Anticancer effects of CH based on in vivo studies
Type of cancer | Animal models | Effects | Mechanisms | Dosage | Duration | References |
---|---|---|---|---|---|---|
Melanoma | C57BL/6JRj mice xenografted with B16F10 | Inhibits angiogenesis | ↓ Tumor volume, ↓ vascular segments, ↓ vascular network length, ↓ VEGF-A, ↓ phosphorylated histone H2AX on Serine 139 (pS139-H2AX), ↓ HIF-1α, ↓ Nrf1, ↓ superoxide dismutase 1 (Sod1), ↓ peroxiredoxin 4 (Prdx4), ↓ glutathione peroxidase (Gpx) | 50 mg/kg | 16 days | [12] |
C57BL/6 mice xenografted with B16F10 | Improve tumor immune response | ↓ Cancer cell growth in tumors, ↑ survival rate in mice↑ vaccine efficacy, ↑ cluster of differentiation 80 (CD80), ↑ CD86, ↑ MHCI, ↑ MHCII, ↑ CD8+ T cells | 650 mg/kg | 21 days | [14] | |
C57BL/6 mice xenogafted with B16F10 | Inhibits angiogenesis and inhibited tumor growth | ↓ Tumor volume and weight, ↓ G-MDSCs buildup in marrow and spleen, restore T cell proliferation, ↓ activation of RhoA, ↓ HIF-1α, ↓ microvessel density, ↓ vascular permeability ↑ vascular perfusion | 20 mg/kg and 40 mg/kg | 22 days | [15] | |
Breast | BALB/c nude mice xenogafted with MDA-MB-231 | Induces apoptosis, inhibits metastasis | ↓ Tumor growth, ↓ Ki-67, ↑ apoptosis frequency, ↓ MMP-1, 2, 3, 9, 10, and 13, ↑ MMP-8, ↓ tissue inhibitor of metalloproteinase-1 (TIMP-1), ↓ PI3K, ↓ p-Akt, ↓ GSK-3β, ↓ NF-κB | CH-NPs—10 mg/kg | 21 days | [22] |
Pancreatic | BALB/c-nude mice xenogarfted with MIA PaCa-2 | Induces apoptosis | ↓ Tumour growth, ↓ Ki-67, ↓ c-Myc | 50 mg/kg | 35 days | [28] |
Prostate | Male BALB/c nude mice xenograted with PC-3 cells | Induces apoptosis | ↓ Tumor spheroid formation and growth, inhibited PC-3 tube formation, ↓ HIF-1α, ↓ VE-cadherin (under normoxic as well as hypoxic conditions), ↓ Ki-67, ↓ SPHK-1, ↓ cyclin D1, ↓ c-caspase-3, ↓ VEGF | 50 mg/kg | 25 days | [30] |
↑: over expression; ↓: down expression
AS, AM, US, DA, TS, MS, AAJ, IR and SR: Writing—original draft, Writing—review & editing. HST: Conceptualization, Validation, Writing—review & editing, Supervision. VY: Validation, Writing—original draft, Writing—review & editing, Supervision. MK: Writing—original draft. All authors read and approved the submitted version.
The authors declare that they have no conflicts of interest.
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The study was financially supported by ICMR-DHR, Government of India to TS, ICMR-DHR Young Scientist Fellowship [R. 12014/29/2022/HR]; partly supported by college research and development cell (RDC) Scheme [HRC/RDC/2021/RP/13]; and VY acknowledge the grant from the Royal Physiographic Society of Lund, Sweden. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
© The Author(s) 2024.