In vivo: xenograft mice | Declined the number and size of 4T1 cells, increased radiosensitivity, reduced tumor growth, promoted apoptosis, and inhibited lung metastasis | ↑: INF-γ/IL-4 ratio ↓: | [132] |
 | In vivo: Au-GLPs (30 mg/kg/every four days, 12 days), Dox (4 mg/kg) | In vivo: xenograft mice bearing 4T1 breast cancer tumors | Reduced tumor weight, decreased body weight loss rate, reduced pulmonary metastasis, and increased CD4 + and CD8 + T cell proliferation | ↑: – ↓: – | [137] |
Cervical | In vivo: 0–300 mg/kg/day, 40 days | In vivo: rats bearing cervical cancer | Increased antioxidant activity and reduced inflammation | ↑: CAT, GSH-Px, and SOD ↓: IL-1β, IL-6, and TNF-α | [121] |
 | In vivo: GLPs (30 mg/kg/day, 14 days), cisplatin (5 mg/kg/day, 14 days) | In vivo: xenograft mice | Induced apoptosis, enhanced the spleen and thymus indexes, decreased the toxicity effects on hepatic and renal functions | ↑: Bax ↓: Bcl-2 | |
 | In vivo: 0–500 μg/mL, 0–72 h | In vitro: C-33A and HeLa cell lines | Reduced cell viability, induced apoptosis, arrested the cell cycle, suppressed the development of the EMT process | ↑: Bax, cleaved caspase-3 and –9, E-cadherin, ↓: Bcl-2, N-cadherin, Slug, Vimentin, p- JAK, p-STAT5 | [46] |
Colon and Colorectal | In vitro: 0.625–5 mg/mL, 0–72 h | In vitro: HCT-116 cell lines | Reduced cell viability suppressed cell migration, changed cell morphology | ↑: Ca2+, caspase-8, Fas ↓: - | |
 | In vitro: 0–10 mg/mL, 0–72 h | In vitro: HCT-116 cell lines | Reduced cell viability, arrested the cell cycle at the S phase, promoted apoptosis, and DNA fragmentation | ↑: Bax to Bcl-2 ratios, caspase-3, caspase-9, PARP ↓: | |
 | In vitro: 0–10 mg/mL, 0–72 h | In vitro: LoVo cell lines | Declined cell viability, suppressed cell migration, induced apoptosis and DNA fragmentation | ↑: Caspase-3, Caspase-8, Caspase-9, Fas, PARP ↓: | [65] |
 | In vitro: 200 μg/mL, 24 h | In vitro: HT29 (p53R273H) and SW480 (p53 R273H&P309S) | Promoted apoptosis, recovered p53 | ↑: Bax, p21, p53 ↓: | [44] |
 | In vitro: 0–7.5 mg/mL, 0–48 h In vivo: 0–300 mg/kg/day, six weeks | In vitro: HCT116 cell lines In vivo: Xenograft mice | Reduced cell viability, inhibited the cell cycle progression, stimulated apoptosis, decreased tumor growth | ↑: caspase-3, caspase-9, NAG-1, p21 ↓: Bcl-2, cyclin A2, cyclin B1, Ki67, PCNA, survivin | [77] |
 | In vivo: 393.75 g/kg/day | In vivo: xenograft mice | Inhibited colon shortening, decreasing the mortality rate, declined the abundance of cecal Oscillospira, associated genes | ↑: ↓: Scd1, Fabp4, Mgll, Acaa1b | [72] |
 | In vitro: 0–10 mg/mL, 0–72 h In vivo: 0–300 mg/kg/day, 14 days | In vitro: HT-29 and HCT-116 cell lines In vivo: xenograft mice | Reduced cell viability, induced autophagy, decreased tumor growth, and volume | ↑: LC3-II, GFP-LC3 puncta ↓: - | [85] |
 | In vitro: 0–0.32 mg/mL, 24 h In vivo: 0–300 mg/kg/day, 14 days | In vitro: HT-29 cell lines In vivo: xenograft mice | Reduced inflammation | ↑: ↓: COX-2, IL-1β, IL-6, iNOS, TNF-α, JNK, ERK | [33] |
 | In vitro: GLPs: 3 μg/mL, 72 h Paclitaxel: 0.5 μM, 72 h In vivo: 2 mg/kg/day, 30 days | In vitro: CT26 and HCT-15 cell lines In vivo: xenograft mice | Reduced cell growth and viability, inhibited tumor growth, and triggered apoptosis | ↑: α-catenin, p53 ↓: IL-1β, IL-11, Cox-2 | |
Gastric | In vivo: 400 and 800 mg/kg/every two days, four weeks | In vivo: Wistar rats bearing gastric cancer | Reduced inflammation and increased antioxidant activity | ↑: IL-2, IL-4, IL-6, CAT, GSH-Px, SOD ↓: IL-6 and TNF-α | [84] |
 | In vitro: 0–15 mg/mL | In vitro: AGS cell lines | Reduced cell viability, promoted apoptosis and autophagy | ↑: cleaved-PARP, LC3-II, p62 ↓: Bcl-2, pro-caspase-3 | [143] |
Glioma | In vivo: 0–200 mg/kg/day, two weeks | In vivo: male Fischer rats bearing glioma | Reduces tumor size, and modulated host immune responses | ↑: IL-2, TNF-α, INF-γ ↓: - | [113] |
Hepatocellular | In vivo: 0–200 mg/kg/day, four weeks | In vivo: xenograft mice | Inhibited tumor growth | ↑: IL-2, miR-125 ↓: FoxP3, Notch1 | |
Leukemia | In vitro: 0–200 μg/mL, 0–48 h | In vitro: THP-1 cell lines | Induced apoptosis degraded DNA | ↑: TNF-α, caspase-3, caspase-7, TRAIL ↓: - | [16] |
Lung | In vitro: 0- 12.8 μg/mL, 24 h | In vitro: lung cancer plasma patients | Reduced cell proliferation | ↑: – ↓: – | [110] |
 | In vitro: 0–1000 μg/mL, 24 h In vivo: 2.5 g/kg/day, 14 days | In vitro: A549 cell lines In vivo: xenograft mice | Reduced the cell viability, and tumor weight, increased the immune index of serum | ↑: – ↓: – | [34] |
 | In vitro: 0–300 μg/mL, 0–48 h In vivo: 75 mg/kg/every two days | In vitro: A549 cell lines In vivo: xenograft mice | Reduced the viability and mobility of lung cancer cells | ↑: – ↓: EGF, p-Akt, p-ERK1/2, p-FAK, p-Smad2, TGF-β | [39] |
 | In vivo GLPs: 75 mg/kg/every two days, 20 days Cisplatin: 2.3 mg/kg/day, five days | In vivo: xenograft mice | Attenuated tumor growth and formation of nodular pulmonary metastases, induced apoptosis, and enhanced the therapeutic effects of cisplatin | ↑: – ↓: – | [88] |
 | In vitro: 0–800 μg/mL, 0–72 h | In vitro: A549 and LLC1 cell lines | Alleviated the growth and viability of both cell lines | ↑: - ↓: p-Akt, p-EGFR, p-ERK, p-Smad2, p-FAK, Slug, twist, TGFβRII | [89] |
Oral | In vitro: 0–800 μg/mL, 0–72 h | In vitro: SAS cell lines | Declined the viability of cells, suppressed the cell cycle, prompted apoptotic responses, reduced cytotoxicity of cisplatin | ↑: Bax/Bcl-2 ratio ↓: p-Akt, p-EGFR | [38] |
 | In vitro: 0.01- 15 mg/mL, 72 h | In vitro: SCC-9 cell lines | Reduced the viability and colony formation of SCC-9 cells, delayed cell migration, and inhibited EMT development | ↑: - ↓: ABCG2, AXL, N-cadherin, p75NGFR Twist, Vimentin | [18] |
Ovarian | In vivo: 100–300 mg/kg/ twice a day | In vivo: ovarian cancer rats | Reduced malondialdehyde formation and increased the total antioxidant capacity | ↑: SOD, CAT, GSH ↓: - | [131] |
 | In vitro: 0–10 μg/mL, 0–3 days | In vitro: OVCAR-3 cell lines | Reduced cell growth and viability and inhibited the cell cycle | ↑: CAT, SOD, NQO1, GSTP1, DJ1, Trx, Nrf-2 ↓: cyclin D1 | [36] |
Prostate | In vitro: 0–20 μg/mL, 0–120 h | In vitro: LNCaP cell lines | Reduced cell proliferation and migration,, suppressed the cell cycle at the G1 stage | ↑: p21 ↓: PRMT6, CDK2, FAK, SRC | [138] |
 | In vitro: 1.25–10 mg/mL, 0–72 h | In vitro: PC-3 cell lines | Reduced the cell viability, stimulated late apoptosis | ↑: NAG-1, cleaved PARP ↓: pro-caspase-3, -6, and -9, p-Akt, p-MAPK/ERK | [120] |
Sarcoma | In vivo: 0–100 mg/kg/day, 21 days | In vivo: xenograft mice | Reduced the tumor growth and size | ↑: – ↓: – | [25] |
Skin | In vivo: 33.3–300 mg/kg/day, eight days | In vivo: xenograft mice | Inhibited tumor growth | ↑:– ↓:– | [86] |