Differentially expressed genes from the glioblastoma cell line SHG-44 treated with all-trans retinoic acid in vitro

Zeng, Yi; Ye, Zhong; Xu, Jianguo; Yang, Moon-Sik; Zeng, Zhen; You, Chao

doi:10.1016/j.jocn.2007.11.014

Cited by 11 publications

(6 citation statements)

References 25 publications

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“…Our results showed that U251 cells undergo morphological changes after ATRA treatment. Although association between morphological changes and the induction of neural differentiation has been demonstrated in several glioma cell lines [7,[28][29][30], we did not detect that U251 cells undergo neural differentiation. A possible explanation is that neural differentiation of U251 cells could be induced only with concentrations of ATRA that are smaller than 10 μM, as previously described for glioma stem/progenitor cells [31].…”

Section: Discussioncontrasting

confidence: 97%

All-trans retinoic acid influences viability, migration and adhesion of U251 glioblastoma cells

Marjanovic-Vicentic

Schwirtlich

Kovacevic-Grujicic

et al. 2017

Arch biol sci (Beogr)

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Glioblastoma (GBM) is one of the most aggressive and deadly forms of cancer. Literature data reveals that all-trans retinoic acid (ATRA) has anticancer effects on different types of tumor cells. However, data about the effects of ATRA on glioblastoma cells are contradictory. In this study, we examined whether ATRA treatment affects features of human glioblastoma U251 cells. To that end, the cells were treated with different concentrations of ATRA. Results obtained by MTT and the crystal violet assays imply that ATRA affected the viability of U251 glioblastoma cells in a dose- and time-dependent manner. Fluorescence staining of microtubule cytoskeleton protein ?-tubulin revealed that ATRA induced changes in cell morphology. Using semi-quantitative RT-PCR we found that the expression of SOX3 and GFAP genes, as markers of neural differentiation, was not changed upon ATRA treatment. Thus, the observed changes in cell morphology after ATRA treatment are not associated with neural differentiation of U251 glioblastoma cells. The scratch-wound healing assay revealed that ATRA changed the mode of U251 cell migration from collective to single cell motility. The cell-matrix adhesion assay demonstrated that the pharmacologically relevant concentration of ATRA lowered the cell-matrix adhesion capability of U251 cells. In conclusion, our results imply that further studies are needed before ATRA could be considered for the treatment of glioblastoma.

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Section: Discussioncontrasting

confidence: 97%

All-trans retinoic acid influences viability, migration and adhesion of U251 glioblastoma cells

Marjanovic-Vicentic

Schwirtlich

Kovacevic-Grujicic

et al. 2017

Arch biol sci (Beogr)

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“…This diversity can be accounted on diversity of retinoic acid receptors present in the specific cell/tissue. Treatment with retinoic acid simultaneously suppresses proliferation and significantly induced differentiation in astrocytoma cell line deriving from glioblastoma multiforme and exhibits the same effects in retinoblastoma cells (Zhang et al, 2008; Zeng et al, 2009). Pre‐treatment of follicular thyroid carcinoma cell lines with RA resulted in decreased in vitro proliferation rates and reduced tumor cell growth (Trojanowicz et al, 2009) Incubation with all‐trans retinoic acid (RA) induces embryonic carcinoma cells to cease proliferation, induce differentiation, and undergo apoptosis (Herget et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Retinoid‐responsive transcriptional changes in epidermal keratinocytes

Lee

Stojadinović

Krzyzanowska

et al. 2009

Journal Cellular Physiology

103

101

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Retinoids (RA) have been used as therapeutic agents for numerous skin diseases, from psoriasis to acne and wrinkles. While RA is known to inhibit keratinocyte differentiation, the molecular effects of RA in epidermis have not been comprehensively defined. To identify the transcriptional targets of RA in primary human epidermal keratinocytes, we compared the transcriptional profiles of cells grown in the presence or absence of all-trans retinoic acid for 1, 4, 24, 48 and 72 hours, using large DNA microarrays. As expected, RA suppresses the protein markers of cornification; however the genes responsible for biosynthesis of epidermal lipids, long-chain fatty acids, cholesterol, and sphingolipids, are also suppressed. Importantly, the pathways of RA synthesis, esterification and metabolism are activated by RA; therefore, RA regulates its own bioavailability. Unexpectedly, RA regulates many genes associated with the cell cycle and programmed cell death. This led us to reveal novel effects of RA on keratinocyte proliferation and apoptosis. The response to RA is very fast: 315 genes were regulated already after 1 h. More than one-third of RA-regulated genes function in signal transduction and regulation of transcription. Using in silico analysis, we identified a set of over-represented transcription factor binding sites in the RA-regulated genes. Many psoriasis-related genes are regulated by RA, some induced, others suppressed. These results comprehensively document the transcriptional changes caused by RA in keratinocytes, add new insights into the molecular mechanism influenced by RA in the epidermis and demonstrate the hypothesis-generating power of DNA microarray analysis.

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“…Recent gene-expression profiling analyses showed that serum factors, most likely bone morphogenetic protein 4, induce astrocyte differentiation of human normal neural progenitor cells by upregulating the expression of inhibitor of differentiation (ID) family genes (Obayashi et al, 2009) and that ATRA treatment of a glioblastoma cell line induces up-or downregulation of 42 genes, among which are the astrocytic lineage marker GFAP and the oncogene MDM2 (Zeng et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

De-repression of CTGF via the miR-17-92 cluster upon differentiation of human glioblastoma spheroid cultures

et al. 2010

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All-trans retinoic acid is a potent promoter of cellular differentiation processes, which is used in cancer therapy. Glioblastoma spheroid cultures are enriched in tumorinitiating cells, and provide a model to test new treatment options in vitro. We investigated the molecular mechanisms of response to exposure to differentiation-promoting conditions in such cultures. Microarray analyses of five independent cultures showed that after induction of differentiation, inhibitors of transforming growth factorb/bone morphogenetic protein, Wnt/b-catenin and IGF signaling were upregulated, whereas expression of several microRNAs decreased, particularly that of the miR-17-92 cluster. In primary astrocytic gliomas (n ¼ 82), expression of several members of miR-17-92 was significantly higher relative to those of normal brain (n ¼ 8) and significantly increased with tumor grade progression (Po0.05). A high-level amplification of the miR-17-92 locus was detected in one glioblastoma specimen. Transfection of inhibitors of miR-17-92 induced increased apoptosis and decreased cell proliferation in glioblastoma spheroids. Mir-17-92 inhibition was also associated with increased messenger RNA (mRNA) and/or protein expression of CDKN1A, E2F1, PTEN and CTGF. The CTGF gene was shown to be a target of miR-17-92 in glioblastoma spheroids by luciferase reporter assays. Our results suggest that miR-17-92 and its target CTGF mediate effects of differentiation-promoting treatment on glioblastoma cells through multiple regulatory pathways.

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Differentially expressed genes from the glioblastoma cell line SHG-44 treated with all-trans retinoic acid in vitro

Cited by 11 publications

References 25 publications

All-trans retinoic acid influences viability, migration and adhesion of U251 glioblastoma cells

All-trans retinoic acid influences viability, migration and adhesion of U251 glioblastoma cells

Retinoid‐responsive transcriptional changes in epidermal keratinocytes

De-repression of CTGF via the miR-17-92 cluster upon differentiation of human glioblastoma spheroid cultures

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