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lung neoplasms/proline
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A small proline-rich protein regulated by vitamin A in tracheal epithelial cells is induced in lung tumors.
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In cell-free translations of RNA from primary cultures of pig trachea surface epithelial cells, we observed that a 20 kD proline-rich protein (sPRP) is induced during culturing (Biochem. Biophys. Res. Commun. 1990; 172:1304-1309). Subsequently, a cDNA encoding sPRP has been cloned from pig tracheal
Up-regulation of proline-rich tyrosine kinase 2 in non-small cell lung cancer.
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Proline-rich tyrosine kinase 2 (PYK2) is a non-receptor tyrosine kinase, plays different roles in intracellular signaling pathways, that regulates a number of biological processes, such as cell proliferation, differentiation, adhesion and migration, which have been shown to correlate with tumor
Antibodies to the protein core of the small cell lung cancer workshop antigen cluster-w4 and to the leucocyte workshop antigen CD24 recognize the same short protein sequence leucine-alanine-proline.
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We recently described the identity of the small cell lung cancer (SCLC) cluster-w4 antigen and the human B cell differentiation marker CD24, a glycosylphosphatidylinositol (GPI)-anchored, highly glycosylated surface molecule of only 31-35 amino acids [15]. The specificities of three anti-cluster-w4
Apoptotic action of peroxisome proliferator-activated receptor-gamma activation in human non small-cell lung cancer is mediated via proline oxidase-induced reactive oxygen species formation.
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Peroxisome proliferator-activated receptor (PPAR)-gamma ligands have been shown to inhibit human lung cancers by inducing apoptosis and differentiation. In the present study, we elucidated the apoptotic mechanism of PPARgamma activation in human lung cancers by using a novel PPARgamma agonist,
Proline-rich tyrosine kinase 2 and its phosphorylated form pY881 are novel prognostic markers for non-small-cell lung cancer progression and patients' overall survival.
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BACKGROUND
Our previous study revealed that proline-rich tyrosine kinase 2 (Pyk2) is implicated in both anchorage-independent growth and anoikis resistance in lung cancer cells. This study aims to explore the expression and clinical significance of Pyk2 and its phosphorylated forms in non-small-cell
Cancer progression is mediated by proline catabolism in non-small cell lung cancer.
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Dysregulated metabolism contributes to cancer initiation and progression, but the key drivers of these pathways are just being discovered. Here, we report a critical role for proline catabolism in non-small cell lung cancer (NSCLC). Proline dehydrogenase (PRODH) is activated to reduce proline levels
Increased expression of proline-, glutamic acid- and leucine-rich protein PELP1 in non-small cell lung cancer.
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It has been demonstrated that estrogens are able to enhance lung tumorigenesis by estrogen receptor (ER) pathway. ER signaling is a highly complex process that requires a number of different coactivators, including proline-, glutamic acid- and leucine-rich protein-1 (PELP1). We studied PELP1
The p53 codon 72 proline allele is associated with p53 gene mutations in non-small cell lung cancer.
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The p53 gene plays a critical role in cell cycle control, the initiation of apoptosis, and in DNA repair. An Arg/Pro polymorphism at codon 72 of the p53 gene alters the ability of the p53 protein to induce apoptosis, influences the behavior of mutant p53, decreases DNA repair capacity, and may be
Plasma and tissue free amino acid profiles and their concentration correlation in patients with lung cancer.
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Variation of plasma free amino acids (PFAAs) is an essential feature of protein metabolic abnormalities in cancer patients. But there still little data about the cancer tissue free amino acid (TFAAs) profiles, including their patterns and correlations with PFAAs. To evaluate the variation in PFAAs
Etoposide (VP-16) elicits apoptosis following prolonged G2-M cell arrest in p53-mutated human non-small cell lung cancer cells.
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In this work, we described the proliferation of human non-small-cell-lung-cancer (NSCLC) cells H1437 harboring p53 alleles (proline-267) can be inhibited by low-dosage topoisomerase II inhibitor etoposide (VP-16) in vitro and in vivo. The cytotoxicity was demonstrated by prolonged cell arrest at
Total synthesis and cyclization strategy of samoamide A, a cytotoxic cyclic octapeptide rich in proline and phenlalanine isolated from marine cyanobacterium.
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Samoamide A is a cyclic octapeptide rich in proline and phenylalanine residues isolated from an American Samoa marine cyanobacterium, which exhibits potent activity against H460 human non-small-cell lung cancer cells (IC50 of 1.1 μM). The first total synthesis of samoamide A was achieved by
Correlation of the mutation of p53 gene and the polymorphism at codon 72 in smoking-related non-small cell lung cancer patients.
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The polymorphism of p53 gene at codon 72 consisting of either arginine (Arg)- or proline (Pro)-encoded allele is suggested to be associated with the susceptibility of tobacco-related lung cancer. In this study we examined the polymorphism of 224 non-small cell lung cancer (NSCLC) patients and that
The p53 codon 72 polymorphism and lung cancer risk.
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The p53 tumor suppressor gene frequently is mutated in many forms of human carcinomas. A common polymorphism occurs at codon 72 of exon 4, with two alleles encoding either arginine (CGC) or proline (CCC). This p53 polymorphism reportedly is associated with lung cancer susceptibility. However, not
Relationships of TP53 codon 72 and HRAS1 polymorphisms with lung cancer risk in an ethnically diverse population.
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Tobacco smoking is a strong cause of lung cancer. However, because only a small proportion of smokers develop the disease, other factors, including genetic susceptibility, may be important in determining lung cancer risk. Polymorphisms in the TP53 tumor suppressor gene and HRAS1 proto-oncogene have
Essential role of Pyk2 and Src kinase activation in neuropeptide-induced proliferation of small cell lung cancer cells.
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Neuropeptide hormones like bombesin/gastrin-releasing peptide, galanin or bradykinin, acting via auto and paracrine growth loops, represent the principal mitogens of small cell lung cancer (SCLC). These mitogenic neuropeptides activate G(q/11)-coupled receptors which stimulate phospholipase Cbeta
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