バイオインフォマティクス分析により,結腸腺がんにおけるlncRNA SNHG25の腫瘍性作用と治療の可能性が明らかになった

Renshan Hao¹, Ye Zhang², Qi Zhu¹

¹Division of Gastroenterology and Hepatology, Baoshan Branch, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

International journal of genomics

|September 2, 2025

まとめ

長い非コーディングRNASNHG25は,結腸腺がん (COAD) で高度に発現し,腫瘍の成長と免疫微環境の改造を促進します. COAD細胞の増殖,移動,侵入を抑制し,新しい治療標的を提示します.

科学分野:

腫瘍学
分子生物学
ゲノミクス

背景:

大腸腺がん (COAD) は治療の選択肢が限られ,予後が悪い.
癌における長い非コーディングRNA (lncRNAs) の役割は重要であるが,COADにおけるSNHG25の特定の機能はほとんど不明である.

研究の目的:

大腸腺がんにおける lncRNA SNHG25の役割と潜在的な治療効果を調査する.

主な方法:

UCSCのXenaデータベースからのCOADトランスクリプトームデータ解析
DESeq2を用いた微分発現分析,ROC曲線による診断有効性評価
CIBERSORTとESTIMATEアルゴリズムを用いた免疫細胞浸透分析
TIDE と oncoPredict を用いて免疫療法と薬物感受性の評価
Encoriと分子ドッキングによる標的mRNAの識別と薬物予測.
qRT-PCR,CCK-8,傷の治癒,およびトランスウェルアッセイを用いた in vitro 検証

主要な成果:

SNHG25は,COAD組織において著しく上昇し,強力な診断能力を示した (AUC=0. 937).
SNHG25の高い発現は酸化性リン酸化と相関し,低い発現はアポトーシスと免疫経路と関連していた.
SNHG25は免疫細胞のサブタイプと有意な関連性を示し,腫瘍の免疫マイクロ環境の改造における役割を示唆した.
ZMYND8は主要な下流標的として特定され,デメコルシン,ピロキシカム,ヴォリノスタットは潜在的な治療薬として予測された.
In vitro 試験では,COAD 細胞系における SNHG25 の上昇が確認され,SNHG25 のノックダウンが増殖,移動,侵入を抑制することが示されました.

結論:

SNHG25はCOADで高度に発現し,複数のメカニズムを通じて腫瘍の進行を促進します.
SNHG25は腫瘍の免疫微環境に影響を与え,COADの診断と治療のターゲットとして潜在的に存在します.

キーワード:

SNHG25 大腸腺がん長い非コーディングRNA 予測薬

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