Retinoic acid receptors and tissue-transglutaminase mediate short-term effect of retinoic acid on migration and invasion of neuroblastoma SH-SY5Y cells

Joshi, Suchitra; Guleria, Rakeshwar S.; Pan, Jing; DiPette, Donald; Singh, Uaday

doi:10.1038/sj.onc.1209027

Cited by 78 publications

(61 citation statements)

References 63 publications

(69 reference statements)

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“…In the second study, the authors observed that the transforming growth factor b-induced increase in the cell surface expression of TG2 was responsible for augmenting the attachment and migration of retinal pigment epithelial cells on Fn-coated surfaces (Priglinger et al, 2004). Moreover, retinoic acid-induced TG2 expression in neuroblastoma SH-SY5 cells strongly augmented their migration and invasion functions (Joshi et al, 2006). The authors concluded that in addition to TG2 some other factor(s) was needed to promote retinoic acid-induced migration and invasion because inhibition of TG2 by antisense blocked these functions, but overexpression of TG2 in untreated cells failed to induce any change.…”

Section: Integ β5mentioning

confidence: 97%

Tissue transglutaminase expression promotes cell attachment, invasion and survival in breast cancer cells

et al. 2006

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Distant metastasis is frequently observed in patients with breast cancer and is a major cause of cancer-related deaths in these patients. Currently, very little is known about the mechanisms that underlie the development of the metastatic phenotype in breast cancer cells. We previously found that metastatic breast cancer cells express high levels of tissue transglutaminase (TG2), but established no direct link between TG2 and metastasis. In this study, we hypothesized that TG2 plays a role in conferring the metastatic phenotype to breast cancer cells. The results obtained suggested that increased expression of TG2 in breast cancer cells contributes to their increased survival, invasion and motility. We further found that TG2 protein in a metastatic breast cancer MDA-MB231 cells was present on the cell surface in close association with integrins b1, b4 and b5. Downregulation of endogenous TG2 by small interfering RNA inhibited fibronectin (Fn)-mediated cell attachment, survival and invasion. Conversely, ectopic expression of TG2 augmented invasion of breast cancer cells and attachment to Fn-coated surfaces. We conclude that TG2 expression in breast cancer cells plays an important role in the development of the metastatic phenotype.

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Section: Integ β5mentioning

confidence: 97%

Tissue transglutaminase expression promotes cell attachment, invasion and survival in breast cancer cells

et al. 2006

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“…Administration of RA to neuroblastoma cells in vitro leads to proliferative arrest and neuronal differentiation as judged by their morphology and the expression of biochemical and functional neuronal markers (20,21). In addition, to inhibit cell proliferation and induce differentiation, long term RA treatment reduces the biological aggressiveness of neuroblastoma cells by reducing their migratory and invasive abilities (22,23). All these results prompted the introduction of RA and its derivatives into therapeutic protocols for neuroblastoma patients, with some success especially in the treatment of minimal residual disease (24 -26).…”

Section: Micrornas (Mirnas Mirs)mentioning

confidence: 99%

MicroRNAs-10a and -10b Contribute to Retinoic Acid-induced Differentiation of Neuroblastoma Cells and Target the Alternative Splicing Regulatory Factor SFRS1 (SF2/ASF)

Meseguer

Mudduluru

Escamilla

et al. 2011

Journal of Biological Chemistry

105

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MicroRNAs (miRNAs) are an emerging class of non-coding endogenous RNAs involved in multiple cellular processes, including cell differentiation. Treatment with retinoic acid (RA) results in neural differentiation of neuroblastoma cells. We wanted to elucidate whether miRNAs contribute to the gene expression changes induced by RA in neuroblastoma cells and whether miRNA regulation is involved in the transduction of the RA signal. We show here that RA treatment of SH-SY5Y neuroblastoma cells results in profound changes in the expression pattern of miRNAs. Up to 42 different miRNA species significantly changed their expression (26 up-regulated and 16 down-regulated). Among them, the closely related miR-10a and -10b showed the most prominent expression changes. Induction of miR-10a and -10b by RA also could be detected in LA-N-1 neuroblastoma cells. Loss of function experiments demonstrated that miR-10a and -10b are essential mediators of RA-induced neuroblastoma differentiation and of the associated changes in migration, invasion, and in vivo metastasis. In addition, we found that the SR-family splicing factor SFRS1 (SF2/ASF) is a target for miR-10a -and -10b in HeLa and SH-SY5Y neuroblastoma cells. We show here that changes in miR10a and -10b expression levels may regulate SFRS1-dependent alternative splicing and translational functions. Taken together, our results give support to the idea that miRNA regulation plays a key role in RA-induced neuroblastoma cell differentiation. The discovery of SFRS1 as direct target of miR-10a and -10b supports the emerging functional interaction between two post-transcriptional mechanisms, microRNAs and splicing, in the neuronal differentiation context. MicroRNAs (miRNAs, miRs)5 are an emerging class of small non-coding endogenous RNAs that are involved in multiple biological processes. These tiny regulatory elements are transcribed as primary longer transcripts, which are then processed by Dicer and Drosha complexes into 21-23-nt mature miRNAs. One strand of the mature miRNA is then incorporated into the RNA-induced silencing complex to regulate gene expression by targeting the 3Ј-untranslated region (3Ј-UTR) of mRNAs with consequent translational repression and/or target mRNA degradation. This mode of action demonstrates the great regulatory potential of miRNAs, as a unique mRNA can be targeted by diverse miRNAs, and conversely, each miRNA may have 100s of different target mRNAs (for review, see Refs. 1 and 2).In vertebrates, the highest variety of miRNAs is expressed in the brain than in any other tissue, suggesting an important role in nervous system development (3, 4). Recent studies have revealed the importance of miRNA expression in neural development and differentiation. For instance, it has been reported that Dicer-deleted mice exhibit malformations of the midbrain and cerebellum and failure of neural crest and dopaminergic differentiation (5). In addition, three brain-specific miRNAs (miR-124a, miR-9, and miR-132) have been proposed to regulate the transcription factor R...

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“…The increase in migration appears to be nonspecific, since also occurs in the absence of laminin chemoattractant. Similar RA-induced rapid transient increases in migration and invasion in neuroblastoma cells have been reported (Joshi et al, 2006;Meseguer et al, 2011), and correlated to the expression of tissue transglutaminase (Joshi et al, 2006). Blocking of RA signaling in vivo also impaired neuroblast migration from the subventricular zone of the brain to the olfactory bulb (Wang et al, 2005a), suggesting that short term RA-induced increases in migration probably reflects a physiological feature of RA action on the regulation of neurogenesis.…”

Section: Discussionmentioning

confidence: 74%

“…After washing with PBS, the slides were counter-stained with Hoechst 33258 and sequentially photographed in a Leica fluorescence microscope equipped with FITC-and UV-specific excitation filters. (Joshi et al, 2006;Joshi et al, 2007;Meseguer et al, 2011;Voigt & Zintl, 2003). To look for RA-induced biological effects in neuroblastoma cells that could be related to the observed downregulation of the 67LR, we used assays for migration/haptotaxis towards Matrigel and for invasion through Matrigel.…”

Section: Ra Treatment Of Neuroblastoma Cells Reduces Migration Towardmentioning

confidence: 99%

Retinoic-Acid-Induced Downregulation of the 67 KDa Laminin Receptor Correlates with Reduced Biological Aggressiveness of Human Neuroblastoma Cells

Escamilla¹,

Bäuerl²,

Lopez³

et al. 2012

Neuroblastoma - Present and Future

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Retinoic acid receptors and tissue-transglutaminase mediate short-term effect of retinoic acid on migration and invasion of neuroblastoma SH-SY5Y cells

Cited by 78 publications

References 63 publications

Tissue transglutaminase expression promotes cell attachment, invasion and survival in breast cancer cells

Tissue transglutaminase expression promotes cell attachment, invasion and survival in breast cancer cells

MicroRNAs-10a and -10b Contribute to Retinoic Acid-induced Differentiation of Neuroblastoma Cells and Target the Alternative Splicing Regulatory Factor SFRS1 (SF2/ASF)

Retinoic-Acid-Induced Downregulation of the 67 KDa Laminin Receptor Correlates with Reduced Biological Aggressiveness of Human Neuroblastoma Cells

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