LncRNA-BX111 Promotes Metastasis And Progression Of Pancreatic Cancer Through Regulating ZEB1 Transcription

PurposesTo figure out the role of BX111 in pancreatic cancer malignant progression.This study may make a contribute to our intensively understanding the mechanism of pancreatic cancer biological malignant progress and provide a potential strategy for comprehensive treatment of pancreatic cancer.MethodsIn our study,pancreatic cancer tissues and the matched adjacent non-cancerous tissues were collected from 48 patients,who received surgical excision in Wuhan Union hospital during 2014 and 2015.q RT-PCR assay were used to detect the differential expression of BX111 in tissue specimens and pancreatic cell lines.BX111 expression was downregulated or upregulated by transfection of BX111-si RNA or pc DNA-BX111 and then MTT assay,wound healing assay and transwell assay were used to observe the effects of BX111 on tumor biological behaviors such as proliferation,migration and invasion ability in pancreatic cancer cells.After upregulating BX111 with pc DNA-BX111 or downregulating BX111 with BX111-si RNA,the expression levels of ZEB1 m RNA and protein were detected by q RT-PCR assay and Western blot assay respectively.In the reverse experiment,after pc DNA-BX111 and BX111-si RNA were co-transfected into the PANC-1 cells,the biological behaviors as well as morphological changes were observed by light microscopy.At the same time,the expression of ZEB1 and some epithelial and mesenchymal markers were identified by Western blot assay.ResultsBX111 was obviously higher expressed in pancreatic cancer tissues and pancreatic cell lines.Cell functional experiments demonstrated that BX111 knockdown or overexpression can inhibit or promote pancreatic cancer cell proliferation,invasion and migration ability.BX111 knockdown downregulated ZEB1 m RNA and protein level distinctly.Similarly,BX111 overexpression upregulated the expression level of ZEB1.The reverse experiment indicated that ZEB1 downregulation can suppress the increasing invasion ability caused by BX111 overexpression.At the same time,it also revealed that BX111 could enhance the aggressive progress of cancer cells through the upregulation of ZEB1,leading to the increase of epithelial markers and the decline of mesenchymal markers.ConclusionsBX111 can promote pancreatic cells proliferation,invasion and migration ability by targeting ZEB1 expression.While the exact mechanism behind it needs further study.Therefore,inhibiting cancer cell invasion and migration by targeting BX111 expression might be a potential strategy for the biological treatment of pancreatic cancer.