AI Article Synopsis
- Non-small cell lung cancer (NSCLC) has a high mortality rate due to late detection and ineffective treatments, prompting research into new drug targets like SRD5A1, which is up-regulated in NSCLC compared to normal tissue.
- Researchers used siRNA to silence SRD5A1 in lung cancer cell lines and tested the effects on cell proliferation, cycle distribution, and apoptosis/necrosis, while also using 4-azasteroids to inhibit SRD5A1 activity.
- Despite efficient silencing of SRD5A1, results showed no significant impact on cell proliferation or survival, indicating that SRD5A1 may not be essential for the growth of NSCLC cell lines.
Article Abstract
Background: Non-small cell lung cancer (NSCLC) is one of the most frequent malignancies and has a high mortality rate due to late detection and lack of efficient treatments. Identifying novel drug targets for this indication may open the way for new treatment strategies. Comparison of gene expression profiles of NSCLC and normal adjacent tissue (NAT) allowed to determine that 5-alpha-reductase type I (SRD5A1) was up-regulated in NSCLC compared to NAT. This raised the question whether SRD5A1 was involved in sustained proliferation and survival of NSCLC.
Methods: siRNA-mediated silencing of SRD5A1 was performed in A549 and NCI-H460 lung cancer cell lines in order to determine the impact on proliferation, on distribution during the different phases of the cell cycle, and on apoptosis/necrosis. In addition, lung cancer cell lines were treated with 4-azasteroids, which specifically inhibit SRD5A1 activity, and the effects on proliferation were measured. Statistical analyses using ANOVA and post-hoc Tamhane-T2-test were performed. In the case of non-parametric data, the Kruskal-Wallis test and the post-hoc Mann-Whitney-U-test were used.
Results: The knock-down of SRDA51 expression was very efficient with the SRD5A1 transcripts being reduced to 10% of control levels. Knock-down efficiency was furthermore confirmed at the protein level. However, no effect of SRD5A1 silencing was observed in the proliferation assay, the cell cycle analysis, and the apoptosis/necrosis assay. Treatment of lung cancer cell lines with 4-azasteroids did not significantly inhibit proliferation.
Conclusions: In summary, the results suggest that SRD5A1 is not a crucial enzyme for the sustained proliferation of NSCLC cell lines.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3269976 | PMC |
| http://dx.doi.org/10.1186/1475-2867-12-1 | DOI Listing |
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