时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
In this study, we investigated the tumor-suppressive effects of β-ionone–mediated OR51E2 activation using human CRC cell lines (SW480, SW620, and RKO) and patient-derived organoids (PDOs).；OR51E2 Activation Induces CRC Senescence This study investigated whether the anti-cancer effect of OR51E2 activation by β-ionone in CRC is mediated through cellular senescence.
方法
In this study, we investigated the tumor-suppressive effects of β-ionone–mediated OR51E2 activation using human CRC cell lines (SW480, SW620, and RKO) and patient-derived organoids (PDOs).；We demonstrate that β-ionone treatment stimulates intracellular calcium levels in an OR51E2-dependent manner, upregulating MAPK-directed phosphatases (DUSP1/2/4 and PPP1CA).；We previously demonstrated that β-ionone suppresses CRC cell growth through OR51E2 activation by inducing apoptosis [5]; however, the molecular mechanisms underlying this effect, particularly its potential involvement in cellular senescence, remain unclear.
核心结论
We demonstrate that β-ionone treatment stimulates intracellular calcium levels in an OR51E2-dependent manner, upregulating MAPK-directed phosphatases (DUSP1/2/4 and PPP1CA).；Collectively, this study demonstrates that OR51E2 activation coordinates a heterogeneous cell-fate decision encompassing both apoptosis and a senescence-like phenotype.；We previously demonstrated that β-ionone suppresses CRC cell growth through OR51E2 activation by inducing apoptosis [5]; however, the molecular mechanisms underlying this effect, particularly its potential involvement in cellular senescence, remain unclear.
局限
We previously demonstrated that β-ionone suppresses CRC cell growth through OR51E2 activation by inducing apoptosis [5]; however, the molecular mechanisms underlying this effect, particularly its potential involvement in cellular senescence, remain unclear.；However, current senotherapeutics often lack selectivity, leading to off-target cytotoxicity in normal cells [16].
对本项目的价值
中高价值：属「衰老细胞清除 / SASP 轴」方向；细胞衰老 / senolytics / SASP栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.0/5（★★★☆☆）
全文来源
出版商/仓储 OA PDF（正文 24,504 字符，题名指纹 1.0，正文内 DOI 命中，已过题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：β-紫罗兰酮激活嗅受体 51E2 诱导结直肠癌衰老样表型并增强衰老清除治疗敏感性
- 英文标题：Olfactory Receptor 51E2 Activation by β-Ionone Induces a Senescence-Like Phenotype and Increases Susceptibility to Senolytic Treatment in Colorectal Cancer.
- 期刊与标识：Aging and disease · PMID 42970311 · DOI 10.14336/AD.2026.1095