Abstract
BackgroundAbnormal expression of long non-coding RNA (lncRNA) FTX (five prime to Xist), which is involved in X chromosome inactivation, has been reported in various tumors. However, the effect of FTX on the development of pancreatic cancer (PC) has not been elucidated. The purpose of this study was to explore the possible molecular mechanism of FTX in PC.MethodsQuantitative real-time PCR (qRT-PCR) was used to measure the expression levels of FTX and miR-513b-5p in PC cell lines. Proliferation and apoptosis of PC cells were determined by CCK-8, Edu assay, and flow cytometry. Invasion and migration ability of PC cells were detected by Transwell assay and scratch test. Bioinformatics analysis, luciferase reporter gene assay, and RNA immunoprecipitation (RIP) assay were used to verify the direct binding between FTX and miR-513b-5p. The xenotransplantation mouse model was established to explore the effect of FTX and miR-513b-5p on the PC tumor growth in vivo.ResultsThe expression levels of FTX were increased in PC cell lines, and silencing of FTX remarkably suppressed the invasion ability and cell viability. Besides, FTX could bind to miR-513b-5p as a competitive endogenous RNA, thus promoting the invasion and proliferation ability of PC cells. Moreover, knockdown of FTX inhibited the tumor growth and increased the expression levels of miR-513b-5p and apoptosis-related proteins in vivo.ConclusionsFTX could directly combine with miR-513b-5p as a competitive endogenous RNA, thus promoting the occurrence and development of PC in vitro and in vivo.
Highlights
Abnormal expression of long non-coding RNA FTX, which is involved in X chromosome inactivation, has been reported in various tumors
Effects of silencing of FTX on proliferation, apoptosis and cell cycle of pancreatic cancer (PC) cells To explore the effect of FTX on the biological function of PC cells, LV-FTX was transfected into PANC-1 and SW1990 cells to evaluate the effects of silencing of FTX on the proliferation and apoptosis of PC cells
The effects of silencing of FTX on the cell viability and proliferation ability were assessed. It showed that the cell viability and Edu positive cell number of PANC-1 and SW1990 cells in LV-FTX group were observably reduced compared with that in the negative control group (P < 0.05) (Fig. 2b and c), suggesting that cell viability and proliferation ability were significantly suppressed after silencing of FTX
Summary
Abnormal expression of long non-coding RNA (lncRNA) FTX (five prime to Xist), which is involved in X chromosome inactivation, has been reported in various tumors. The key to improve the prognosis of PC is to further study the biological characteristics of PC and the molecular regulatory mechanism of its occurrence and development, and to search for reliable markers for early diagnosis and prognosis evaluation. Studies have shown that a variety of lncRNAs played important regulatory roles in the invasion and metastasis of PC [19, 20]. Studies have found that lncRNA FTX (five prime to Xist) was abnormally expressed in various cancers, such as hepatocellular carcinoma, renal cell carcinoma and colorectal cancer [23,24,25], but the regulation of lncRNA FTX in PC remains unclear
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
