Differentiation-associated modulation of lactoside binding lectins in cancer cells

Lotan, Reuben

doi:10.1007/978-3-642-76739-5_11

Cited by 5 publications

(3 citation statements)

References 98 publications

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“…RAR Regulation of AP-1 Transcriptional Activity-RARs can repress AP-1 transcriptional activity, and this mechanism of action has been proposed to underlie at least some of the antitumorigenic effects of retinoids (8,9,43,51). In transient transfection assays, we found that RA (10 Ϫ6 M) inhibited AP-1 activity 8 -10-fold in wild-type and RAR␣ Ϫ/Ϫ cultures (Fig.…”

Section: Generation Of Rar Null Cell Lines-primary Cultures Ofmentioning

confidence: 74%

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Characterization of Retinoic Acid Receptor-deficient Keratinocytes

Goyette

Chen

Wang

et al. 2000

Journal of Biological Chemistry

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Vitamin A derivatives (retinoids) play central roles in embryonic development and maintenance of various tissues in the adult (1-3). Retinoids also exhibit potent antitumorigenic properties in diverse model systems and show potential for the treatment of a number of human malignancies, including diverse epithelial cancers or pre-cancerous lesions (4 -9).The retinoid signal is transduced by two families of nuclear receptors, the retinoic acid (RA) 1 receptors (RAR␣, -␤, and -␥ and their isoforms) and the retinoid x receptors (RXR␣, -␤, and -␥) (10 -13). RARs function as ligand-inducible transcription regulators by binding, together with an RXR partner, to specific cis-acting response elements (RAREs). RARs can be activated by both RA and its stereoisomer, 9-cis RA, whereas RXRs are activated only by 9-cis RA (14). RXRs are also essential heterodimeric partners for a number of other nuclear receptor signaling pathways, including thyroid hormone, vitamin D, and certain orphan receptors (15, 16). Although 9-cis RA is not obligatory for transcriptional regulation via these pathways, some results suggest that RXR-specific ligands can elicit transcriptional activation in certain settings (e.g. .RARs, like several other nuclear receptors, can function in a ligand-dependent manner to inhibit AP-1 activity, and it has been suggested that the affect of retinoids on the growth of transformed cells may occur through this trans-repression mechanism (21-23). This inhibition is believed to be due, at least in part, to competition for limiting amounts of transcriptional co-factors, such as CBP and/or its homologue p300, common to both pathways (24, 25). Other mechanisms, such as inhibition of the expression of AP-1 family members or c-Jun N-terminal kinase (JNK), may also contribute to this cross-talk (26 -29).Gene targeting of the various RARs has revealed essential and diverse roles for these receptors (2, 30, 31). However, because of perinatal or embryonic lethality inherent to many of these RAR null backgrounds, there is a void in our knowledge of RAR function in a number of contexts, such as tumorigenesis.Exogenous retinoids can attenuate the effects of tumor promoters in the two stage skin carcinogenesis protocol (9, 32). Among the retinoid receptors, normal epidermis expresses RAR␥ and RAR␣␥ as well as RXR␣ and RXR␤, with RAR␥ and RXR␣ as the predominant heterodimer (33,34). This pattern of expression prompted us to investigate the roles of RAR␣ and RAR␥ in mediating the antitumorigenic effects of retinoids in epithelial keratinocytes. To this end, we established RAR␣, RAR␥, and RAR␣␥ null keratinocyte lines by transformation with a dominant-negative p53 expression vector and compared the properties of these various lines. Our results demonstrate that RAR␣ and RAR␥ affect different aspects of retinoid response in these transformed cells, with RAR␥ being the primary mediator of RA-induced growth inhibition. However, other synthetic ligands affected proliferation independent of the RARs. RAR-dependent, but not -independent,...

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Section: Generation Of Rar Null Cell Lines-primary Cultures Ofmentioning

confidence: 74%

“…Exogenous retinoids can attenuate the effects of tumor promoters in the two stage skin carcinogenesis protocol (9,32). Among the retinoid receptors, normal epidermis expresses RAR␥ and RAR␣␥ as well as RXR␣ and RXR␤, with RAR␥ and RXR␣ as the predominant heterodimer (33,34).…”

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confidence: 99%

Characterization of Retinoic Acid Receptor-deficient Keratinocytes

Goyette

Chen

Wang

et al. 2000

Journal of Biological Chemistry

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“…Li studied lectin receptors in normal, dysplastic, and neoplastic cervices with a panel of 12 lectins; some receptors were found to correlate with tumorigenicity, others with differentiation, and others with invasion 127. Lectins are of interest as markers because they are modulated by retinoids 128–130. CD44 is a glycoprotein that functions as a surface receptor for the extracellular matrix glycan hyaluron, which mediates important aspects of lymphocyte activation and cellular migration.…”

Section: Differentiation Markersmentioning

confidence: 99%

Surrogate endpoint biomarkers and their modulation in cervical chemoprevention trials

Follen

Schottenfeld

2001

Cancer

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BACKGROUND. Surrogate endpoint biomarkers (SEBs) are used as intermediate indicators of a reduction in cancer incidence in chemoprevention studies. SEBs should be expressed differentially in normal and high risk tissue; appear at a well defined stage of carcinogenesis; be studied with reasonable sensitivity, specificity, and accuracy; and be modulated in chemoprevention trials. The concept of SEBs may be useful in the trials of many new therapies. METHODS.The current review includes a comprehensive review of the literature.Many SEBs have been the subject of intense study and include quantitative histopathology and cytology, proliferation markers, regulation markers, differentiation markers, general genomic instability markers, and tissue maintenance markers. Because of the critical biologic and epidemiologic role of the human papillomavirus (HPV) in cervical carcinogenesis, the relation between these markers and HPV should be considered. In addition, biomarkers of HPV infection and its regression should be sought. RESULTS. Several chemoprevention trials have beenpublished that have included the use of SEBs. The biomarkers that appear most promising in these clinical trials can be measured quantitatively and reproducibly: quantitative histology and cytology, proliferating cell nuclear antigen (PCNA), MIB-1, MPM-2, HPV viral load, epidermal growth factor receptor, polyamines, and ploidy. The markers that have been demonstrated to be modulated in chemoprevention trials in the literature are quantitative histology and cytology, PCNA, MPM-2, HPV viral load, and polyamines. CONCLUSIONS.The surrogate endpoint biomarkers of most interest in future research should correlate well with HPV infection, be modulated by several therapeutic agents, and have limited variability and ease in measurement. Cancer 2001;

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Modulation of galectin-1 content in human head and neck squamous carcinoma cells by sodium butyrate

Gillenwater

Estrov

et al. 1998

Int. J. Cancer

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Differentiation-associated modulation of lactoside binding lectins in cancer cells

Cited by 5 publications

References 98 publications

Characterization of Retinoic Acid Receptor-deficient Keratinocytes

Characterization of Retinoic Acid Receptor-deficient Keratinocytes

Surrogate endpoint biomarkers and their modulation in cervical chemoprevention trials

Modulation of galectin-1 content in human head and neck squamous carcinoma cells by sodium butyrate

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