SLURP-1 and -2 in normal, immortalized and malignant oral keratinocytes

Arredondo, Juan; Chernyavsky, Alexander I.; Grando, Sergei A.

doi:10.1016/j.lfs.2007.01.003

Cited by 59 publications

(61 citation statements)

References 13 publications

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“…In a previous study, we found that recombinant SLURP-1 and -2 can lessen tumorigenic activities of tobacco-derived nitrosamines [6]. The intact Het-1A cells had decreased SLURP-1 and -2 mRNA levels that further decreased after treatment of cells with carcinogenic nitrosamines.…”

Section: Discussionmentioning

confidence: 81%

“…We could not detected either SLURP protein in the 120-fold concentrated supernatants of Het-1A cell cultures, whereas the protein bands corresponding to SLURP-1 and -2 could be visualized in 80-fold concentrated supernatants of cultures of normal keratinocytes. The levels of SLURP-1 and -2 mRNA levels in Het-1A cells decreased further after treatment of cells with NNK [6]. These preliminary results suggested that SLURPs may protect keratinocytes from malignant transformation.…”

Section: Introductionmentioning

confidence: 66%

“…The biologic effects of SLURP-1 and -2, however, may differ due to their differential binding to the nAChR subtypes expressed in each cell type. Since patients with autosomal dominant palmoplantar keratodermas, such as Mal de Meleda that features mutations of the gene encoding SLURP-1 [19], have an increased risk for developing esophageal carcinoma and other types of mucocutaneous and internal malignancies [20,21], and since the SLURP-1 and -2 levels are decreased in malignant and immortalized cells [6], mutations affecting the integrity of SLURP proteins may play a role in an increased susceptibility to cancer.…”

Section: Discussionmentioning

confidence: 99%

“…Both SLURPs diminished tumorigenic effects of tobacco nitrosamines on Het-1A cells [6]. Compared to normal keratinocytes, the levels of gene expression of SLURP-1 and -2 in Het-1A cells as well as in the malignant keratinocytes SCC-25 and FaDu are significantly decreased [6]. We could not detected either SLURP protein in the 120-fold concentrated supernatants of Het-1A cell cultures, whereas the protein bands corresponding to SLURP-1 and -2 could be visualized in 80-fold concentrated supernatants of cultures of normal keratinocytes.…”

Section: Introductionmentioning

confidence: 93%

“…We have recently demonstrated that recombinant SLURP-1 and -2 can compete with the nicotinic radioligands [ 3 H]nicotine and [ 3 H]epibatidine for binding to the keratinocyte plasma membrane [4,5]. Both SLURPs diminished tumorigenic effects of tobacco nitrosamines on Het-1A cells [6]. Compared to normal keratinocytes, the levels of gene expression of SLURP-1 and -2 in Het-1A cells as well as in the malignant keratinocytes SCC-25 and FaDu are significantly decreased [6].…”

Section: Introductionmentioning

confidence: 99%

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Overexpression of SLURP-1 and -2 alleviates the tumorigenic action of tobacco-derived nitrosamine on immortalized oral epithelial cells

Arredondo

Chernyavsky

Grando

2007

Biochemical Pharmacology

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Recent research has demonstrated that mucocutaneous epithelial cells express functional nicotinic acetylcholine receptors (nAChRs) and that tobacco-derived carcinogenic nitrosamines, such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), and SLURP (secreted mammalian Ly-6/ urokinase plasminogen activator receptor-related protein)-1 and -2 can act as non-canonical ligands of these receptors. It was found that recombinant SLURP-1 and -2 can lessen tumorigenic activity of nitrosamines. The immortalized esophageal keratinocytes (Het-1A cells) exhibit low SLURP-1 and -2 mRNA levels that decrease further after treatment with NNK. Based on these observations, we hypothesized that overexpression of full length SLURP proteins may protect Het-1A cells from malignant transformation by NNK. The Het-1A cells transfected with either SLURP-1 or -2 vector produced the highest amounts of respective proteins between 24 and 48 h, at which point they were exposed to 1 μM NNK for 24 h and their tumorigenic activities were subsequently evaluated by plating in soft agar and injecting subcutaneously to Nu/Nu mice. Transfection with either SLURP-1 or -2 cDNA in both cases significantly (p<0.05) diminished the number of colonies produced by NNK exposed cells. SLURP-1 was more efficient than SLURP-2 in abolishing the tumorigenic effect in nude mice. Thus, the anti-tumorigenic activities of SLURP-1 and -2 were demonstrated both in vitro and in vivo. The obtained results suggest that SLURP-like proteins may become useful for developing novel anti-cancer therapies.

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Section: Discussionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Overexpression of SLURP-1 and -2 alleviates the tumorigenic action of tobacco-derived nitrosamine on immortalized oral epithelial cells

Arredondo

Chernyavsky

Grando

2007

Biochemical Pharmacology

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Application of large-scale and multicohort plasma proteomics data to discover novel causal proteins in gastric cancer

Tang,

2024

Discov Onc

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Targeting Brain α7 Nicotinic Acetylcholine Receptors in Alzheimer’s Disease: Rationale and Current Status

2014

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Alzheimer's disease (AD) is the most common form of dementia among older persons. Pathognomonic hallmarks of the disease include the development of amyloid senile plaques and deposits of neurofibrillary tangles. These changes occur in the brain long before the clinical manifestations of AD (cognitive impairment in particular) become apparent. Nicotinic acetylcholine receptors (AChRs), particularly the α7 subtype, are highly expressed in brain regions relevant to cognitive and memory functions and involved in the processing of sensory information. There is strong evidence that implicates the participation of AChRs in AD. This review briefly introduces current strategies addressing the pathophysiologic findings (amyloid-β-peptide plaques, neurofibrillary tangles) and then focuses on more recent efforts of pharmacologic intervention in AD, specifically targeted to the α7 AChR. Whereas cholinesterase inhibitors such as donepezil, galantamine, or rivastigmine, together with the non-competitive N-methyl-D-aspartate receptor antagonist memantine are at the forefront of present-day clinical intervention for AD, new insights into AChR molecular pharmacology are bringing other drugs, directed at AChRs, to center stage. Among these are the positive allosteric modulators that selectively target α7 AChRs and are aimed at unleashing the factors that hinder agonist-mediated, α7 AChR channel activation. This calls for more detailed knowledge of the distribution, functional properties, and involvement of AChRs in various signaling cascades-together with the corresponding abnormalities in all these properties-to be able to engineer strategies in drug design and evaluate the therapeutic possibilities of new compounds targeting this class of neurotransmitter receptors.

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SLURP-1 and -2 in normal, immortalized and malignant oral keratinocytes

Cited by 59 publications

References 13 publications

Overexpression of SLURP-1 and -2 alleviates the tumorigenic action of tobacco-derived nitrosamine on immortalized oral epithelial cells

Overexpression of SLURP-1 and -2 alleviates the tumorigenic action of tobacco-derived nitrosamine on immortalized oral epithelial cells

Application of large-scale and multicohort plasma proteomics data to discover novel causal proteins in gastric cancer

Targeting Brain α7 Nicotinic Acetylcholine Receptors in Alzheimer’s Disease: Rationale and Current Status

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