Department of Gynecologic Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan 250117, China.
Comput Math Methods Med. 2022 May 23;2022:2318170. doi: 10.1155/2022/2318170. eCollection 2022.
The present study was aimed at exploring the role of FTX in cisplatin (DDP) resistance in ovarian cancer (OC).
QPCR was applied to evaluate mRNA expression in OC tissue and cells. CCK-8 assay was conducted to evaluate cell proliferation. Transwell chamber assay was performed to evaluate invasion of SKOV3/DDP cells. The protein expression was evaluated via western blot assay. Flow cytometry was performed to evaluate the apoptosis of SKOV3/DDP cells.
The expression of FTX in DDP-resistant cells was observably higher in contrast to DDP-sensitive cells and normal ovarian cells. FTX was higher expressed in DDP-resistant tissues by comparison with DDP-sensitive tissues. Knockdown of FTX obviously suppressed the proliferation ability invasion ability of SKOV3/DDP cells. Knockdown of FTX obviously enhanced apoptosis of SKOV3/DDP cells. miR-153-3p was proved to be directly regulated by FTX via the luciferase reporter assays. By comparison with normal cells, miR-153-3p was lower expressed in OC cells. miR-153-3p was lower expressed in SKOV3/DDP cells in contrast to SKOV3 cells. More interestingly, FTX reversed the inhibiting influence of miR-153-3p on cisplatin resistance of OC cells. Moreover, miR-153-3p was proved to directly regulate FOXR2. Knockdown of miR-153-3p attenuated the inhibitory influence of knockdown FOXR2 on cisplatin resistance of OC cells.
FTX regulated miR-153-3p/FOXR2 to promote cisplatin resistance via inhibiting the apoptosis and promoting the viability and invasion in OC.
本研究旨在探讨 FTX 在卵巢癌（OC）顺铂（DDP）耐药中的作用。
采用 QPCR 评估 OC 组织和细胞中的 mRNA 表达。通过 CCK-8 测定法评估细胞增殖。Transwell 室测定法用于评估 SKOV3/DDP 细胞的侵袭能力。通过 Western blot 测定法评估蛋白表达。通过流式细胞术评估 SKOV3/DDP 细胞的凋亡。
与 DDP 敏感细胞和正常卵巢细胞相比，耐药细胞中 FTX 的表达明显更高。与 DDP 敏感组织相比，耐药组织中 FTX 的表达更高。FTX 敲低明显抑制了 SKOV3/DDP 细胞的增殖能力和侵袭能力。FTX 敲低明显增强了 SKOV3/DDP 细胞的凋亡。荧光素酶报告测定法证实 miR-153-3p 可被 FTX 直接调控。与正常细胞相比，OC 细胞中的 miR-153-3p 表达水平较低。与 SKOV3 细胞相比，SKOV3/DDP 细胞中的 miR-153-3p 表达水平较低。更有趣的是，FTX 逆转了 miR-153-3p 对 OC 细胞顺铂耐药性的抑制作用。此外，miR-153-3p 被证实可直接调控 FOXR2。miR-153-3p 敲低减弱了 FOXR2 敲低对 OC 细胞顺铂耐药性的抑制作用。
FTX 通过抑制凋亡和促进 OC 细胞的活力和侵袭来调节 miR-153-3p/FOXR2，从而促进顺铂耐药。
