Table 2 A brief of different studies related to the application of GLPs in cancer treatment

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

[144, 145]

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

↓: -

[63, 64]

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

↓:

[63, 64]

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

[66, 69]

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

[56, 57]

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]