Overexpression of long non-coding RNA-CTD903 inhibits colorectal cancer invasion and migration by repressing Wnt/β-catenin signaling and predicts favorable prognosis

Yuan, Zixu; Yu, Xihu; Ni, Beibei; Chen, Daici; Yang, Zihuan; Huang, Jintuan; Wang, Jianping; Chen, Dianke; Wang, Lei

doi:10.3892/ijo.2016.3447

Cited by 62 publications

(58 citation statements)

References 34 publications

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“…There is currently no evidence showing the direct targeting of ZO-1 by Twist1. However, emerging evidence showing that repression of ZO-1 expression in cancer cells during EMT involves transcription factors including Twist14950. Consistently, our REST overexpression data showed that overexpression of REST in CWR22Rv1 cells significantly reduced Twist1 and N-cadherin expression, along with increased ZO-1 level (Figs 4A and 5A).…”

Section: Discussionsupporting

confidence: 83%

REST is a crucial regulator for acquiring EMT-like and stemness phenotypes in hormone-refractory prostate cancer

Chang¹,

Lin

Campbell

et al. 2017

Sci Rep

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Castration-resistance prostate cancer (CRPC), also known as hormone-refractory prostate cancer (HRPC), requires immediate attention since it is not only resistant to androgen ablation, chemo- and radiotherapy, but also highly metastatic. Increasing evidence suggests that enrichment of neuroendocrine (NE) cells is associated with CRPC. Here, combined RNA-seq and ChIP-seq analysis reveals that REST is involved in epithelial-mesenchymal transition (EMT) and stemness acquisition in NE differentiated prostate cancer (PCa) cells via direct transcriptional repression of Twist1 and CD44. Specifically we show that short-term knockdown of REST induces NE differentiation of LNCaP cells. Long-term REST knockdown enhanced the expression of Twist1 and CD44, cell migration and sphere formation. Overexpression of REST in hormone-refractory CWR22Rv1 PCa cells significantly reduces Twist1 and CD44 expression, cell migration and sphere formation. Collectively, our study uncovers REST in regulating EMT and stemness properties of NE PCa cells and suggests that REST is a potential therapeutic target for CRPC.

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Section: Discussionsupporting

confidence: 83%

REST is a crucial regulator for acquiring EMT-like and stemness phenotypes in hormone-refractory prostate cancer

Chang¹,

Lin

Campbell

et al. 2017

Sci Rep

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“…β-catenin is a proliferation-related transcription factor. However, its effects on tumor invasion and EMT have been gradually recognized [27]. E-cadherin repressor Snail or Slug is also activated by β-catenin–Lefs/Tcfs-mediated transcription [28, 29].…”

Section: Discussionmentioning

confidence: 99%

NTS/NTR1 co-expression enhances epithelial-to-mesenchymal transition and promotes tumor metastasis by activating the Wnt/β-catenin signaling pathway in hepatocellular carcinoma

Long

Zhang

et al. 2016

Oncotarget

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Neurotensin (NTS) is a neuropeptide distributed in central nervous and digestive systems. In this study, the significant association between ectopic NTS expression and tumor invasion was confirmed in hepatocellular carcinoma (HCC). In primary HCC tissues, the NTS and neurotensin receptor 1 (NTR1) co-expression (NTS+NTR1+) is a poor prognostic factor correlated with aggressive biological behaviors and poor clinical prognosis. Enhanced epithelial-to-mesenchymal transition (EMT) features, including decreased E-cadherin, increased β-catenin translocation and N-cadherin expression, were identified in NTS+NTR1+ HCC tissues. Varied NTS-responsible HCC cell lines were established using NTR1 genetically modified Hep3B and HepG2 cells which were used to elucidate the molecular mechanisms regulating NTS-induced EMT and tumor invasion in vitro. Results revealed that inducing exogenous NTS stimulation and enhancing NTR1 expression promoted tumor invasion rather than proliferation by accelerating EMT in HCC cells. The NTS-induced EMT was correlated with the remarkable increase in Wnt1, Wnt3, Wnt5, Axin, and p-GSK3β expression and was significantly reversed by blocking the NTS signaling via the NTR1 antagonist SR48692 or by inhibiting the activation of the Wnt/β-catenin pathway via specific inhibitors, such as TSW119 and DKK-1. SR48692 also inhibited the metastases of NTR1-overexpressing HCC xenografts in the lungs in vivo. This finding implied that NTS may be an important stimulus to promote HCC invasion and metastasis both in vitro and in vivo, and NTS signaling enhanced the tumor EMT and invasion potentials by activating the canonical Wnt/β-catenin signaling pathway. Therefore, NTS may be a valuable therapeutic target to prevent tumor progression in HCC.

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“…Moreover, CCAT2 [7], H19 [129], CASC11 [134], TINCR [111], CCAL [128], cir-ITCH [82], and CTD903 [135] are involved in the WNT pathway, which also regulates gene expression changes during EMT[111]. WNT signaling can promote cancer progression-associated EMT processes via β-catenin-mediated increased gene expression at the invasive front of colorectal tumors [136].…”

Section: Lncrnas Involved In the Invasion Metastasis Early Diagnosimentioning

confidence: 99%

Long non-coding RNAs: a rising biotarget in colorectal cancer

Luo

et al. 2017

Oncotarget

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Colorectal cancer (CRC) is a common gastrointestinal cancer, with a high incidence and high mortality. Long non-coding RNAs (lncRNAs) are involved in the development, invasion and metastasis, early diagnosis, prognosis, the chemoresistance and radioresistance of CRC through interference with mRNA activity, directly combining with proteins to regulate their activity or alter their localization, influencing downstream gene expression by inhibiting RNA polymerase and regulating gene expression as competing endogenous RNAs. Recent progress in next generation sequencing and transcriptome analysis has revealed that tissue and cancer-type specific lncRNAs could be useful prognostic markers. Here, the CRC-associated lncRNAs from recent studies until October 2016 are reviewed and multiple studies that have confirmed CRC-associated lncRNAs are summarized. This review may be helpful in understanding the overall relationships between the lncRNAs involved in CRC.

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Overexpression of long non-coding RNA-CTD903 inhibits colorectal cancer invasion and migration by repressing Wnt/β-catenin signaling and predicts favorable prognosis

Cited by 62 publications

References 34 publications

REST is a crucial regulator for acquiring EMT-like and stemness phenotypes in hormone-refractory prostate cancer

REST is a crucial regulator for acquiring EMT-like and stemness phenotypes in hormone-refractory prostate cancer

NTS/NTR1 co-expression enhances epithelial-to-mesenchymal transition and promotes tumor metastasis by activating the Wnt/β-catenin signaling pathway in hepatocellular carcinoma

Long non-coding RNAs: a rising biotarget in colorectal cancer

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