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检测[具体物质]在介导宫颈鳞癌细胞对紫杉醇耐药中的作用及机制。 （原文中“of”后面缺少具体内容）

Examination of the functions and mechanism of in mediating paclitaxel resistance in cervical squamous carcinoma cells.

作者信息

He Yue, Xu Jian-Qing, Zhang Jing-Jing, Liu Zhen-You, Ji Chen, Liu Yang, Wang Yun-Fan, Wang Ming, Wu Yu-Mei, Wang Yan

机构信息

Department of Gynecological Oncology, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital, Beijing, China.

出版信息

Front Oncol. 2025 Apr 14;15:1550032. doi: 10.3389/fonc.2025.1550032. eCollection 2025.

DOI:10.3389/fonc.2025.1550032
PMID:40297811
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12034699/
Abstract

OBJECTIVE

To evaluate the mechanism of Kielin/chordin-like protein () in the resistance of cervical cancer cells to paclitaxel.

METHOD

A cervical squamous carcinoma cell line (SiHa) with knockout was constructed and treated with paclitaxel. Key cell functions were assessed by colony formation assay, measurement of cell proliferation by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and FACS-based detection of apoptosis. The downstream mechanism of -mediated resistance to paclitaxel was then examined using human gene chip detection and IPA bioinformatics analysis, and qPCR analysis was used to validate its downstream genes.

RESULTS

①Functional studies of SiHa cells showed that knockout (sgRNA) inhibited colony formation and proliferation of SiHa cells in the presence of paclitaxel (<0.05). ②Using a whole human genome microarray, a total of 491 differentially expressed genes were identified in knockout versus the NC SiHa cells. IPA-based bioinformatics analysis of upstream regulators showed that SPI1 was strongly activated and that SPI1 inhibited and activated and , which is consistent with results from gene chip analysis showing , , and expression after knockout. ③A total of 30 differentially expressed genes associated with tumor cell proliferation were identified by gene microarray and IPA analyses. The changes in the aforementioned genes after knockout were verified by qPCR, and and expression were significantly lower and higher, respectively, compared to in the control group.

CONCLUSION

increased resistance of cervical cancer to paclitaxel by enhancing cell proliferation and colony formation. We observed that could act positively on the downstream gene and negatively on the downstream gene to affect the resistance of cervical carcinoma cells to paclitaxel.

摘要

目的

评估奇林/脊索样蛋白（）在宫颈癌细胞对紫杉醇耐药中的作用机制。

方法

构建敲除的宫颈鳞状癌细胞系（SiHa）并用紫杉醇处理。通过集落形成试验评估关键细胞功能，用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐（MTT）法测量细胞增殖，并通过基于流式细胞术的方法检测细胞凋亡。然后使用人类基因芯片检测和IPA生物信息学分析研究介导的紫杉醇耐药下游机制，并用qPCR分析验证其下游基因。

结果

①SiHa细胞的功能研究表明，敲除（sgRNA）在紫杉醇存在的情况下抑制了SiHa细胞的集落形成和增殖（<0.05）。②使用全人类基因组微阵列，在敲除的SiHa细胞与NC SiHa细胞中总共鉴定出491个差异表达基因。基于IPA的上游调节因子生物信息学分析表明，SPI1被强烈激活，并且SPI1抑制并激活和，这与基因芯片分析结果一致，即敲除后、和表达。③通过基因微阵列和IPA分析共鉴定出30个与肿瘤细胞增殖相关的差异表达基因。敲除后上述基因的变化通过qPCR验证，与对照组相比，和的表达分别显著降低和升高。

结论

通过增强细胞增殖和集落形成增加了宫颈癌对紫杉醇的耐药性。我们观察到可以对下游基因起正向作用，对下游基因起负向作用，从而影响宫颈癌细胞对紫杉醇的耐药性。

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