Characterization of genes which exhibit reduced expression during the retinoic acid-induced differentiation of F9 teratocarcinoma cells: involvement of cyclin D3 in RA-mediated growth arrest

Faria, Teresa N.; LaRosa, Gregory J.; Wilen, E.; Liao, Jack; Gudas, Lorraine J.

doi:10.1016/s0303-7207(98)00127-0

Cited by 49 publications

(37 citation statements)

References 57 publications

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“…RA is known to cause G0 arrest in S91 melanoma cells (Spanjaard et al 1997), F9 murine teratocarcinoma cells (Faria et al 1998), and HL-60 human myeloblastic leukemia cells (Yen et al 1999). In contrast, RA causes cell differentiation in PCC7-Mz1 embryonic carcinoma cells (Herget et al 1998), P19 mouse embryonic carcinoma cells (Jho et al 1997) and porcine preadipocytes (Suryawan & Hu 1997).…”

Section: Discussionmentioning

confidence: 99%

“…RA has been shown to be essential for the growth and differentiation of many types of cells. Numerous studies have reported that RA induces terminal differentiation of many cell types, including P19 embryonal carcinoma (Paterno et al 1997), F9 murine tetracarcinoma cells (Faria et al 1998), and HL-60 human myeloblastic leukemia cells (Yen et al 1999). However, the nature of the proliferation and differentiation responses elicited by RA are dependent on the cell type.…”

Section: Introductionmentioning

confidence: 99%

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Inhibitory effect of retinoic acid on the development of immature porcine granulosa cells to mature cells

Hattori

Takesue²,

Nishida³

et al. 2000

Journal of Molecular Endocrinology

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The present study investigated the effect of retinoic acid (RA) on the differentiation of granulosa cells prepared from porcine ovaries. The granulosa cells were precultured for 15 h, then cultured for 48 h with FSH and further treated for 24 h with LH in order to induce their transformation into luteal cells. After the cells had been exposed to 1 µM retinoids (RA, retinal and retinol) for 87 h, analysis of the LH receptor mRNA expression, an indicator of granulosa cell differentiation, was carried out by using semiquantitative RT-PCR. The results showed that there was a decrease in LH receptor mRNA levels, and that RA had a more potent effect on these levels than the other two retinoids. When cells were exposed to RA in the immature stage (before the addition of FSH) or the early stage of development (0-24 h after the addition of FSH), expression of LH receptor mRNA was greatly diminished. When the immature cells were cultured for 15 h with RA, then washed and cultured for 48 h with FSH and for 24 h with LH, the expression of LH receptor mRNA was not reversed. In the differentiated cells (24 h after the addition of FSH), however, RA no longer had any inhibitory effect. When the immature cells were exposed to RA, FSH-induced expression of c-fos mRNA was markedly decreased. In contrast, expression of c-jun and activating transcription factor-4 mRNAs remained constant. However, the expression of c-fos mRNA was not decreased by forskolin. The results indicate that RA is a potent inhibitor in the immature stage of porcine granulosa cell differentiation, probably through decreased expression of FSH receptor, but that RA does not inhibit differentiation in the mature stage of the cells.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of retinoic acid on the development of immature porcine granulosa cells to mature cells

Hattori

Takesue²,

Nishida³

et al. 2000

Journal of Molecular Endocrinology

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“…BEX1: Initially BEX1 was described as a gene downregulated following retinoic acid treatment of F9 murine teratocarcinoma cells [17]. This gene was also highly expressed in parthenogenetic blastocysts [18,19].…”

Section: Bex Genes and Proteinsmentioning

confidence: 99%

Brain-Expressed X-linked (BEX) proteins in human cancers

Kazi

Kabir

2015

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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The Brain-Expressed X-linked (BEX) family proteins are comprised of five human proteins including BEX1, BEX2, BEX3, BEX4 and BEX5. BEX family proteins are expressed in a wide range of tissues and are known to play a role in neuronal development. Recent studies suggest a role of BEX family proteins in cancers. BEX1 expression is lost in a subgroup of patients with acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). Expression of BEX1 controls cell surface receptor signaling and restores imatinib response in resistant cells. BEX2 is overexpressed in a group of breast cancer patients and also in gliomas. Increased BEX2 expression led to enhanced NF-κB signaling as well as cell proliferation. Although BEX2 acts as tumor promoter in a subset of breast cancer, BEX3 expression displayed an opposite role. Overexpression of BEX3 resulted in inhibition of tumor formation in breast cancer mouse xenograft models. The role of BEX4 and BEX5 in cancer has not yet been defined. Collectively this suggests that BEX family members have distinct roles in cancers.While BEX1 and BEX3 act as a tumor suppressors, BEX2 seems to act as an oncogene.

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“…The search revealed sequence similarity to brain-expressed (Bex) proteins, Bex1-3 (Figure 2a). The Bex proteins belong to a small family of genes comprised of bex1 (Faria et al, 1998), bex2 and bex3 (Rapp et al, 1990;Mukai et al, 2000). We therefore named the newly identified gene, mapping between bex2, and bex3 on X22.1-22.2, as bex4.…”

Section: Similarity Alignment Of Tceal7 To Other Proteinsmentioning

confidence: 99%

Epigenetic silencing of TCEAL7 (Bex4) in ovarian cancer

et al. 2005

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Epigenetic silencing by hypermethylation of CpGs represents a mechanism of inactivation of tumor suppressors. Here we report on the cloning of a novel candidate tumor suppressor gene TCEAL7 inactivated by methylation in ovarian cancer. TCEAL codes for a 1.35 kb transcript that was previously reported to be downregulated in ovarian cancer by cDNA microarray and suppression subtraction cDNA (SSH) analyses. This report focuses on the elucidation of mechanisms associated with TCEAL7 downregulation. Expression of TCEAL7 is downregulated in a majority of ovarian tumors and cancer cell lines but induced by 5-aza-2 0 -deoxycytidine treatment in a dosedependant manner, implicating methylation as a mechanism of TCEAL7 inactivation. Sequence analyses of bisufite-modified genomic DNA from somatic cell hybrids with either the active or the inactive human X chromosome reveal that TCEAL7 is subjected to X chromosome inactivation. Loss of TCEAL7 expression in primary tumors and cell lines correlates with methylation of a CpG site within the promoter. In vitro methylation of the CpG site suppresses promoter activity whereas selective demethylation of the SmaI site attenuates the suppression. Finally, re-expression of TCEAL7 in cancer cell lines induces cell death and reduces colony formation efficiency. These data implicate TCEAL7 as a cell death regulatory protein that is frequently inactivated in ovarian cancers, and suggest that it may function as a tumor suppressor.

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Characterization of genes which exhibit reduced expression during the retinoic acid-induced differentiation of F9 teratocarcinoma cells: involvement of cyclin D3 in RA-mediated growth arrest

Cited by 49 publications

References 57 publications

Inhibitory effect of retinoic acid on the development of immature porcine granulosa cells to mature cells

Inhibitory effect of retinoic acid on the development of immature porcine granulosa cells to mature cells

Brain-Expressed X-linked (BEX) proteins in human cancers

Epigenetic silencing of TCEAL7 (Bex4) in ovarian cancer

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