<br>STEAP3 在肺鳞状细胞癌中的分子特征：调节 EGFR 影响细胞增殖和铁死亡,Archives of Biochemistry and Biophysics

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STEAP3 在肺鳞状细胞癌中的分子特征：调节 EGFR 影响细胞增殖和铁死亡
Archives of Biochemistry and Biophysics ( IF 3.8 ) Pub Date : 2023-11-29 , DOI: 10.1016/j.abb.2023.109842
Hanqiang Shi ₁ , Siyu Lei ₂ , Lie Xiong ₁ , Shuqin Du ₁ , Yanbo Shi ₁

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据报道，前列腺 3 的六跨膜上皮抗原（STEAP3）在各种类型的癌症中起调节作用。然而，它与肺鳞状细胞癌（LUSC）的参与仍未得到充分研究。在这里，我们旨在探讨 STEAP3 在 LUSC 中的生物学功能和潜在机制。使用 Venn 方法、 STRING 、 GEPIA 和 UALCAN 数据库分析与 LUSC 和铁死亡相关的交叉基因。qPCR 和 western blotting 法检测 STEAP3 的表达。使用细胞计数试剂盒 8 测定和 EDU 染色测定细胞增殖和活力。通过相应的试剂盒和 DCFH-DA 染色测量氧化应激和脂质过氧化。通过 Phen Green SK 和 Western blot 法评估铁死亡。STEAP3 和 EGFR 之间的相关性由 TIMER 和 starBase 数据库预测。进行免疫共沉淀以验证 STEAP3 和 EGFR 的结合。数据表明 LUSC 细胞系中 STEAP3 表达显著上调。沉默 STEAP3 抑制 H2170 细胞活力和增殖，同时通过增加 MDA 和 ROS 水平促进氧化应激和脂质过氧化，并抑制 SOD 活性。此外，STEAP3 的敲除通过调节铁死亡相关蛋白诱导铁死亡。此外，在 LUSC 中预测并证实了 STEAP3 和 EGFR 之间的结合。EGFR 过表达逆转了 STEAP3 沉默对 H2170 细胞活力、增殖、氧化应激和铁死亡的影响。综上所述，抑制 STEAP3/EGFR 可作为 LUSC 治疗的有前途的治疗靶点，因为它可以抑制 LUSC 增殖并促进脂质过氧化和铁死亡。

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Molecular characterization of STEAP3 in lung squamous cell carcinoma: Regulating EGFR to affect cell proliferation and ferroptosis

Six-transmembrane epithelial antigen of the prostate 3 (STEAP3) has been reported to play a regulatory role in various types of cancers. However, its involvement in lung squamous cell carcinoma (LUSC) remains understudied. Here, we aimed to explore the biological functions and underlying mechanisms of STEAP3 in LUSC. Intersection genes associated with LUSC and ferroptosis were analyzed using the Venn method, STRING, GEPIA and UALCAN databases. The expression of STEAP3 was detected by qPCR and western blotting assay. Cell proliferation and viability were determined using the cell counting kit-8 assay and EDU staining. Oxidative stress and lipid peroxidation were measured by corresponding kits and DCFH-DA staining. Ferroptosis was evaluated by Phen Green SK and Western blot assay. The correlation between STEAP3 and EGFR was predicted by the TIMER and starBase database. Co-immunoprecipitation was conducted to verify the binding of STEAP3 and EGFR. The data demonstrated a significant upregulation of STEAP3 expression in LUSC cell lines. Silencing of STEAP3 suppressed H2170 cell viability and proliferation while promoting oxidative stress and lipid peroxidation through increased levels of MDA and ROS, as well as inhibited SOD activity. In addition, knockdown of STEAP3 induced ferroptosis through the regulation of ferroptosis-related proteins. Moreover, the binding between STEAP3 and EGFR was predicted and confirmed in LUSC. EGFR overexpression reversed the effects of STEAP3 silencing on H2170 cell viability, proliferation, oxidative stress, and ferroptosis. To summarize, the inhibition of STEAP3/EGFR may serve as a promising therapeutic target for LUSC treatment, as it can suppress LUSC proliferation and promote lipid peroxidation and ferroptosis.

更新日期：2023-11-29

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