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.
CONCLUSIONS: In summary, SULT2B1 silencing repressed OC progression by targeting ANXA9.
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.
CONCLUSIONS: In summary, SULT2B1 silencing repressed OC progression by targeting ANXA9.
摘要：
背景：据报道，磺基转移酶家族2B成员1（SULT2B1）在许多类型的癌症中发挥致癌作用。然而，SULT2B1在卵巢癌（OC）中的作用及其隐藏的分子机制尚不清楚。
方法：通过GEPIA数据库分析SULT2B1在OC中的表达。qRT-PCR和蛋白质印迹（WB）用于OC细胞系中SULT2B1和膜联蛋白A9（ANXA9）的评价。细胞的增殖能力，迁移和侵入用CCK-8测定进行评估，伤口愈合试验，以及transwell分析。利用流式细胞术估计细胞凋亡水平。WB用于评估迁移和凋亡相关蛋白。生物信息学分析和免疫共沉淀用于预测和验证SULT2B1和ANXA9的组合。
结果：数据显示SULT2B1和ANXA9在OC细胞中上调。SULT2B1耗竭抑制了增殖，迁徙,和SKOV3细胞的侵袭能力，但促进细胞凋亡。SULT2B1调节ANXA9表达并被证明与ANXA9结合。此外,ANXA9缺乏对细胞迁移表现出相同的影响，侵袭能力和凋亡水平作为SULT2B1沉默。此外，ANXA9过表达逆转了SULT2B1沉默对增殖的抑制作用，迁徙,侵入性,和SKOV3细胞的凋亡能力。
结论：总之，SULT2B1沉默通过靶向ANXA9抑制OC进展。
方法：通过GEPIA数据库分析SULT2B1在OC中的表达。qRT-PCR和蛋白质印迹（WB）用于OC细胞系中SULT2B1和膜联蛋白A9（ANXA9）的评价。细胞的增殖能力，迁移和侵入用CCK-8测定进行评估，伤口愈合试验，以及transwell分析。利用流式细胞术估计细胞凋亡水平。WB用于评估迁移和凋亡相关蛋白。生物信息学分析和免疫共沉淀用于预测和验证SULT2B1和ANXA9的组合。
结果：数据显示SULT2B1和ANXA9在OC细胞中上调。SULT2B1耗竭抑制了增殖，迁徙,和SKOV3细胞的侵袭能力，但促进细胞凋亡。SULT2B1调节ANXA9表达并被证明与ANXA9结合。此外,ANXA9缺乏对细胞迁移表现出相同的影响，侵袭能力和凋亡水平作为SULT2B1沉默。此外，ANXA9过表达逆转了SULT2B1沉默对增殖的抑制作用，迁徙,侵入性,和SKOV3细胞的凋亡能力。
结论：总之，SULT2B1沉默通过靶向ANXA9抑制OC进展。
