RETRACTED ARTICLE: LncRNA TUG1 promoted KIAA1199 expression via miR-600 to accelerate cell metastasis and epithelial-mesenchymal transition in colorectal cancer

Abstract

BackgroundLncRNA TUG1 has been reported to be highly expressed in CRC samples and cells and promoted metastasis by affecting EMT, indicating a poor prognosis for colorectal cancer (CRC). In this study, we determined the underlying mechanism for tumor oncogenesis of lncRNA TUG1 in CRC metastasis.MethodsThe expressions of miR-600 and KIAA1199 in 76 CRC patients and CRC cells and CRC metastatic tissues were determined using qRT-PCR. Epithelial-mesenchymal transition (EMT)-related proteins were determined using western blot. CRC cell metastasis was assessed by colony formation, wound healing and transwell assay. Luciferase reporter gene assay was used to confirm miR-600 binding to KIAA1199 3’UTR.ResultsOur data showed that lncRNA TUG1 was upregulated in CRC cells, miR-600 was downregulated in CRC tissues, cell lines and CRC metastatic tissues, and low miR-600 expression predicted a poor clinical prognosis. Overexpression of miR-600 suppressed CRC cell migration/invasion and EMT-related proteins in vitro, inhibited tumor volume and weight, and decreased the number of CRC liver metastasis in vivo. KIAA1199 was upregulated in CRC tissues, and was negatively regulated by miR-600. KIAA1199 overexpression promoted CRC cell migration and invasion, which reversed the inhibition effect of miR-600 mimic on migration and invasion of CRC cells. Moreover, TUG1 negatively regulated miR-600, and inhibition of TUG1 suppressed CRC cell migration and invasion and EMT-related proteins via regulating miR-600.ConclusionOur study proved that TUG1 promoted KIAA1199 expression to accelerate EMT and metastasis of CRC cell through inhibition of miR-600 expression.

Circular RNA circPIP5K1A promotes non‐small cell lung cancer proliferation and metastasis through miR‐600/HIF‐1α regulation

“…Increasing evidence supports the important role of EMT in oncogenesis . Induction of the EMT promotes cell invasion, migration, and metastasis, which confers stem‐cell‐like characteristics on cancer cells, and induces therapeutic resistance .…”

“…However, downregulation miR-600 expression reversed the circPIP5K1A-silencing-induced inhibition of metastasis and Increasing evidence supports the important role of EMT in oncogenesis. 35,36 Induction of the EMT promotes cell invasion, migration, and metastasis, which confers stem-celllike characteristics on cancer cells, and induces therapeutic resistance. 37,38 Cellular signaling responses to hypoxia and inflammation involve crosstalk through upregulation of HIF-1α and associated tumorigenic activities, which are mediated by the inflammatory cytokine interferon-α.…”

SMAD3/SP1 complex‐mediated constitutive active loop between lncRNA PCAT7 and TGF‐β signaling promotes prostate cancer bone metastasis

“…Previous studies have revealed that cytoplasmic lncRNAs generally function as ceRNAs to regulate mRNA expression via sponging versatile miRNAs, thereby playing a pivotal role in cancer metastasis (Lian et al , ; Shan et al , ; Sun et al , ; Wang and Kong, ; Yan et al , ). In fact, lncRNAs exert their functions in several biological processes via interaction with DNA, proteins, and RNAs, which is dependent on the subcellular localization of the lncRNAs within the cells to a large extent (Chen et al , ).…”

LINC00961 inhibits the migration and invasion of colon cancer cells by sponging miR‐223‐3p and targeting SOX11

“…In‐depth studies have demonstrated that lncRNAs acted as a vital regulatory role in malignancies as competing endogenous RNAs. LncRNA TUG1 accelerates cells invasion in colorectal cancer via targeting miR‐600 . LncRNA SNHG16 accelerates the cancer cells migration and invasion abilities through sponging miR‐520d‐3p and targeting STAT3 in hemangioma .…”

“…LncRNA TUG1 accelerates cells invasion in colorectal cancer via targeting miR-600. 23 LncRNA SNHG16 accelerates the cancer cells migration and invasion abilities through sponging miR-520d-3p and targeting STAT3 in hemangioma. 24 HOTAIR facilitates the tumor progression in breast cancer cells via downregulation of miR-20a-5p and upregulation of HMGA2.…”