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Title: Zunyimycin C inhibits the proliferation of lung cancer cells by inducing apoptosis through an AKT-related mechanism

Journal Article · · Medicinal Chemistry Research (Print)
;  [1];  [2];  [3];  [1]
  1. Zunyi Medical University, Research Center for Medicine & Biology (China)
  2. Zunyi Medical University, Guizhou Provincial College-based Key Lab for Tumor Prevention & Treatment with Distinctive Medicines (China)
  3. Fudan University School of Pharmacy, Laboratory of Neuropharmacology (China)

Objective: Zunyimycin C is a novel halogenated type II polyketide derived from the fermentation product of the Streptomyces species with notable antibiotic activity. However, it is still unclear whether zunyimycin C could inhibit the activity of cancer cells. In this study, human lung adenocarcinoma cell line A549, the large-cell lung cancer cell line NCI-H460 and the non-small-cell lung cancer cell line NCI-H1299 were employed to determine the in vitro anticancer properties of zunyimycin C and underlying molecular mechanisms. Materials and methods: The cellular viability and proliferative properties of lung cancer cells were investigated using the Cell Counting Kit-8 and colony formation assay, respectively. The mRNA expression of apoptotic genes related to lung cancer was studied using reverse-transcription polymerase chain reaction. The apoptotic ratio was measured through flow cytometry. The protein expression was visualized via western blotting using specific antibodies. Results: Zunyimycin C could inhibit cell proliferation and induce apoptosis in a dose-dependent manner. The expression levels of apoptosis-related proteins (i.e., BAX, cleaved-caspase-3, and cleaved-caspase-9) were increased compared with the control group. However, the levels of Bcl-2 and phosphorylated AKT were decreased by administration by zunyimycin C. Conclusions: Collectively, these results implied that zunyimycin C could inhibit cell proliferation and induce apoptosis via AKT phosphorylation.

OSTI ID:
22936164
Journal Information:
Medicinal Chemistry Research (Print), Vol. 28, Issue 11; Other Information: Copyright (c) 2019 Springer Science+Business Media, LLC, part of Springer Nature; Country of input: International Atomic Energy Agency (IAEA); ISSN 1054-2523
Country of Publication:
United States
Language:
English