Anti-proliferative Effects of Common Plant Extracts on Tumor Cells in Vitro

In 2018, the World Health Organization identified cancer as responsible for 1 in 6 deaths globally, encouraging the exploration of creative forms of cancer treatment. Our research interests include identifying anti-proliferative plant extracts and illuminating mechanisms of growth inhibition. In this study we measured the effects of Vitis vinifera (grapeseed), Juniperus communis (juniper berry), and Curcuma longa (turmeric) extracts on the proliferation of several normal and tumorigenic cell strains and lines (HFF-S2, HeLa, HepG2, MDA MB 231, and RAW 264.7). We performed dose response CyQUANT assays to analyze the effects on cell growth. We are using DNA analysis, recovery experiments, and DAPI staining to investigate whether our extracts induce apoptosis in these cells. Our results showed dose-dependent inhibition of cell growth in vitro with all three extracts but not with extracts from other plants. The results of this study suggest the potential for further study of components of grapeseed, juniper berry, and turmeric extracts as potential chemo preventive agents

PKCμ promotes keratinocyte cell migration through Cx43 phosphorylation-mediated suppression of intercellular communication

Summary: Downregulation of intercellular communication through suppression of gap junctional conductance is necessary during wound healing. Connexin 43 (Cx43), a prominent gap junction protein in skin, is downregulated following wounding to restrict communication between keratinocytes. Previous studies found that PKCμ, a novel PKC isozyme, regulates efficient cutaneous wound healing. However, the molecular mechanism by which PKCμ regulates wound healing remains unknown. We have identified that PKCμ suppresses intercellular communication and enhances cell migration in an in vitro wound healing model by regulating Cx43 containing gap junctions. PKCμ can directly interact with and phosphorylate Cx43 at S368, which leads to Cx43 internalization and downregulation. Finally, utilizing phosphomimetic and non-phosphorylatable S368 substitutions and gap junction inhibitors, we confirmed that PKCμ regulates intercellular communication and in vitro wound healing by controlling Cx43-S368 phosphorylation. These results define PKCμ as a critical regulator of Cx43 phosphorylation to control cell migration and wound healing in keratinocytes