Erianin Inhibits Proliferation and Induces Apoptosis of HaCaT Cells via ROS-Mediated JNK/c-Jun and AKT/mTOR Signaling Pathways

• Published in: Molecules (Basel, Switzerland) Switzerland), 2019-07, Vol.24 (15), p.2727
• Main Authors: Mo, Canlong, Shetti, Dattatrya, Wei, Kun
• Format: Article
• Language: English
• Subjects: Acetylcysteine; AKT protein; AKT/mTOR; Angiogenesis; Antitumor activity; Apoptosis; Apoptosis - drug effects; Bibenzyls - chemistry; Bibenzyls - pharmacology; c-Jun protein; Cell cycle; Cell growth; Cell Line, Tumor; Cell proliferation; erianin; Flow cytometry; Humans; Inflammation; Investigations; JNK Mitogen-Activated Protein Kinases - metabolism; JNK protein; JNK/c-Jun; keratinocyte; Kinases; MAP Kinase Signaling System - drug effects; Mediators; Pathogenesis; Proteins; Psoriasis; Rapamycin; Reactive oxygen species; Reactive Oxygen Species - metabolism; ROS; Signal transduction; Signal Transduction - drug effects; Skin diseases; TOR protein; TOR Serine-Threonine Kinases - metabolism; Transcription factors
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules24152727

Psoriasis is a recurrent skin disease described as keratinocyte hyperproliferation and aberrant differentiation. Erianin, a bibenzyl compound extracted from , has displayed antitumor and anti-angiogenesis effects. However, the effects of erianin on a human keratinocyte cell line (HaCaT) are not fully understood. In the present study, we explored the effect of erianin on proliferation and apoptosis in HaCaT cells. Our results indicated that treatment with erianin ranging from 12.5 nM to 50 nM inhibited proliferation and induced apoptosis of HaCaT cells. In addition, erianin-induced apoptosis was accompanied by elevated reactive oxygen species (ROS). The ROS scavenger -acetyl-cysteine (NAC) attenuated this elevation. Moreover, treatment with erianin induced activation of the c-Jun N-terminal kinase (JNK)/c-Jun signaling pathway and suppressed the protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway, while pretreatment with NAC also reversed these effects. Collectively, these data demonstrated that erianin inhibited proliferation and induced apoptosis of HaCaT cells through ROS-mediated JNK/c-Jun and AKT/mTOR signaling pathways. Erianin could be recognized as a potential anti-psoriasis drug.