ArticleBriefings in functional genomics2026
Effect of EGR1/LIPT1 regulatory axis on cuproptosis in chromophobe renal cell carcinoma.
Article in Briefings in functional genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Renal cell carcinoma (RCC) is one of the most prevalent solid tumors, and chromophobe renal cell carcinoma (chRCC) is its third most common subtype. The cuproptosis has become a hot topic in the field of cancer treatment. This study aimed to investigate the potential targets of cuproptosis in chRCC cells. We first downloaded the chRCC mRNA transcriptome data from The Cancer Genome Atlas. Based on the previous reports, we speculated that the expression of LIPT1 was considerably down-regulated in chRCC tissues. The upstream transcription factor (TF) EGR1 was predicted by the hTFtarget web tool, and the interaction between EGR1 and LIPT1 was further verified by dual-luciferase and chromatin immunoprecipitation experiments. The mRNA expression levels of EGR1 and LIPT1 were detected by quantitative polymerase chain reaction. The expression levels of target protein LIPT1 and cuproptosis-associated protein were detected by western blot and immunofluorescence. Cell Counting Kit-8 assay was employed to detect the viability of RCC98 cells. The Transwell assay was utilized to assess the migration and invasion abilities of RCC98 cells. LIPT1 and its upstream TF, EGR1, were significantly down-regulated in chRCC tissues and cells. EGR1 could transcriptionally activate LIPT1. Additionally, overexpression of LIPT1 significantly reduced the cancer-associated malignant phenotype of chRCC and elevated the sensitivity of RCC98 cells to cuproptosis. However, on this basis, knocking down EGR1 restored the anti-cancer effect conferred by overexpression of LIPT1. This work aimed to investigate the transcriptional activation of LIPT1 by EGR1 in RCC98 cells to repress the malignant progression of cancer cells while enhancing the sensitivity of RCC98 cells to cuproptosis.
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