antroquinonol-d and Lung-Neoplasms

Antrodia camphorata is an expensive mushroom that grows on the inner cavity of an endangered native tree of Taiwan namely Cinnamomum kanehirai Hayata. It is used as a traditional medicine in Taiwan and has several health benefits including free radical scavenging, anti-inflammatory, antimicrobial, hepatoprotective, neuroprotective, antidiabetic, and free radical-induced DNA damage protecting activities. Antroquinonol is a tetrahydro ubiquinone derivative found predominately in the mycelium of Antrodia camphorata, and is characterized by numerous biological and pharmacological activities. Several studies have revealed potential anticancer effects of antroquinonol in various carcinogenic models. Moreover, a phase II clinical trial is ongoing in the US and Taiwan to treat the lung cancer patients with this active compound. The present review aims at depicting a detailed view of the synthetic procedures of antroquinonol as well as deciphering its potential health benefits with a special emphasis on anticancer properties.

Topics: Animals; Antineoplastic Agents, Phytogenic; Antrodia; Cell Proliferation; DNA Damage; Humans; Lung Neoplasms; Ubiquinone

Lung and breast cancer are the leading causes of mortality in women worldwide. The discovery of molecular alterations that underlie these two cancers and corresponding drugs has contributed to precision medicine. We found that CCND2 is a common target in lung and breast cancer. Hypermethylation of the

Topics: Antineoplastic Agents; Biomarkers, Tumor; Breast Neoplasms; Cell Movement; Cell Proliferation; Cyclin D2; DNA Methylation; Dose-Response Relationship, Drug; Gene Expression Regulation, Neoplastic; Humans; Lung Neoplasms; Prognosis; Promoter Regions, Genetic; Proportional Hazards Models; RNA, Messenger; Ubiquinone

Antroquinonol a derivative of Antrodia camphorata has been reported to have antitumor effects against various cancer cells. However, the effect of antroquinonol on cell signalling and survival pathways in non-small cell lung cancer (NSCLC) cells has not been fully demarcated. Here we report that antroquinonol treatment significantly reduced the proliferation of three NSCLC cells. Treatment of A549 cells with antroquinonol increased cell shrinkage, apoptotic vacuoles, pore formation, TUNEL positive cells and increased Sub-G1 cell population with respect to time and dose dependent manner. Antroquinonol treatment not only increased the Sub-G1 accumulation but also reduced the protein levels of cdc2 without altering the expression of cyclin B1, cdc25C, pcdc2, and pcdc25C. Antroquinonol induced apoptosis was associated with disrupted mitochondrial membrane potential and activation of Caspase 3 and PARP cleavage in A549 cells. Moreover, antroquinonol treatment down regulated the expression of Bcl2 proteins, which was correlated with the decreased PI3K and mTOR protein levels without altering pro apoptotic and anti apoptotic proteins. Results from the microarray analysis demonstrated that antroquinonol altered the expression level of miRNAs compared with untreated control in A549 cells. The data collectively suggested the antiproliferative effect of antroquinonol on NSCLC A549 cells, which provides useful information for understanding the anticancer mechanism influenced by antroquinonol and is the first report to suggest that antroquinonol may be a promising chemotherapeutic agent for lung cancer.

Topics: Antineoplastic Agents; Apoptosis; Carcinoma, Non-Small-Cell Lung; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Gene Expression Regulation, Neoplastic; Humans; Lung Neoplasms; Membrane Potentials; MicroRNAs; Phosphatidylinositol 3-Kinases; Signal Transduction; TOR Serine-Threonine Kinases; Ubiquinone