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Hsa_circ_0020095调节了CRC在PDO模型中的化学阻力

Xinyu Li^1,2, Tao Li^1,2, Yan Zhao^2,3

¹School of Clinical Medicine, Shandong Second Medical University, Weifang, Shandong, China.

Frontiers in medicine

|June 11, 2025

概括

Hsa_circ_0020095 促进结肠直肠癌 (CRC) 的进展和化学抵抗. 在患者衍生器官中准这种癌基因逆转了耐药性,这表明它有可能成为治疗CRC治疗的治疗标.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

结肠直肠癌 (CRC) 是全球癌症死亡的主要原因.
化学抗药性显著导致治疗失败和CRC患者的疾病进展.
Hsa_circ_0020095之前被确定为一种通过miR-487a-3p/SOX9通路促进CRC进展和西斯普拉丁耐药性的瘤基因.

研究的目的:

调查Hsa_circ_0020095在结直肠癌的化学抵抗中的作用.
探索Hsa_circ_0020095作为CRC治疗点的潜力.

主要方法:

使用H&E,IHC和WES从CRC瘤中生成和验证患者衍生器官 (PDOs).
使用shRNA在PDO中的Hsa_circ_0020095的淘汰,其表达水平通过RT-qPCR得到确认.
通过CellTiter-Glo® 3D测定和使用转录组测序和生物信息学分析的机械探索来评估PDO的耐药性.

主要成果:

成功建立了五个CRC PDO线,反映了父母瘤的形态学,组织病理学和遗传特征.
沉默Hsa_circ_0020095显著抑制了其在PDO中的表达.
淘汰Hsa_circ_0020095扭转了PDOs对5-FU和oxaliplatin的耐药性,表明它在调节化学抵抗方面的作用.

结论:

Hsa_circ_0020095在结直肠癌中介化疗抵抗方面发挥着至关重要的作用.
Hsa_circ_0020095代表了克服CRC治疗中药物耐药性的潜在治疗目标.

关键词:

在CRC中,CRC就是CRC.Hsa_circ_002009595 在线观看在线观看这是POD的缩写.化学电阻是一种化学电阻.有机生物有机物

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