关键词: LUAD TSPAN6 bidirectional effect cisplatin lung cancer

Mesh : Humans Cisplatin / pharmacology Drug Resistance, Neoplasm / drug effects genetics Tetraspanins / metabolism genetics Lung Neoplasms / drug therapy metabolism pathology genetics Computational Biology NF-kappa B / metabolism Antineoplastic Agents / pharmacology A549 Cells Signal Transduction / drug effects RNA, Small Interfering / metabolism Cell Line, Tumor

来  源:   DOI:10.1111/cbdd.14570

Abstract:
Cisplatin-based chemotherapy is frequently employed as the primary therapeutic approach for advanced lung cancer. Nevertheless, a significant proportion of patients may develop resistance to cisplatin, leading to diminished efficacy of chemotherapy. Through analysis of Gene Expression Omnibus databases, TSPAN6 has been identified as a key factor in conferring resistance to cisplatin, attributed to its activation of the NF-κB signaling pathway. Knockdown of TSPAN6 using siRNA resulted in decreased expression levels of NF-κB in A549 cells. This indicates that TSPAN6 may have dual effects on lung cancer cisplatin resistance and could serve as a promising therapeutic target for individuals with cisplatin resistance.
摘要:
基于顺铂的化疗经常被用作晚期肺癌的主要治疗方法。然而,相当比例的患者可能对顺铂产生耐药性,导致化疗疗效下降。通过分析基因表达综合数据库,TSPAN6已被确定为赋予顺铂耐药性的关键因素,归因于其对NF-κB信号通路的激活。使用siRNA敲低TSPAN6导致A549细胞中NF-κB的表达水平降低。这表明TSPAN6可能对肺癌顺铂耐药性具有双重作用,并且可以作为具有顺铂耐药性的个体的有希望的治疗靶标。
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