LincRNA-ROR promotes invasion, metastasis and tumor growth in pancreatic cancer through activating ZEB1 pathway

Background: LncRNA ROR, a tumor oncogene associated with various human cancers, has been reported to be involved in regulating various cellular processes, such as proliferation, apoptosis and invasion through targeting multiple genes. However, the molecular biological function in bladder cancer has not been clearly elucidated. The aim of this study is to explore ROR expression levels and evaluated its function in bladder cancer. Methods: LncRNA ROR expression levels in the 36 pairs of bladder cancer tissues (and corresponding non-tumor tissues) and bladder cancer cells were assessed by qRT-PCR. MTT assay, colony formation assay, flow cytometric analysis, wound healing assay, cell transwell assays, attachment/detachment and western blotting were performed to assess the effects of ROR on proliferation, apoptosis, migration/invasion and epithelial-to-mesenchymal (EMT) phenotypes in BC cells in vitro. ZEB1 is target of ROR. Rescue assays were performed to further confirm that ROR contributes to the progression of BC cells through targeting ZEB1. Results: LncRNA ROR was up-regulated in bladder cancer tissues (compared to adjacent non-tumor tissues) and was almost overexpression in bladder cancer cells (compared with normal urothelial cell line SVHUC-1 cells). Increased lncRNA ROR expression significantly promoted tumor cells proliferation, inhibited cells apoptosis, facilitated cells metastasis and contributed to the formation of EMT phenotype. While down-regulated ROR could obviously inhibit cells proliferation, promote cells apoptosis, inhibit metastasis and reverse EMT to MET. ZEB1 was a target gene of ROR and was positive correlation with the level of ROR in cancer tissues. Conclusion: These results indicated that lncRNA ROR was associated with tumor progression in bladder cancer cells.

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“…It has been identified that ZEB1 was a target of ROR [16]. To detect whether ROR exerts its function in BC cells is dependent on ZEB1.…”

Section: Resultsmentioning

confidence: 99%

LncROR Promotes Bladder Cancer Cell Proliferation, Migration, and Epithelial-Mesenchymal Transition

Chen

Peng

et al. 2017

Cell Physiol Biochem

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“…Linc-ROR has a regulatory role in multiple cancer types. [91][92][93][94][95][96] Recent studies have shown that linc-ROR may function as a molecular sponge for miR-145 targets, such as OCT4, SOX2 and Nanog. 92 Hou et al 91 examined linc-ROR in breast tissue specimens and breast cancer cell lines.…”

Section: Hox Transcript Antisense Intergenic Rna (Hotair)mentioning

confidence: 99%

The evolving concept of cancer stem-like cells in thyroid cancer and other solid tumors

Hardin

Zhang

Helein

et al. 2017

Laboratory Investigation

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The cancer stem-like cell (CSC) hypothesis postulates that a small population of cells in a cancer has self-renewal and clonal tumor initiation properties. These cells are responsible for tumor initiation, growth, recurrence and for resistance to chemotherapy and radiation therapy. CSCs can be characterized using markers such as SSEA-1, SSEA-4, CD44, CD24, ALDEFLUOR and others. CSCs form spheres when they are cultured in serum-free condition in low attachment plates and can generate tumors when injected into immune-deficient mice. During epithelial to mesenchymal transition (EMT), cells lose cellular adhesion and polarity and acquire an invasive phenotype. Recent studies have established a relationship between EMT and increased numbers of CSCs in some solid malignancies. Non-coding RNAs such as microRNAs and long non-coding RNAs (lncRNAs) have been shown to have important roles during EMT and some of these molecules also have regulatory roles in the proliferation of CSCs. Specific lncRNAs enhanced cell migration and invasion in breast carcinomas, which was associated with the generation of stem cell properties. The tumor microenvironment of CSCs also has an important role in tumor progression. Recent studies have shown that the interaction between tumor cells and the local microenvironment at the metastatic site leads to the development of premetastatic niche(s) and allows for the proliferation of the metastatic cells during colonization. The role of exosomes in the microenvironment during the EMT program is currently a major area of research. This review examines CSCs and the relationship between EMT and CSCs in solid tumors with emphasis on thyroid CSCs. The role of non-coding RNAs and of the microenvironment in EMT and in tumor progression are also examined. This review also highlights the growing number of studies that show the close association of EMT and CSCs and the role of exosomes and other elements of the tissue microenvironment in CSC metastasis. A better understanding of these mechanisms will lead to more effective targeting of primary and metastatic malignancies.

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“…A series of studies has established the importance of linc-ROR as a marker of cancers. Marked upregulation of linc-ROR is observed in various cancers, including breast cancer [32][33][34], pancreatic cancer [48,70], hepatocellular cancer [36,37], endometrial cancer [38], and nasopharyngeal carcinoma [76], while linc-ROR acts as a tumor suppressor in glioma [40]. Although linc-ROR is overexpressed in various types of cancer, the target genes are rather variable depending on the host cell type.…”

Section: Linc-ror-related Cancersmentioning

confidence: 99%

“…Futher, Chen et al demostrated that linc-ROR is an important marker for multidrug resistance of breast cancer by inducing the EMT [33], which was relevant to paclitaxel and 5-FU resistances in human malignancies [67][68][69]. Moreover, linc-ROR may mediate migration and metastasis in pancreatic cancer cells partly by activation of ZEB1 through inhibition of p53 expression [70]. ZEB1 can repress the members of miR-200 family, resulting in activation of EMT and maintenance of stemness in pancreatic cancer [71].…”

Section: Linc-ror Triggers the Emt Progressmentioning

confidence: 99%

The Emerging Roles of Long Noncoding RNA ROR (lincRNA-ROR) and its Possible Mechanisms in Human Cancers

Pan

Li²,

Chen³

et al. 2016

Cell Physiol Biochem

119

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To date, there is only up to 2% of protein-coding genes that are stably transcribed, whereas the vast majority are non-coding RNAs (ncRNAs). These ncRNAs, also known as non-messenger RNAs (nmRNAs) or functional RNAs (fRNAs), include transfer RNAs, ribosomal RNAs, microRNAs and long non-coding RNAs (lncRNAs). With the advance of high-resolution microarrays and massively parallel sequencing technology, lncRNAs have gained extended attentions nowadays and are found to play important roles in tumorigenesis and progression of human cancers. Long intergenic non-protein coding RNA, regulator of reprogramming (linc-ROR), was first discovered in induced pluripotent stem cells (iPSCs), where it was controlled by the key pluripotency factors Oct4, Sox2 and Nanog. Linc-ROR has been shown to be dysregulated in many types of cancers, including breast cancer (BC), pancreatic cancer (PC), hepatocellular cancer (HCC), endometrial cancer (EC), and nasopharyngeal carcinoma (NPC). Also, linc-ROR functions as regulatory molecule in a large amount of biological processes. However, the underlying mechanisms of its contribution to carcinogenesis remain to be elucidated. In this review, we will emphasize on the characteristics of linc-ROR and their roles in different types of human cancers.

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LincRNA-ROR promotes invasion, metastasis and tumor growth in pancreatic cancer through activating ZEB1 pathway

Cited by 114 publications

References 27 publications

LncROR Promotes Bladder Cancer Cell Proliferation, Migration, and Epithelial-Mesenchymal Transition

LncROR Promotes Bladder Cancer Cell Proliferation, Migration, and Epithelial-Mesenchymal Transition

The evolving concept of cancer stem-like cells in thyroid cancer and other solid tumors

The Emerging Roles of Long Noncoding RNA ROR (lincRNA-ROR) and its Possible Mechanisms in Human Cancers

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