ArticleCell death & disease2022
Restoring the epigenetically silenced lncRNA COL18A1-AS1 represses ccRCC progression by lipid browning via miR-1286/KLF12 axis.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 27 citations in OpenAlex.
- Review
- Article
- Long Non-Coding RNAs in Pathogenesis of Renal Cell Carcinoma: Epigenetic Regulation, Signaling Pathways, and Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Unveiling the epigenetic landscape: transforming renal cell carcinoma treatment.Clinical epigenetics · 2026Review
- Multi-omics analysis and experiments validate the tumor-suppressive role of mitochondrial lipid metabolism gene ACSM5 in lung adenocarcinoma and its impact on the immune microenvironment.Human genomics · 2026Article
- Review
- The multifaceted regulation of white adipose tissue browning and their therapeutic potential.Journal of physiology and biochemistry · 2025Review
- The Long Noncoding RNA ΒFaar Promotes White Adipose Tissue Browning and Prevents Diet-Induced Obesity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The prognostic and immune significance ofTranslational cancer research · 2025Article
- KLF12 Aggravates Angiotensin II-Induced Cardiac Remodeling in Male Mice by Transcriptionally Inhibiting SMAD7.Journal of the American Heart Association · 2025Article
- The Multifaced Role of Collagen in Cancer Development and Progression.International journal of molecular sciences · 2024Review
- Identification of Specific microRNAs in Adipose Tissue Affected by Lipedema.Current issues in molecular biology · 2024Article
- LINC01806 Promotes Breast Cancer Growth and Metastasis via Sponging miR-1286 to Disinhibit ZEB1 Expression.Biochemical genetics · 2024Article
- Pulling the trigger: Noncoding RNAs in white adipose tissue browning.Reviews in endocrine & metabolic disorders · 2024Review
- Development of a novel disulfidptosis-related lncRNA signature for prognostic and immune response prediction in clear cell renal cell carcinoma.Scientific reports · 2024Article
- LncRNAs-circRNAs as Rising Epigenetic Binary Superstars in Regulating Lipid Metabolic Reprogramming of Cancers.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- The function of miRNAs in the process of kidney development.Non-coding RNA research · 2023Review
- Fatty Acid Oxidation Mediated by Malonyl-CoA Decarboxylase Represses Renal Cell Carcinoma Progression.Cancer research · 2023Article
- KLF12 overcomes anti-PD-1 resistance by reducing galectin-1 in cancer cells.Journal for immunotherapy of cancer · 2023Article
- Long non-coding RNAs enable precise diagnosis and prediction of early relapse after nephrectomy in patients with renal cell carcinoma.Journal of cancer research and clinical oncology · 2023Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal accumulation of lipids has been highlighted in the progression of clear cell renal cell carcinoma (ccRCC). However, the underlying mechanism remains unclear. Emerging evidence suggests long noncoding RNAs (lncRNAs) participate in the regulation of lipid metabolism. In this study, we found lncRNA COL18A1-AS1 was downregulated in ccRCC and that higher COL18A1-AS1 expression indicated better prognosis. Decreased COL18A1-AS1 expression was caused by DNA methylation at the CpG islands within its promoter. Restoring the epigenetically silenced COL18A1-AS1 repressed tumor progression, promoted lipid browning and consumption in vitro and in vivo. Mechanistically, COL18A1-AS1 could competitively bind miR-1286 to increase the expression of Krüppel-like factor 12 (KLF12). Downregulation of COL18A1-AS1 in ccRCC resulted in the low expression of KLF12. COL18A1-AS1/KLF12 positively regulated uncoupling protein 1 (UCP1)-mediated lipid browning, which promotes tumor cell "slimming" and inhibits tumor progression. When tumor cell "slimming" occurred, lipid droplets turned into tiny pieces, and lipids were consumed without producing ATP energy. Taken together, our findings on COL18A1-AS1-miR-1286/KLF12 axis revealed a potential mechanism of abnormal accumulation of lipids in ccRCC and could be a promising therapeutic target for ccRCC patients.
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