Activation of PTHrP Gene Expression in Squamous Carcinoma Cell Lines by Mutant Isoforms of the Tumor Suppressor p53

Foley, John; King, Connie S.; Jiménez, Julio Díaz; Wysolmerski, John J.; Philbrick, William M.

doi:10.3727/096504001108747549

Cited by 6 publications

(4 citation statements)

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“…Our results are in accordance with previous studies that measured alternative promoter usage in various cell lines and in lung carcinoma (16,17 ). Furthermore, several reports on the regulation of individual promoters in different cancers have identified some of the transcription factors regulating PTHrP expression and have highlighted the importance of the P3 promoter in gene transactivation (20,(22)(23)(24)(25). The results given in previous reports analyzing the prevalence of all three isoforms in healthy and neoplastic tissues by use of nonquantitative RT-PCR or Northern blots are comparable to our results.…”

supporting

confidence: 82%

“…Previous studies have examined the differential usage of the three PTHrP promoters in healthy tissue and tumor samples from individual patients based on semiquantitative RT-PCR (16 ), Northern blots (19 ), RNase protection assay (20 ), or quantitative competitive PCR (21 ), but no clear consensus on tissue-specific patterns of promoter usage has been reached. Our results are in accordance with previous studies that measured alternative promoter usage in various cell lines and in lung carcinoma (16,17 ).…”

mentioning

confidence: 99%

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Quantitative Evaluation of Alternative Promoter Usage and 3′ Splice Variants for Parathyroid Hormone-related Protein by Real-Time Reverse Transcription-PCR

Richard¹,

Luchin²,

Brena

et al. 2003

Clinical Chemistry

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confidence: 82%

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confidence: 99%

Quantitative Evaluation of Alternative Promoter Usage and 3′ Splice Variants for Parathyroid Hormone-related Protein by Real-Time Reverse Transcription-PCR

Richard¹,

Luchin²,

Brena

et al. 2003

Clinical Chemistry

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“…Immunoblotting for erbB and extracellular signal-regulated kinase (ERK) proteins was performed as in Gilmore and Riese (2004) and Foley et al (2000). For measurement of phosphorylation of MAPK, RWGT2 cells were seeded at a density of 5 Â 10 5 cells/100-mm dish 24 h before treatment with PD.…”

Section: Immunoblot Analysismentioning

confidence: 99%

Inhibition of epidermal growth factor receptor signalling reduces hypercalcaemia induced by human lung squamous-cell carcinoma in athymic mice

et al. 2007

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The purpose of this study was to evaluate the role of the epidermal growth factor receptor (EGFR) in parathyroid hormone-related protein (PTHrP) expression and humoral hypercalcaemia of malignancy (HHM), using two different human squamous-cell carcinoma (SCC) xenograft models. A randomised controlled study in which nude mice with RWGT2 and HARA xenografts received either placebo or gefitinib 200 mg kg À1 for 3 days after developing HHM. Effectiveness of therapy was evaluated by measuring plasma calcium and PTHrP, urine cyclic AMP/creatinine ratios, and tumour volumes. The study end point was at 78 h. The lung SCC lines, RWGT2 and HARA, expressed high levels of PTHrP mRNA as well as abundant EGFR protein, but very little erbB2 or erbB3. Both lines expressed high transcript levels for the EGFR ligand, amphiregulin (AREG), as well as, substantially lower levels of transforming growth factor-a (TGF-a), and heparin binding-epidermal growth factor (HB-EGF) mRNA. Parathyroid hormone-related protein gene expression in both lines was reduced 40 -80% after treatment with 1 mM of EGFR tyrosine kinase inhibitor PD153035 and precipitating antibodies to AREG. Gefitinib treatment of hypercalcaemic mice with RWGT2 and HARA xenografts resulted in a significant reduction of plasma total calcium concentrations by 78 h. Autocrine AREG stimulated the EGFR and increased PTHrP gene expression in the RWGT2 and HARA lung SCC lines. Inhibition of the EGFR pathway in two human SCC models of HHM by an anilinoquinazoline demonstrated that the EGFR tyrosine kinase is a potential target for antihypercalcaemic therapy.

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“…In all, 20 ml of 1 mg/ml of protein was combined with 10 ml of 3 Â Laemlli sample buffer and then boiled for 5 minutes before subsequently loaded onto 8% Laemlli polyacrylamide gels. Running the gels and blotting was performed as in Foley et al (2000). The efficiency of transfer was assessed by incubating the blotted gel in 0.1% Coomassie brilliant blue for 1 hour followed by 30 minutes in destaining solution.…”

Section: Western Blottingmentioning

confidence: 99%

Parathyroid Hormone Hormone-Related Protein and the PTH Receptor Regulate Angiogenesis of the Skin

Diamond

Gonterman

Anderson

et al. 2006

Journal of Investigative Dermatology

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In developing organs, parathyroid hormone (PTH)/parathyroid hormone-related protein (PTHrP) receptor (PPR) signaling inhibits proliferation and differentiation of mesenchyme-derived cell types resulting in control of morphogenic events. Previous studies using PPR agonists and antagonists as well as transgenic overexpression of the PPR ligand PTHrP have suggested that this ligand receptor combination might regulate the anagen to catagen transition of the hair cycle. To further understand the precise role of PTHrP and the PPR in the hair cycle, we have evaluated hair growth in the traditional K14-PTHrP (KrP) and an inducible bitransgenic PTHrP mice. High levels of PTHrP trangene expression limited to the adult hair cycle resulted in the production of shorter hair shafts. Morphometric analysis indicated that reduced proliferation in the matrix preceded the appearance of thinner hair follicles and shafts during late anagen. CD31 staining revealed that the late anagen hair follicles of the KrP mice were surrounded by reduced numbers of smaller diameter capillaries as compared to controls. Moreover, the fetal skins of the PTHrP and PPR knockouts (KOs) had reciprocal increases in the length, diameter, and density of capillaries. Finally, crossing the KrP transgene onto a thrombospondin-1 KO background reversed the vascular changes as well as the delayed catagen exhibited by these mice. Taken together, these findings suggest that PTHrP's influence on the hair cycle is mediated in part by its effects on angiogenesis.

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Activation of PTHrP Gene Expression in Squamous Carcinoma Cell Lines by Mutant Isoforms of the Tumor Suppressor p53

Cited by 6 publications

References 0 publications

Quantitative Evaluation of Alternative Promoter Usage and 3′ Splice Variants for Parathyroid Hormone-related Protein by Real-Time Reverse Transcription-PCR

Quantitative Evaluation of Alternative Promoter Usage and 3′ Splice Variants for Parathyroid Hormone-related Protein by Real-Time Reverse Transcription-PCR

Inhibition of epidermal growth factor receptor signalling reduces hypercalcaemia induced by human lung squamous-cell carcinoma in athymic mice

Parathyroid Hormone Hormone-Related Protein and the PTH Receptor Regulate Angiogenesis of the Skin

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