Munakarmi, Suvesh; Shrestha, Juna; Shin, Hyun-Beak; Lee, Geum-Hwa; Jeong, Yeon-Jun published the article 《3,3′-diindolylmethane suppresses the growth of hepatocellular carcinoma by regulating its invasion, migration, and er stress-mediated mitochondrial apoptosis》. Keywords: DIM; EMT; ER stress; apoptosis; hepatocellular carcinoma; unfolded protein response.They researched the compound: 3,3′-Diindolylmethane( cas:1968-05-4 ).Category: chlorides-buliding-blocks. Aromatic heterocyclic compounds can be divided into two categories: single heterocyclic and fused heterocyclic. In addition, there is a lot of other information about this compound (cas:1968-05-4) here.
Hepatocellular carcinoma (HCC) is the leading cause of cancer-related death worldwide with limited treatment options. Biomarker-based active phenolic flavonoids isolated from medicinal plants might shed some light on potential therapeutics for treating HCC. 3,3′-diindolylmethane (DIM) is a unique biol. active dimer of indole-3-carbinol (I3C), a phytochem. compound derived from Brassica species of cruciferous vegetables-such as broccoli, kale, cabbage, and cauliflower. It has anti-cancer effects on various cancers such as breast cancer, prostate cancer, endometrial cancer, and colon cancer. However, the mol. mechanism of DIM involved in reducing cancer risk and/or enhancing therapy remains unknown. The aim of the present study was to evaluate anti-cancer and therapeutic effects of DIM in human hepatoma cell lines Hep3B and HuhCell proliferation was measured with MTT and trypan blue colony formation assays. Migration, invasion, and apoptosis were measured with Transwell assays and flow cytometry analyses. Reactive oxygen species (ROS) intensity and the loss in mitochondrial membrane potential of Hep3B and Huh7 cells were determined using dihydroethidium (DHE) staining and tetramethylrhodamine Et ester dye. Results showed that DIM significantly suppressed HCC cell growth, proliferation, migration, and invasion in a concentration-dependent manner. Furthermore, DIM treatment activated caspasedependent apoptotic pathway and suppressed epithelial-mesenchymal transition (EMT) via ER stress and unfolded protein response (UPR). Taken together, our results suggest that DIM is a potential anticancer drug for HCC therapy by targeting ER-stress/UPR.
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