Open AccessRETRACTED: Long non‐coding RNA CRNDE sponges miR‐384 to promote proliferation and metastasis of pancreatic cancer cells through upregulating IRS 1
Author(s) -
Wang Gang,
Pan Jingen,
Zhang Lu,
Wei Yajun,
Wang Cheng
Publication year - 2017
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12389
Subject(s) - pancreatic cancer , gene knockdown , cancer research , long non coding rna , cell growth , carcinogenesis , downregulation and upregulation , biology , cancer , metastasis , cell culture , in vivo , gene , genetics
Objective Colorectal neoplasia differentially expressed ( CRNDE ), a vital cancer‐related long non‐coding RNA (lncRNA), has been brought to reports for playing quintessential functions in the growth and progression of several human malignancies. Nevertheless, the expression as well as the functional mechanisms of CRNDE in pancreatic cancer is not known so for. This study aimed at investigating the biological and clinical importance of CRNDE in human pancreatic cancer. Materials and methods The expression levels of CRNDE in pancreatic cancer tissues as well as cell lines were identified with the help of quantitative real‐time PCR (qRT‐PCR). Furthermore, the analysis of the relationship between CRNDE expression and clinicopathologic characteristics of patients with pancreatic cancer was also performed. Novel target of CRNDE was identified with the use of bioinformatics analysis and confirmed by a dual‐luciferase reporter assay. Colorectal neoplasia differentially expressed was knocked down using si RNA in pancreatic cancer cells. Thereafter, cell proliferation, migration and invasion were examined. Tumour xenograft was created to explore the function of CRNDE in tumorigenesis in vivo. Results Upregulation of the expression of CRNDE was found in pancreatic cancer tissues as well as cell lines, in comparison with the adjacent non‐tumour tissues and human pancreatic duct epithelial cells. High expression of CRNDE was correlated with poor clinicpathological characteristics and shorter overall survival. We identified miR‐384 as a direct target for CRNDE . Moreover, the CRNDE knockdown considerably inhibited pancreatic cancer cell proliferation, migration and invasion not only in vitro but also in vivo. In addition, CRNDE positively regulated IRS 1 expression through sponging miR‐384. Conclusions Colorectal neoplasia differentially expressed performed an oncogenic function in cell proliferation as well as metastasis of pancreatic cancer. Our results suggest that CRNDE is likely to serve as an efficient therapeutic approach in respect of pancreatic cancer treatment.