Cloning and characterization of a novel retinoid-inducible gene 1(RIG1) deriving from human gastric cancer cells

Huang, Shengping; Shyu, Rong-Yaun; Yeh, Ming‐Yang; Jiang, Shun-Yuan

doi:10.1016/s0303-7207(99)00207-5

Cited by 66 publications

(53 citation statements)

References 30 publications

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“…13,14,19 Note that if RAR-RXR dimer has bound an RXR agonist but not an RAR agonist, then that RAR-RXR dimer cannot bind to DR5 RARE and no transcription increase ensues. 13 …”

Section: Atramentioning

confidence: 99%

“…19 Performing a similar function as the better known outer cell membrane TLR-3 (Toll-like receptor-3), RIG is a dsRNA sensing cytosolic receptor, an early warning and essential component in mammalian defense and innate immunity to many viruses. protein and greater IRF-3, and stronger signaling to nuclear Type I interferon promoters, and proportionate increases in interferon protein.…”

Section: Rigmentioning

confidence: 99%

See 1 more Smart Citation

Potential for all-trans retinoic acid [tretinoin] to enhance interferon-alpha treatment response in chronic myelogenous leukemia, melanoma, myeloma, and renal cell carcinoma

Kast¹

2008

Cancer Biology & Therapy

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“…13,14,19 Note that if RAR-RXR dimer has bound an RXR agonist but not an RAR agonist, then that RAR-RXR dimer cannot bind to DR5 RARE and no transcription increase ensues. 13 …”

Section: Atramentioning

confidence: 99%

Section: Rigmentioning

confidence: 99%

Potential for all-trans retinoic acid [tretinoin] to enhance interferon-alpha treatment response in chronic myelogenous leukemia, melanoma, myeloma, and renal cell carcinoma

Kast¹

2008

Cancer Biology & Therapy

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“…Overexpression of TIG3 suppressed the ability to form colonies in T47D breast cancer cells, HaCaT, immortalized skin keratinocytes, or Chinese hamster ovary cells (Di Sepio et al, 1998;Deucher et al, 2000) Also, decreased proliferation with increased TIG3 expression was observed in 293 cells expressing TIG3 linked to an inducible promoter (Di Sepio et al, 1998). The same gene has also been identified by differential display as a retinoic acidinducible gene called retinoid-inducible gene 1 (RIG-1) in gastric cancer cells (Huang et al, 2000). Furthermore, transient expression of the RIG-1 (TIG3) decreased cell growth and induced cellular apoptosis by negatively regulating signal pathways of extracellular signalregulated kinase, c-Jun N-terminal kinase, and p38 mitogen-activated kinase (Huang et al, 2002).…”

Section: Introductionmentioning

confidence: 98%

Induction of TIG3, a putative class II tumor suppressor gene, by retinoic acid in head and neck and lung carcinoma cells and its association with suppression of the transformed phenotype

et al. 2003

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Retinoids can regulate the proliferation and differentiation of various tumor cells. It is thought that nuclear retinoid receptors mediate these effects by regulating gene transcription. The identity of specific retinoid target genes is only beginning to be unraveled. One candidate for mediating retinoid-induced growth suppression is the novel class II tumor suppressor gene tazarotene-induced gene 3 (TIG3). We examined the constitutive and all-trans retinoic acid (ATRA)-inducible expression of TIG3 mRNA in five head and neck squamous cell carcinoma (HNSCC) and five nonsmall cell lung carcinoma (NSCLC) cell lines to determine whether it is associated with their responsiveness to ATRA. The expression patterns of retinoic acid receptor b (RARb), another putative retinoid-inducible tumor suppressor gene, were also examined. The constitutive TIG3 expression was high in one HNSCC cell line and two NSCLC cell lines, and moderate to very low in the other cells. Some RARbexpressing cells had either low or undetectable TIG3 levels and vice versa. ATRA (1 lm; 48 h) increased TIG3 mRNA in 4/5 HNSCCs and 3/5 NSCLCs and RARb mRNA in some of the same cell lines, but also in cells that did not show TIG3 induction. TIG3 mRNA was induced by ATRA between 6 and 12 h in most of the responsive cells. ATRA concentrations required for TIG3 induction ranged from 1 to 500 nm depending on the cell line. The pan-RAR antagonists AGN193109 and the RARa antagonist Ro 41-5253 blocked TIG3 induction by ATRA. ATRA suppressed anchorage-independent colony formation in most cells that had a high or moderate constitutive or induced TIG3 expression level. In contrast, RARb mRNA expression pattern was not correlated with sensitivity to ATRA. These results suggest that TIG3 is regulated by ATRA via retinoid receptors in certain aerodigestive tract cancer cells, and its induction by ATRA is associated with the suppression of anchorageindependent growth.

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“…Their re-expression can be achieved either via activation of positive regulators or by abrogation of negative regulation, for instance through treatment with pharmaceutical agents. [3][4][5][6] Once reactivated, the class II tumor suppressors affect main signal transduction pathways regulating cell differentiation, proliferation, and programmed cell death. For instance, caveolin-1 is down-regulated in breast, ovarian, and small cell lung carcinomas.…”

mentioning

confidence: 99%

H-REV107-1 Stimulates Growth in Non-Small Cell Lung Carcinomas via the Activation of Mitogenic Signaling

Nazarenko

Kristiansen

Fonfara

et al. 2006

The American Journal of Pathology

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H-REV107-1 , a known member of the class II tumor suppressor gene family , is involved in the regulation of differentiation and survival. We analyzed H-REV107-1 in non-small cell lung carcinomas , in normal lung , and in immortalized and tumor-derived cell lines. Sixty-eight percent of lung tumors revealed positive H-REV107-1-specific staining. Furthermore , survival analysis demonstrated a significant association of cytoplasmic H-REV107-1 with decreased patient survival. This suggested that H-REV107-1 , known as a tumor suppressor , plays a different role in non-small cell lung carcinomas. Knock-down of H-REV107-1 expression in lung carcinoma cells inhibited anchorage-dependent and anchorage-independent growth whereas overexpression of H-REV107-1 induced tumor cell proliferation. Consistent with results of the survival analysis , cytoplasmic localization of the protein was essential for this growth-inducing function. Analysis of signaling pathways potentially involved in this process demonstrated that overexpression of H-REV107-1 stimulated RAS-GTPase activity , ERK1 ,2 phosphorylation, and caveolin-1 expression in the cell lines analyzed. These results indicate that H-REV107-1 is deficient in its function as a tumor suppressor in nonsmall cell lung carcinomas and is required for proliferation and anchorage-independent growth in cells expressing high levels of the protein, thus contributing to tumor progression in a subset of non-small cell lung carcinomas.

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Cloning and characterization of a novel retinoid-inducible gene 1(RIG1) deriving from human gastric cancer cells

Cited by 66 publications

References 30 publications

Potential for all-trans retinoic acid [tretinoin] to enhance interferon-alpha treatment response in chronic myelogenous leukemia, melanoma, myeloma, and renal cell carcinoma

Potential for all-trans retinoic acid [tretinoin] to enhance interferon-alpha treatment response in chronic myelogenous leukemia, melanoma, myeloma, and renal cell carcinoma

Induction of TIG3, a putative class II tumor suppressor gene, by retinoic acid in head and neck and lung carcinoma cells and its association with suppression of the transformed phenotype

H-REV107-1 Stimulates Growth in Non-Small Cell Lung Carcinomas via the Activation of Mitogenic Signaling

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