Pilot study of jadomycin B pharmacokinetics and anti-tumoral effects in zebrafish larvae and mouse breast cancer xenograft models.

Despite numerous therapeutic options, multidrug resistance (MDR) remains an obstacle to successful breast cancer therapy. Jadomycin B, a natural product derived from ISP5230, maintains cytotoxicity in MDR human breast cancer cells. Our objectives were to evaluate the pharmacokinetics, toxicity, anti-tumoral, and anti-metastatic effects of jadomycin B in zebrafish larvae and mice.

Jadomycins: A potential chemotherapy for multi-drug resistant metastatic breast cancer.

Breast cancer causes the most cancer fatalities in women worldwide. Approximately one-third of breast cancers metastasize, or spread from primary tumors to other tissues, and have a 70% 5-year mortality rate. Current breast cancer treatments like doxorubicin and paclitaxel become ineffective when breast cancer cells develop multi-drug resistance and overexpress ATP-binding cassette transporters, as the transporters cause a substantial efflux of the chemotherapies.

Celosiadines A and B, unusual guanidine alkaloids from .

Two unusual di-isopentenyl guanidine alkaloids, named celosiadines A () and B (), were isolated from aerial parts. The structures of the compounds were elucidated from extensive spectroscopic analyses including HRMS, NMR and ECD. Celosiadines A and B showed favorable binding affinity to the androgen receptor (AR) and were cytotoxic towards AR-sensitive (LNCaP) but not AR-insensitive (PC3) human prostate cancer cells .

More Than an Adipokine: The Complex Roles of Chemerin Signaling in Cancer.

Chemerin is widely recognized as an adipokine, with diverse biological roles in cellular differentiation and metabolism, as well as a leukocyte chemoattractant. Research investigating the role of chemerin in the obesity-cancer relationship has provided evidence both for pro- and anti-cancer effects. The tumor-promoting effects of chemerin primarily involve direct effects on migration, invasion, and metastasis as well as growth and proliferation of cancer cells.

Magnolol affects expression of IGF-1 and associated binding proteins in human prostate cancer cells in vitro.

Background/aim: This study investigated the effects of magnolol, a compound from Magnolia officinalis, on the behavior of LNCaP and PC3 human prostate cancer cells in vitro.

Materials And Methods: In vitro cell culture approach with biochemical tests and Western blot analyses was used.

Results: Magnolol, (80 μM, 6 hour exposure) was found to affect the expression of insulin-like growth factor-1 (IGF-1) and associated proteins.

Magnolol causes alterations in the cell cycle in androgen insensitive human prostate cancer cells in vitro by affecting expression of key cell cycle regulatory proteins.

Prostate cancer, one of the most common cancers in the Western world, affects many men worldwide. This study investigated the effects of magnolol, a compound found in the roots and bark of the magnolia tree Magnolia officinalis, on the behavior of 2 androgen insensitive human prostate cancer cell lines, DU145 and PC3, in vitro. Magnolol, in a 24-h exposure at 40 and 80 μM, was found to be cytotoxic to cells.