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SRPK1参与人卵巢癌细胞中与长链非编码RNA UCA1相关的顺铂耐药。

Involvement of SRPK1 in cisplatin resistance related to long non-coding RNA UCA1 in human ovarian cancer cells.

作者信息

Wang F, Zhou J, Xie X, Hu J, Chen L, Hu Q, Guo H, Yu C

出版信息

Neoplasma. 2015;62(3):432-8.

Abstract

The therapeutic potential of cisplatin in ovarian cancer treatment is restricted by the occurrence of cellular resistance. We aimed to explore the role of SRPK1 in cisplatin resistance related to the long non-coding RNA UCA1 in ovarian cancer cell.Totally, 24 ovarian cancer tissues and 16 normal tissues were used to assess the expression of UCA1 RNA. UCA1 stable transfected SKOV3 cells were established and the ability of cell migration, invasion and cisplatin resistance was assessed. The expression of SRPK1 and apoptosis pathway proteins was then assessed to explore the mechanism. In addition, SRPK1 knockdown cell line was also established and the effects of SRPK1 on cell migration, invasion and cisplatin resistance was evaluated.Elevated expression of UCA1 RNA was identified in ovarian cancer tissues compared with normal tissues. Expression of UCA1 RNA in SKOV3 cells enhanced the cell migration, invasion and cisplatin resistance. Increased expression of SRPK1 and anti-apoptosis proteins were found in SKOV3/pcDNA-UCA1 cells. Knocking-down SRPK1 could partly rescue the effect of UCA1 expression on cell migration, invasion and cisplatin resistance in SKOV3 cells.Elevated expression of UCA1 RNA was found in ovarian cancer tissues. UCA1 can improve the cell migration, invasion and induce cisplatin resistance. SRPK1 and apoptosis pathway proteins may be involved in the effect of UCA1.

摘要

顺铂在卵巢癌治疗中的治疗潜力受到细胞耐药性的限制。我们旨在探讨SRPK1在卵巢癌细胞中与长链非编码RNA UCA1相关的顺铂耐药中的作用。总共使用24个卵巢癌组织和16个正常组织来评估UCA1 RNA的表达。建立了UCA1稳定转染的SKOV3细胞,并评估了细胞迁移、侵袭和顺铂耐药能力。然后评估SRPK1和凋亡通路蛋白的表达以探究其机制。此外,还建立了SRPK1敲低细胞系,并评估了SRPK1对细胞迁移、侵袭和顺铂耐药的影响。与正常组织相比,在卵巢癌组织中鉴定出UCA1 RNA表达升高。SKOV3细胞中UCA1 RNA的表达增强了细胞迁移、侵袭和顺铂耐药性。在SKOV3/pcDNA-UCA1细胞中发现SRPK1和抗凋亡蛋白的表达增加。敲低SRPK1可部分挽救UCA1表达对SKOV3细胞迁移、侵袭和顺铂耐药性的影响。在卵巢癌组织中发现UCA1 RNA表达升高。UCA1可改善细胞迁移、侵袭并诱导顺铂耐药。SRPK1和凋亡通路蛋白可能参与了UCA1的作用。

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