Long non-coding RNA TMEM51-AS1 inhibits colorectal cancer progression
Colorectal cancer (CRC) is the third most common cause of death worldwide and has high mortality and a poor prognosis. Long non-coding RNAs (lncRNAs) are non-coding RNAs longer than 200 nucleotides that play roles in cancer through multiple mechanisms. TMEM51-AS1 is a newly discovered 40,650 bp lncRNA. Our results showed that TMEM51-AS1 expression was significantly downregulated in CRC tissues (fold change = 0.74, P < 0.0001). This finding was confirmed in 20 pairs of CRC carcinoma and paracancerous tissues (fold change = 0.5, P < 0.001). Additionally, TMEM51-AS1 expression was found to be significantly reduced in CRC cell lines compared to normal human intestinal epithelial cells (P < 0.001). Bioinformatic analysis revealed that TMEM51-AS1 expression was associated with immune escape, RNA methylation, and DNA damage and repair. TMEM51-AS1 may also activate energy metabolism pathways to participate in cancer development. Drug sensitivity analysis confirmed that several drugs are more effective in CRC patients with high expression of TMEM51-AS1. In conclusion, our study demonstrates that TMEM51-AS1 can suppress the progression of CRC.
Authors
- Yunan Mao (ORCID: https://orcid.org/0000-0002-5466-0886)
- Shiwei Duan (ORCID: https://orcid.org/0000-0001-7682-2877)
- Qiannan Ding
- Jiwei Mao
- Xiaoyu Zhang (ORCID: https://orcid.org/0009-0004-3923-651X)
- Qing Xia (ORCID: https://orcid.org/0000-0003-4373-2722)
- Xinming Su
- Jianjiang Liu (ORCID: https://orcid.org/0000-0003-3854-0937)
- Wangyan Zhong (ORCID: https://orcid.org/0009-0009-2405-6504)
- H. Li
- Dongping Wu (ORCID: https://orcid.org/0009-0006-9873-0846)
Institutions
- Hangzhou City University
- Zhejiang University of Technology (CN)
- Zhejiang University (CN)
Publication Details
- Journal
- Discover Oncology
- Published
- 2025-05-23
- DOI
- https://doi.org/10.1007/s12672-025-02676-z
- Primary Topic
- Cancer-related molecular mechanisms research
- Type
- article
- Field-Weighted Citation Impact
- 0.00