Related Experiment Video
Updated: Feb 26, 2026

RNA Pull-down Procedure to Identify RNA Targets of a Long Non-coding RNA
Published on: April 10, 2018
SLC45A3-ELK4 functions as a long non-coding chimeric RNA
Fujun Qin1, Yanmei Zhang2, Jia Liu1
1Department of Pathology, University of Virginia, Charlottesville, VA, 22908, USA.
Abstract:
Gene fusions in cancer typically lead to the expression of a fusion protein or disrupt the expression of one of the parental genes. Here we report a new phenomenon whereby a fusion transcript functions as a long non-coding chimeric RNA (lnccRNA). This fusion RNA, SLC45A3-ELK4, generated by cis-splicing between neighboring genes, was found in prostate cancer. The fusion RNA encodes the same protein as ELK4. Intriguingly, we found that the fusion RNA level is less than 1% of wild type ELK4, unlikely to perturb the general pool of ELK4 protein. Nonetheless, when the fusion RNA, but not ELK4 is silenced, cell proliferation is inhibited in both androgen-dependent and castration-resistant prostate cancer cells. This growth arrest can be rescued by exogenous expression of the fusion and a mutant designed to prevent translation of the ELK4 protein. In the same setting, the mutant could also suppress CDKN1A and several other targets of SLC45A3-ELK4. In addition, similar to many long non-coding RNAs, the fusion RNA is enriched in the nuclear fraction. Altogether, these results indicate that SLC45A3-ELK4 regulates cancer cell proliferation by its transcript, not translated protein.
Insights
A novel long non-coding chimeric RNA (lnccRNA), SLC45A3-ELK4, drives prostate cancer cell proliferation. This fusion RNA regulates cancer growth through its transcript, not its protein product.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Gene fusions in cancer can create fusion proteins or disrupt gene expression.
- A newly identified phenomenon involves fusion transcripts acting as long non-coding chimeric RNAs (lnccRNAs).
Purpose of the Study:
- To investigate the role of the SLC45A3-ELK4 fusion transcript in prostate cancer.
- To determine whether the SLC45A3-ELK4 fusion RNA functions via its protein product or as a non-coding RNA.
Main Methods:
- Identification of the SLC45A3-ELK4 fusion RNA in prostate cancer.
- Silencing of the fusion RNA and wild-type ELK4 to assess effects on cell proliferation.
- Rescue experiments using exogenous expression of the fusion RNA and a non-translatable mutant.
- Analysis of CDKN1A and other target gene expression.
Main Results:
- The SLC45A3-ELK4 fusion RNA, while encoding the same protein as ELK4, is present at low levels.
- Silencing the fusion RNA, but not ELK4, inhibits prostate cancer cell proliferation.
- The fusion RNA, acting as a transcript, suppresses CDKN1A and other targets, leading to growth arrest.
Conclusions:
- The SLC45A3-ELK4 fusion RNA regulates prostate cancer cell proliferation through its non-coding transcript function.
- This finding reveals a novel mechanism where lncRNA function, not protein production, drives cancer progression.
Related Concept Videos
lncRNA - Long Non-coding RNAs
lncRNA - Long Non-coding RNAs
RNA Splicing
Ribosomal RNA Synthesis
Ribosome biogenesis begins with the synthesis of 5S and 45S pre-rRNAs by distinct RNA polymerases. The primary transcripts are extensively processed and modified before they are bound and folded by ribosomal proteins and assembly factors,...
Leaky Scanning
Non-LTR Retrotransposons

