인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
DBpia AI
AI 에이전트
AI 아이디어
AI 리더
AI 뷰어
Citeasy
크롬 서지관리 다운로드
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
This study aimed to investigate the relationship between methylation quantitative trait loci (meQTL) and lung adenocarcinoma (LUAD) susceptibility. Candidate SNPs linked to differentially methylated CpG sites in LUAD were identified through meQTL datasets. Genome-wide association study (GWAS) data were analyzed to assess the correlation between selected meQTLs and LUAD risk. The effects of target genes on malignant LUAD phenotypes were examined through both in vitro and in vivo experiments. Additionally, machine learning and radiomics models were employed to evaluate the association of target genes on LUAD progression. The variant A allele of rs939408 was associated with decreased methylation levels of cg09596674 in LRRC2 (β < 0, P < 0.001). While cg09596674 was highly methylated, LRRC2 showed lower expression in LUAD tumor tissues. Consistently, a negative correlation was observed between methylation of cg09596674 and LRRC2 expression (r = -0.32, P < 0.001), indicating that lower methylation of cg09596674 modulated by rs939408 may reduce non-smoking LUAD risk (OR = 0.89, P = 0.019). Increased LRRC2 expression inhibited LUAD cell line malignancy and suppressed tumor growth in mice. Furthermore, lower LRRC2 expression was linked to metastasis (P = 0.02) and higher levels of two poorer survival-related imaging features (P = 0.03). The meQTL rs939408 may modulate DNA methylation of LRRC2, thereby influencing its expression and potentially affecting non-smoking LUAD risk. These findings offer valuable insights into the role of meQTLs in LUAD carcinogenesis.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
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