Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/87996
Title: Comparative transcriptomics unravels prodigiosin's potential cancer-specific activity between human small airway epithelial cells and lung adenocarcinoma cells
Authors: Davient, Bala
Ng, Jessica Pei Zhen
Xiao, Qiang
Li, Liang
Yang, Liang
Keywords: Prodigiosin
Small Molecule
DRNTU::Science::Biological sciences
Issue Date: 2018
Source: Davient, B., Ng, J. P. Z., Xiao, Q., Li, L., & Yang, L. (2018). Comparative Transcriptomics Unravels Prodigiosin's Potential Cancer-Specific Activity Between Human Small Airway Epithelial Cells and Lung Adenocarcinoma Cells. Frontiers in Oncology, 8, 573-. doi:10.3389/fonc.2018.00573
Series/Report no.: Frontiers in Oncology
Abstract: Objective: Non-Small Cell Lung Cancer (NSCLC) is extremely lethal upon metastasis and requires safe and effective systemic therapies to improve a patient's prognosis. Prodigiosin (PG) appears to selectively and effectively target cancer but not healthy cells. However, PG's cancer-specific activity has remained elusive until recently. Methods: PG's cancer-specific performance was compared to Docetaxel (DTX), Paclitaxel (PTX), and Doxorubicin (DOX) against human lung adenocarcinoma (A549) and human small airway epithelial cells (HSAEC). Combination of PG with DTX, PTX, or DOX in a 1:1 ED50 ratio was also evaluated. MTT assay was used to determine the post-treatment cell viability. RNA-sequencing was used for comparative transcriptomics analysis between A549 and HSAEC treated with 1.0 μM PG for 24 h. Results: PG reduced A549 cell viability by four-folds greater than HSAEC. In comparison to DTX, PTX and DOX, PG was ~1.7 times more toxic toward A549, and 2.5 times more protective toward HSAEC. Combination of PG in a 1:1 ED50 ratio with DTX, PTX, or DOX failed to exhibit synergistic toxicity toward A549 or protection toward HSAEC. In A549, genes associated in DNA replication were downregulated, while genes directly or indirectly associated in lipid and cholesterol biogenesis were upregulated. In HSAEC, co-upregulation of oncogenic and tumor-suppressive genes was observed. Conclusion: An overactive lipid and cholesterol biogenesis could have caused A549's autophagy, while a balancing-act between genes of oncogenic and tumor-suppressive nature could have conferred HSAEC heightened survival. Overall, PG appears to be a smart chemotherapeutic agent that may be both safe and effective for NSCLC patients.
URI: https://hdl.handle.net/10356/87996
http://hdl.handle.net/10220/47030
DOI: http://dx.doi.org/10.3389/fonc.2018.00573
Rights: © 2018 Davient, Ng, Xiao, Li and Yang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SCELSE Journal Articles

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