LncRNA RP11-708J19.2 promotes colorectal cancer progression by binding to SIRT7 via regulating H3K18ac
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Authors
Colorectal cancer (CRC) is a prevalent malignancy with a complex genetic basis. Recent genome-wide association studies (GWAS) have identified a susceptibility locus at 3p21.31, however, the functional SNP(s) underlying the association between the 3p21.31 region and CRC remain to be elucidated. In this study, we identified rs2101247 as the potential functional SNP and further demonstrated that rs2101247 is significantly associated with the expression of the nearby long non-coding RNA (lncRNA) RP11-708J19.2 (ENSG00000271161.1). Functional experiments showed that RP11-708J19.2 is upregulated in CRC tumor tissues, and its knockdown reduces cell viability while promoting apoptosis in SW1116 and HCT116 cell lines. Mechanistically, RP11-708J19.2 interacts directly with the deacetylase SIRT7, modulating histone H3K18 acetylation (H3K18ac). Specifically, RP11-708J19.2 knockdown leads to a significant upregulation of H3K18ac levels, implicating a SIRT7-mediated epigenetic pathway in CRC progression. Our findings elucidate a novel functional SNP-lncRNA axis that contributes to CRC pathogenesis, providing potential biomarkers for early detection and therapeutic targets for intervention.
CRediT authorship contribution
Jiali Ma, Rongrong Jia, conceptualization, investigation, funding acquisition. Jiali Ma, Xianglong Tian, Yiwen Qiu, Chen Zhao, Jinghui Wang, investigation, formal analysis. Rongrong Jia, supervision, writing-original draft. All authors have read and approved the final version of the manuscript.
Supporting Agencies
Changning District Science and Technology Commission Fund (CNKW2022Y01), Key Cultivation Project of Science and Technology Commission of Xuhui District, Shanghai (SHXH202510)Data Availability Statement
The data generated in the present study may be requested from the corresponding author.
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