RETRACTED ARTICLE: Long noncoding RNA LINC00657 enhances the malignancy of pancreatic ductal adenocarcinoma by acting as a competing endogenous RNA on microRNA-433 to increase PAK4 expression

Abstract

A long noncoding RNAs (lncRNA) called LINC00657 is dysregulated and contributes to tumor progression in a number of human cancer types. However, there is limited information on the expression profile and functions of LINC00657 in pancreatic ductal adenocarcinoma (PDAC). The expression profile of LINC00657 in PDAC was estimated by reverse-transcription quantitative polymerase chain reaction (RT-qPCR). The effects of LINC00657 upregulation on PDAC cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo were explored using CCK-8, flow cytometry, Transwell migration and invasion assays, and a xenograft tumor formation experiment, respectively. The results revealed that LINC00657 was evidently upregulated in the PDAC tumors and cell lines. High LINC00657 expression significantly correlated with the pathological T stage, lymph node metastasis, and shorter overall survival. Functional analysis demonstrated that LINC00657 knockdown inhibited the proliferation, migration, and invasion while promoted the apoptosis of PDAC cells. In addition, LINC00657 knockdown markedly suppressed tumor growth of these cells in vivo. In terms of the mechanism, LINC00657 could directly interact with microRNA-433 (miR-433) and effectively worked as an miR-433 sponge, thus decreasing the competitive binding of miR-433 to PAK4 mRNA and ultimately increasing PAK4 expression. The actions of LINC00657 knockdown on malignant phenotype of PDAC cells were strongly attenuated by miR-433 inhibition and PAK4 restoration. These results indicate that LINC00657 promotes PDAC progression by increasing the output of the miR-433-PAK4 regulatory loop, thus highlighting the importance of the LINC00657-miR-433-PAK4 network in PDAC pathogenesis.

LncRNA LINC00857 strengthens the malignancy behaviors of pancreatic adenocarcinoma cells by serving as a competing endogenous RNA for miR-340-5p to upregulate TGFA expression

“…For example, lncRNA PVT1 sponged miR-519d-3p to promote progression and glycolysis in pancreatic ductal adenocarcinoma (PDAC) [ 7 ]. LncRNA LINC00657 facilitated the malignancy of PDAC via regarding as a competing endogenous RNA (ceRNA) on miR-433 to upregulate PAK4 expression [ 8 ]. Additionally, lncRNA ITGB2-AS2 has been discovered to accelerate cell proliferation and aggressiveness via regulating miR-4319/RAF1 in PDAC [ 9 ].…”

Prognostic Value of Long Noncoding RNA NORAD in Various cancers: a meta-analysis

“…For the correlation of NORAD expression with OS in cancer patients, a total of 14 articles with 867 subjects were enrolled in the present analysis [19-27,33-37]. The overall results showed that elevated level of NORAD was significantly related to worse prognosis (HR = 1.46, 95% CI: 1.06-2.01, P = 0.020) (Figure 2).…”

“…Several studies demonstrated that high NORAD expression acted as a competitive endogenous RNA (ceRNA) by sponging miRNA to regulate target genes of miRNA, and thereby exerted its oncogenic role [19,21,26,[37][38][39][40][41][42]. For instance, it was demonstrated that NORAD positively regulated JunB expression via serving as a ceRNA to sponge miR-615-3p, and then contributed to ESCC progression [38].…”

“…For the correlation of NORAD expression with OS in cancer patients, a total of 14 articles with 867 subjects were enrolled in the present analysis [19][20][21][22][23][24][25][26][27][33][34][35][36][37].…”

LINC01094 Upregulates LIN28B Expression by Sponging miR-577 to Promote Pancreatic Cancer Proliferation and Metastasis

“…In PC, the expression of lncRNAs are often maladjusted, for example lncRNA HULC is abnormally increased in PC, and its high expression is signi cantly related to metastasis and vascular invasion of PC [16]. In addition, lncRNA PVT1 upregulates the progression and glycolysis of PC cells by regulating mir-519d-3p and HIF1α, and LINC00657 acts as a miR-433 sponge to enhance the malignancy of pancreatic ductal adenocarcinoma [17,18]. Although lncRNA plays a decisive role in PC, the study of LINC01094 in PC has not been reported, and the interaction between LINC01094 and miRNA remains unclear.…”