Upregulated MALAT-1 contributes to bladder cancer cell migration by inducing epithelial-to-mesenchymal transition

Liang, Ying; Chen, Qi; Wang, Yawei; Zhou, Zhihua; Huang, Yiran; Qiu, Feng

doi:10.1039/c2mb25070e

Cited by 314 publications

(246 citation statements)

References 30 publications

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“…9 In this review, we related that some lncRNAs, such as MALAT1 and H19, were found to promote EMT by activating the Wnt/b-catenin pathway in bladder cancer cells. 49,53 A recent study has identified the role of HOTAIR within the context of EMT and has suggested that HOTAIR inhibition could reverse the EMT process in gastric carcinoma cells. Furthermore, the expression of Snail, one of the major transcription factors regulating EMT, could be induced by HOTAIR overexpression, implying that HOTAIR could act as a potential regulator of EMT.…”

Section: Discussionmentioning

confidence: 99%

“…However, another report has suggested that MALAT1 promotes EMT by activating the Wnt/bcatenin pathway in bladder cancer cells: the downregulation of MALAT1 resulted in a decrease in the levels of Slug, as well as ZEB1 and ZEB2 (known as transcriptional repressors of E-cadherin), and an increase in CDH1 levels, indicating that MALAT1 promotes EMT by activating Wnt signaling. 49 LncRNA H19 may be involved in a similar regulatory mechanism. H19, an imprinted and maternally expressed oncofetal gene, is located on chromosome 11p15.5 near the IGF II (encoding insulin-like growth factor II) locus.…”

Section: Malat1 H19 and Ccat2-wnt/b-catenin Pathwaymentioning

confidence: 99%

“…Like HOTAIR, MALAT1 was also known to be misregulated in many other cancer metastases, including CRC and bladder cancer. 49,76 HOTAIR and MALAT1 both act as oncogenic lncRNAs, whereas some other lncRNAs were found to exert tumor-suppressive roles in cancer invasion and metastasis. For instance, lncRNA-LET was discovered to be significantly underexpressed in HCC, CRC, as well as squamous cell lung carcinoma tissues compared with its expression in peritumoral tissue, and a lower lncRNA-LET level was found to be associated with tumor metastasis and determined to have tumor suppressor activity.…”

Section: Lncrnas As Diagnostic and Prognostic Markersmentioning

confidence: 99%

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Long non-coding RNAs in cancer invasion and metastasis

Shen

Pan

2015

Modern Pathology

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Recent large-scale transcriptome analyses have revealed that the human genome contains more than just protein-coding genes. Indeed, a large number of transcripts, including long non-coding RNAs (lncRNAs), lack protein-coding capacity, and increasing evidence suggests that lncRNAs could have a critical role in the regulation of diverse cellular processes, such as stem cell pluripotency, development, cell growth and apoptosis, and cancer invasion and/or metastasis. Furthermore, the aberrant expression of several lncRNAs is closely linked to cancer invasion and/or metastasis. Although the underlying molecular mechanisms by which lncRNAs regulate cancer invasion and/or metastasis are not clearly understood, recent studies have revealed that aberrant lncRNAs expression affects the progression of cancer. In this review, we highlight recent findings regarding the roles of lncRNAs in cancer invasion and/or metastasis.

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Section: Discussionmentioning

confidence: 99%

Section: Malat1 H19 and Ccat2-wnt/b-catenin Pathwaymentioning

confidence: 99%

Section: Lncrnas As Diagnostic and Prognostic Markersmentioning

confidence: 99%

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Long non-coding RNAs in cancer invasion and metastasis

Shen

Pan

2015

Modern Pathology

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“…According to statistics, human bladder cancer is the fourth leading cause of malignancy in men and currently the tenth most malignant tumor in women (1). According to its pathological features, bladder cancer can be divided into two major groups: urothelial carcinoma (UC) and invasive bladder cancer.…”

Section: Introductionmentioning

confidence: 99%

miR-24-3p regulates bladder cancer cell proliferation, migration, invasion and autophagy by targeting DEDD

Jia

Dou

2016

Oncology Reports

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Abstract. microRNAs (miRNAs), a class of small non-coding RNA molecules, can regulate gene expression by interacting with the 3'-untranslated regions (3'UTR) of target genes and influence various biological processes. We investigated the potential role of miR-24-3p in the development of bladder cancer by regulating DEDD, a member of the death effector domaincontaining protein family. First, we found that miR-24-3p was highly expressed and that DEDD was expressed at a low level in bladder cancer tissues compared with that in adjacent bladder tissues by qRT-PCR (P<0.0001). Second, we found that miR-24-3p promoted the proliferation ability of bladder cancer cells using the MTT assay and colony forming assay; and showed that miR-24-3p accelerated the migration and invasion of bladder cancer cells using migration and invasion assays (P<0.05). Moreover, miR-24-3p inhibited apoptosis of bladder cancer cells, as shown by flow cytometry (P<0.05). Western blot results demonstrated that miR-24-3p participated in autophagy of bladder cancer cells by DEDD. In addition, the tumor formation assay showed that miR-24-3p promoted the growth of bladder tumor in vivo. Furthermore, the luciferase reporter gene assay indicated that miR-24-3p suppressed DEDD gene transcription. Therefore, our study indicated that miR-24-3p promoted bladder cancer progression by inhibiting DEDD.

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“…Recently, Ying et al [43] found that MALAT-1 levels were up-regulated in bladder cancer tissues compared with adjacent normal tissues, and siRNA-mediated MALAT-1 silencing resulted in a decrease of ZEB1, ZEB2 and Slug levels, and an increase of E-cadherin levels. MALAT-1 promoted EMT by activating Wnt signaling in vitro.…”

Section: Lncrnas In Cancermentioning

confidence: 99%

Non-coding RNAs regulate tumor cell plasticity

Liu

Sun

Song

2013

Sci. China Life Sci.

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Tumor metastasis is one of the most serious challenges for human cancers as the majority of deaths caused by cancer are associated with metastasis, rather than the primary tumor. Recent studies have demonstrated that tumor cell plasticity plays a critical role in tumor metastasis by giving rise to various cell types which is necessary for tumor to invade adjacent tissues and form distant metastasis. These include differentiation of cancer stem cells (CSCs), or epithelial-mesenchymal transition (EMT) and its reverse process, mesenchymal-epithelial transition (MET). A growing body of evidence has demonstrated that the biology of tumor cell plasticity is tightly linked to functions of non-coding RNAs (ncRNAs), especially microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). Therefore, understanding the mechanisms how non-coding RNAs regulate tumor cell plasticity is essential for discovery of new diagnostic markers and therapeutic targets to overcome metastasis. metastasis, tumor cell plasticity, CSCs, EMT, miRNA, lncRNA Citation:

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Upregulated MALAT-1 contributes to bladder cancer cell migration by inducing epithelial-to-mesenchymal transition

Cited by 314 publications

References 30 publications

Long non-coding RNAs in cancer invasion and metastasis

Long non-coding RNAs in cancer invasion and metastasis

miR-24-3p regulates bladder cancer cell proliferation, migration, invasion and autophagy by targeting DEDD

Non-coding RNAs regulate tumor cell plasticity

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