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Downregulation of SOX21-AS1 alleviated cisplatin resistance in cervical cancer through Epithelial-messenchymal transition (EMT) inhibition.

Cisplatin is widely used in chemotherapies in cervical cancer (CC). Nevertheless, drug resistance in cancer patients poses a major threat to efficacy of treatment. To explore the underlying modulatory mechanism of SOX21-AS1 in cisplatin resistance in CC cell and mice models，Gepia database was referred for SOX21-AS1 expression in cancer tissues and normal ones. RT-qPCR was used to measure the differential expression of SOX21-AS1 in parental Siha cells and cisplatin-resistant Siha/DDP cells. Luciferase reporter gene assays were conducted to verify putative bindings between SOX21-AS1 and miR-9-3p. Western blot method was employed to evaluate the changes in cleaved-caspase 7 protein expression. Cisplatin resistance was evaluated in each transfected group using CCK8 method after cells were exposed to cisplatin (0,7.5,15,30,60,120, 240ug/ml) for 24h. Flow cytometry method was used to measure the apoptosis rates. Cell migration and invasion were measured using Transwell assays. Immunofluorescence method was applied to observe EMT markers including E-cadherin, Snail, MMP3 and MMP9. Siha/DDP cell groups stably transfected with sh-NC and sh- SOX21-AS1 were injected through tail vein of Balb/C mice. Lung tissue sections were used for HE staining and IHC analysis. SOX1-AS1 expression was higher in cancer tissues than normal ones and was also higher in Siha/DDP rather than Siha cells. SOX21-AS1 was targeted by miR-9-3p in CC cells. Downregulation of SOX21-AS1 or overexpression of miR-9-3p inhibited cisplatin resistance in Siha/DDP cells and reduced cell invasion and migration and attenuated EMT progression. In vivo, the SOX21-AS1 knockdown led to less severe lung metastasis. Downregulation of SOX21-AS1 alleviated cisplatin resistance in cervical cancer through EMT inhibition.