AI Article Synopsis
- * The study identified that SLC7A11-AS1 lncRNA is significantly overexpressed in CRC and its high levels correlate with poor patient survival, while reducing its expression can inhibit cancer cell growth and movement.
- * SLC7A11-AS1 may enhance CRC development by elevating the levels of NRF2 and SLC7A11, leading to lower reactive oxygen species (ROS) levels in cancer cells, suggesting it could be a valuable target for CRC treatment and a potential diagnostic marker.
Article Abstract
Colorectal cancer (CRC) is ranked as the second leading cause of cancer-related death worldwide. Many abnormally expressed long non-coding RNAs (lncRNAs) in CRC were identified with the development of next-generation sequencing, most functions of which are largely unclear. In this study, we report that the lncRNA SLC7A11-AS1 was significantly overexpressed in CRC by analyzing TCGA database and 6 pairs of clinical samples. High SLC7A11-AS1 level was related to poor CRC overall survival and SLC7A11-AS1 knockdown could inhibit the proliferation, migration and invasion of CRC cell lines. Furthermore, we found there was a positive correlation between the expression of SLC7A11-AS1 and its' sense transcript SLC7A11. In HCT-8 cells, SLC7A11-AS1 knockdown decreased expression of both SLC7A11 and the nuclear level of NRF2, which happens to be the activator of SLC7A11 transcription. Interestingly, in SLC7A11-AS1 overexpressed CRC tissues, SLC7A11 and NRF2 were also upregulated. Moreover, the ROS levels increased with SLC7A11-AS1 knockdown in HCT-8 cells. And the down regulated expression of SLC7A11 and lower ROS level causing by SLC7A11-AS1 knocked down could be relieved by overexpressed NRF2. These results suggested that upregulated SLC7A11-AS1 might promote the formation and progression of CRC by increasing the expression of NRF2 and SLC7A11, which decreases the ROS level in cancer cells. Therefore, SLC7A11-AS1 could be a potential therapeutic target and diagnostic marker of CRC.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10108855 | PMC |
| http://dx.doi.org/10.7717/peerj.15216 | DOI Listing |
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