Oral Cancer (OSCC)

Oral squamous cell carcinoma is one of the most important mechanistic cancer models in the polydatin literature because it links direct G6PD inhibition to reduced invasion and metastasis.

Overview

This is the clearest cancer model for polydatin's PPP-disrupting and anti-metastatic biology.

Key findings

• Decreases survival and proliferation of CAL27 and Ca9-22 oral cancer cells

• Induces cytochrome c release, caspase-related apoptosis, and PARP cleavage

• Triggers autophagy alongside apoptosis

• Inhibits migration and invasion through EMT-related changes

• Prevents lymph node metastases in orthotopic models through direct G6PD inhibition

• Reduced toxicity was reported in normal tissues in vivo

Practical interpretation

This is one of the strongest pages in the whole polydatin evidence base because the mechanism, in vivo effect, and metastasis findings line up unusually well.

References

Polydatin, a Glycoside of Resveratrol, Induces Apoptosis and Autophagy in Oral Squamous Cell Carcinoma
https://pmc.ncbi.nlm.nih.gov/articles/PMC8468100/

A new inhibitor of glucose-6-phosphate dehydrogenase blocks pentose phosphate pathway and suppresses malignant proliferation and metastasis in vivo
https://www.nature.com/articles/s41419-018-0635-5