Purified inotodiol reduced breast tumor proliferation in living diabetic rats by downregulating beta-catenin signaling.
What the researchers found
In rats with streptozotocin-induced diabetes and DMBA-induced breast tumors, inotodiol lowered blood glucose, reduced the proliferation marker PCNA, downregulated beta-catenin and its targets c-Myc and cyclin D1, and induced apoptosis.
Why it matters
This is one of only two in vivo studies of purified inotodiol in cancer, and the only one using a tumor-bearing animal model rather than a chemically induced skin promotion assay.
The numbers in context
Streptozotocin 35 mg/kg; DMBA 10 mg/kg.
How the study worked
Rat model of diabetic breast cancer; fasting blood glucose and oral glucose tolerance testing; immunohistochemistry for PCNA, cleaved caspase-3 and beta-catenin; TUNEL staining for apoptosis.
Who was studied
Female Sprague-Dawley rats with streptozotocin-induced diabetes and DMBA-induced breast tumors.
What this study cannot tell us
Animal model only; the diabetic-tumor combination is a specific disease context that may not generalize; no human data; dose translation to human intake is not established.
Read the original research
Inotodiol suppresses proliferation of breast cancer in rat model of type 2 diabetes mellitus via downregulation of beta-catenin signaling.
Biomedicine & pharmacotherapy, 99, 142-150
Citation
Zhang, Xin; Bao, Chun; Zhang, Jingping. (2018). Inotodiol suppresses proliferation of breast cancer in rat model of type 2 diabetes mellitus via downregulation of beta-catenin signaling.. Biomedicine & pharmacotherapy, 99, 142-150. https://doi.org/10.1016/j.biopha.2017.12.084