Open Access
Croton tiglium essential oil compounds have anti-proliferative and pro-apoptotic effects in A549 lung cancer cell lines
Author(s) -
Qinglin Niu,
Hui Sun,
Chao Liu,
Juan Li,
Changxu Liang,
Ruirui Zhang,
Fu-rong Ge,
Wei Liu
Publication year - 2020
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0231437
Subject(s) - a549 cell , apoptosis , chemistry , cell growth , cytotoxicity , cell cycle , cancer cell , pharmacology , cancer , traditional medicine , microbiology and biotechnology , biology , biochemistry , in vitro , medicine , genetics
As a traditional Chinese medicine, Croton tiglium has the characteristics of laxative, analgesic, antibacterial and swelling. This study aimed to analyze the chemical composition of C . tiglium essential oil (CTEO) extracted from the seeds of C . tiglium and its cytotoxicity and antitumor effect in vitro . Supercritical CO 2 fluid extraction technology was used to extract CTEO and the chemical constituents of the essential oil were identified by comparing the retention indices and mass spectra data taken from the NIST library with those calculated based on the C7-C40 n -alkanes standard. In vitro cytotoxicity of the CTEO was assessed against cancer cell lines (A549) and the human normal bronchial epithelial cells (HBE) using the CCK-8 assay. Proliferation was detected by colony formation experiments. Wound scratch and cell invasion assays were used to detect cell migration and invasion. Levels of apoptotic markers, signaling molecules, and cell cycle regulators expression were characterized by Western blot analysis. As the results, twenty-eight compounds representing 92.39% of the total oil were identified in CTEO. The CTEO has significant antitumor activity on A549 cancer cells (IC 50 48.38 μg/mL). In vitro antitumor experiments showed that CTEO treatment significantly inhibited the proliferation and migration of A549 cells, disrupted the cell cycle process, and reduced the expression levels of cyclin A, cyclin B and CDK1. CTEO can also reduce mitochondrial membrane potential, activate caspase-dependent apoptosis pathway, and finally induce apoptosis. CTEO may become an effective anti-cancer drug and will be further developed for cancer treatment.