LncRNA RP11-708J19.2 promotes colorectal cancer progression by binding to SIRT7 via regulating H3K18ac

Sep 22, 2026

Colorectal cancer (CRC) is a prevalent malignancy with a complex genetic basis. Genome-wide association studies highlight a susceptibility locus at 3p21.31, yet the functional SNP(s) driving this association remain unclear. This work identifies rs2101247 as a potential functional SNP, linking it to the expression of lncRNA RP11-708J19.2. Functional assays show RP11-708J19.2 upregulation in CRC tissues, where knockdown reduces viability and promotes apoptosis through a SIRT7-mediated epigenetic pathway involving H3K18ac.

LanguageEnglish

CategoryResearch & Report

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Pages9

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Introduction

Materials and Methods

In silico analysis

Luciferase reporter gene assay

Fluorescence in situ hybridization (FISH)

European Journal of Histochemistry 2026; volume 70:4560 LncRNA RP11-708J19.2 promotes colorectal cancer progression by binding to SIRT7 via regulating H3K18ac Jiali Ma,1* Xianglong Tian,2* Yiwen Qiu,1 Chen Zhao,1 Jinghui Wang,1 Rongrong Jia1 1Department of Gastroenterology, Shanghai Tongren Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 2Department of Gastroenterology, Shanghai Eighth People’s Hospital (Xuhui Branch of Shanghai Sixth People’s Hospital), Shanghai, China *These authors contributed equally to this study and share first authorship ABSTRACT 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 SNPlncRNA axis that contributes to CRC pathogenesis, providing potential biomarkers for early detection and therapeutic targets for intervention. Key words: colorectal cancer; SNP variant rs2101247; LncRNA RP11-708J19.2 . Correspondence: Rongrong Jia, No. 111, Xianxia Road, Shanghai Tongren Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200336, China. E-mail: [jiarongrongjrr@163.com](jiarongrongjrr@163.com) Contributions: 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. Conflict of interest: the authors declare no competing interests and all authors confirm accuracy. Availability of data and materials: the data generated in the present study may be requested from the corresponding author. Funding: Changning District Science and Technology Commission Fund (CNKW2022Y01) . Key Cultivation Project of Science and Technology Commission of Xuhui District, Shanghai (SHXH202510) . Youth Project Fund of Changning District Health Commission (2024QN02 to J.W.) . [European Journal of Histochemistry 2026; 70:4560] Introduction Colorectal cancer (CRC) is a prevalent malignancy and the second leading cause of cancer-related mortality worldwide.1 Despite significant progress in neoadjuvant chemotherapy and targeted therapy,2-5 the prognosis remains poor, particularly for advanced-stage patients, with a 5-year survival rate of only 12.5% inAJCC stage IV and nearly 50% diagnosed at an advanced stage.6 Therefore, elucidating the molecular mechanisms underlying CRC development and identifying early biomarkers are essential for improving clinical outcomes. Epidemiological and molecular studies suggest that CRC arises from a complex interplay of genetic and environmental factors.7,8 Genome-wide association studies (GWAS) have identified over 60 susceptibility single nucleotide polymorphisms (SNPs) for CRC, highlighting the significant role of genetic variation in disease risk.9 However, the functional mechanisms linking these SNPs to tumorigenesis remain largely unexplored. Notably, many diseaseassociated SNPs reside within non-coding RNA (ncRNA) regio

FAQs

Which SNP is identified as a potential functional variant in the 3p21.31 region for CRC risk?

The study identifies rs2101247 as the potential functional SNP associated with the linkage region at 3p21.31 and related CRC susceptibility.

What is the role of lncRNA RP11-708J19.2 in colorectal cancer cells?

RP11-708J19.2 is upregulated in CRC tumor tissues; its knockdown reduces cell viability and promotes apoptosis in SW1116 and HCT116 cell lines.

How does RP11-708J19.2 mechanistically influence CRC progression?

RP11-708J19.2 directly interacts with the deacetylase SIRT7, modulating histone H3K18 acetylation (H3K18ac) and implicating a SIRT7-mediated epigenetic pathway.

Sep 22, 2026

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