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通过靶向膜联蛋白 A9,磺基转移酶 2B1 的敲低抑制卵巢癌细胞的迁移、侵袭并促进细胞凋亡。

Knockdown of sulfotransferase 2B1 suppresses cell migration, invasion and promotes apoptosis in ovarian carcinoma cells via targeting annexin A9.

机构信息

Department of Gynecology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan Province, P.R. China.

Department of Central Laboratory, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan Province, P.R. China.

出版信息

J Obstet Gynaecol Res. 2024 Aug;50(8):1334-1344. doi: 10.1111/jog.15969. Epub 2024 May 22.

Abstract

BACKGROUND

Sulfotransferase family 2B member 1 (SULT2B1) has been reported to play oncogenic role in many types of cancers. Nevertheless, the role that SULT2B1 played in ovarian cancer (OC) and the hidden molecular mechanism is obscure.

METHODS

Expression of SULT2B1 in OC was analyzed by GEPIA database. qRT-PCR and western blot (WB) was applied for the appraisement of SULT2B1 and Annexin A9 (ANXA9) in OC cell lines. The capabilities of cells to proliferate, migrate and invade were assessed with CCK-8 assay, wound healing assay, along with transwell assay. Cell apoptotic level was estimated utilizing flow cytometry. WB was employed for the evaluation of migration- and apoptosis-related proteins. Bioinformatic analysis and co-immunoprecipitation were used to predict and verify the combination of SULT2B1 and ANXA9.

RESULTS

The data showed that SULT2B1 and ANXA9 were upregulated in OC cells. SULT2B1 depletion suppressed the proliferative, migrative, and invasive capabilities of SKOV3 cells but facilitated the cell apoptosis. SULT2B1-regulated ANXA9 expression and were proved to bind to ANXA9. Additionally, ANXA9 deficiency exhibited the same impacts on cell migrative, invasive capability and apoptotic level as SULT2B1 silencing. Moreover, ANXA9 overexpression reversed the inhibitory impacts of SULT2B1 silencing on the proliferative, migrative, invasive, and apoptotic capabilities of SKOV3 cells.

CONCLUSION

In summary, SULT2B1 silencing repressed OC progression by targeting ANXA9.

摘要

背景

磺基转移酶家族 2B 成员 1(SULT2B1)已被报道在多种类型的癌症中发挥致癌作用。然而,SULT2B1 在卵巢癌(OC)中的作用及其潜在的分子机制尚不清楚。

方法

通过 GEPIA 数据库分析 OC 中 SULT2B1 的表达。qRT-PCR 和 Western blot(WB)用于评估 OC 细胞系中的 SULT2B1 和膜联蛋白 A9(ANXA9)。CCK-8 测定、划痕愈合试验和 Transwell 测定评估细胞增殖、迁移和侵袭能力。流式细胞术评估细胞凋亡水平。WB 用于评估迁移和凋亡相关蛋白。生物信息学分析和共免疫沉淀用于预测和验证 SULT2B1 和 ANXA9 的结合。

结果

数据显示 SULT2B1 和 ANXA9 在 OC 细胞中上调。SULT2B1 耗竭抑制 SKOV3 细胞的增殖、迁移和侵袭能力,但促进细胞凋亡。SULT2B1 调节 ANXA9 的表达,并被证明与 ANXA9 结合。此外,ANXA9 缺失表现出与 SULT2B1 沉默相同的细胞迁移、侵袭能力和凋亡水平的影响。此外,ANXA9 的过表达逆转了 SULT2B1 沉默对 SKOV3 细胞增殖、迁移、侵袭和凋亡能力的抑制作用。

结论

总之,SULT2B1 沉默通过靶向 ANXA9 抑制 OC 进展。

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