Increased expression of epidermal fatty acid binding protein, cofilin, and 14-3-3-σ (stratifin) detected by two-dimensional gel electrophoresis, mass spectrometry and microsequencing of drug-resistant human adenocarcinoma of the pancreas

Sinha, Pranav; Hütter, Gero; Köttgen, E.; Dietel, Manfred; Schadendorf, Dirk; Lage, Hermann

doi:10.1002/(sici)1522-2683(19991001)20:14<2952::aid-elps2952>3.0.co;2-h

Cited by 131 publications

(72 citation statements)

References 38 publications

(35 reference statements)

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“…Loss of 14-3-3 σ expression has been reported in primary gastric (Suzuki et al, 2000), hepatocellular (Iwata et al, 2000), and breast adenocarcinoma (Jeanteur, 2000). In contrast, 14-3-3 σ expression is up-regulated in head and neck squamous cell carcinoma and in chemoresistant pancreatic adenocarcinoma cells (Sinha et al, 1999). In our study, 14-3-3 σ was overexpressed in cholangiocarcinoma.…”

Section: Discussioncontrasting

confidence: 63%

The Clinicopathological and Prognostic Impact of 14-3-3 Protein Isoforms Expression in Human Cholangiocarcinoma by Immunohistochemistry

Liu²,

Luan³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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The 14-3-3 proteins are highly conserved, ubiquitous molecules involved in a variety of biologic phenomena, such as cell cycle control, and apoptosis. However, their expression in cholangiocarcinoma has not been previously characterized. In this paper, immunohistochemistry using specific anti-14-3-3 monoclonal antibodies was performed on formalin-fixed;, paraffin embedded archival tissue from 86 patients of cholangiocarcinoma. We also examined the correlation between expression and survival rate and clinicopathologic factors such as tumor location, tumor size, pathologic differentiation, lymphatic permeation, lymph node metastasis, and tumor stage. Positive 14-3-3 proteins expression was observed for 6 isoforms (β, σ, γ, θ, δ, η) of these proteins in 86 patients of cholangiocarcinoma. β and σ isoform immunoreactivity was correlated with lymph node metastasis, tumor stage and patients' survival rate. In addition, δ isoform immunoreactivity showed trends with tumor location, tumor size, pathologic differentiation and tumor stage, while the θ isoform was correlated with pathologic differentiation. These results indicated that upregulated expression of some isoforms of 14-3-3 may be a common mechanism for evading apoptosis in cholangiocarcinoma, so that targeting 14-3-3 may be a novel promising strategy for the treatment of this tumor.

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Section: Discussioncontrasting

confidence: 63%

The Clinicopathological and Prognostic Impact of 14-3-3 Protein Isoforms Expression in Human Cholangiocarcinoma by Immunohistochemistry

Liu²,

Luan³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…25 E-FABP expression is increased in drug-resistant human adenocarcinoma of the pancreas. 26 It is suggested to be a metastasis-inducing gene in prostate cancer through vegf (vascular endothelial growth factor) gene up-regulation. 27,28 With regard to A-FABP, the protein on which we have focused our attention, its expression is also down-regulated in breast cancer cell lines in comparison with breast normal cell lines.…”

Section: Discussionmentioning

confidence: 99%

A‐FABP, a candidate progression marker of human transitional cell carcinoma of the bladder, is differentially regulated by PPAR in urothelial cancer cells

Boiteux

Lascombe

Roche

et al. 2009

Intl Journal of Cancer

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Superficial pT1 bladder tumors are characterized by a high risk of recurrence and progression in grade and stage. Few studies provided evidence that loss of adipocyte-fatty acid binding protein (A-FABP) expression was associated with bladder cancer progression. A-FABP is a lipid binding protein playing a role in intracellular lipid transport and metabolism, as well as in signal transduction. We reported from bladder tumors that decrease of A-FABP transcript level significantly correlated to tumor stage and to histologic grade (p < 0.05). Namely, in poor prognosis high grade pT1 tumors there was a loss of A-FABP expression compared to good prognosis tumors suggesting that re-expression of A-FABP could be a therapeutic approach in early stage bladder cancer to prevent disease progression. We demonstrated for the first time that this marker is upregulated by Peroxisome Proliferator-Activated Receptor (PPAR) a, b and c in T24 cells (derived from an undifferentiated grade III carcinoma) and only by PPARb in RT4 cells (derived from a well differentiated grade I papillary tumor). This effect occurred through a PPAR-dependent transcriptional mechanism without modifying mRNA stability and interestingly required de novo protein synthesis. Data as a whole suggest a prognostic significance of A-FABP in bladder cancer outcome and the potential utility of overexpression of this protein by PPAR agonists open up new perspectives in the treatment of bladder cancer.

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“…Although their complete tertiary structure, gene organization, and binding properties are known, the functional aspects of these proteins are still undergoing investigation. FABP's protective role is evidenced by: (1) controlling the availability of free fatty acids and their metabolites in the cytosol, and which prevents their cellular toxicity 14,15 ; (2) modulating the interaction of fatty acids with nuclear receptors 16 ; (3) sequestrating or removing cytotoxic drugs 17 ; and (4) trapping or scavenging ROS. 4,[18][19][20][21] However, no significant protective effects of FABP had been observed for chemical-induced anoxia or transport of intracellular fatty acid using the FABP-transfected kidney cell (MDCK) model.…”

Section: Discussionmentioning

confidence: 99%

Antioxidative function of L-FABP in L-FABP stably transfected Chang liver cells

et al. 2005

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C ellular oxidative stress is one of the factors responsible for the propagation of liver diseases, such as hepatitis, cirrhosis, and hepatoma. 1 Several primary antioxidant defense systems such as superoxide dismutase (SOD), catalase, glutathione (GSH), and glutathione peroxidase are present intracellularly. These systems scavenge reactive oxygen species (ROS) such as hydrogen peroxide, superoxide, lipid peroxides, and free radicals. Exposure to oxidative stress may, however, deplete the cellular antioxidant capacity. Therefore, other antioxidant defense systems are expected to play an important role in oxidative stress.Liver fatty acid binding protein (L-FABP) is a 14-kd protein found abundantly in the cytoplasm and the nucleus of hepatocytes. 2,3 L-FABP is very likely to be an effective endogenous antioxidant, because it has high affinity and capacity to bind long-chain fatty acid oxidation products. 4,5 Hepatocyte L-FABP concentration could be as high as 0.4 mmol/L, 6 and it contains a large number of reducing amino acid residues (1 cysteine and 7 methionine residues) in its molecular structure. With an accessible volume enclosed by the molecular surface of L-FABP of 28,600 Å 3,7 the concentration of total methionine residues in L-FABP could be as high as approximately 400 mmol/L. Methionine and cysteine amino acids are regarded as cellular scavengers of activated xenobiotics and

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Increased expression of epidermal fatty acid binding protein, cofilin, and 14-3-3-σ (stratifin) detected by two-dimensional gel electrophoresis, mass spectrometry and microsequencing of drug-resistant human adenocarcinoma of the pancreas

Cited by 131 publications

References 38 publications

The Clinicopathological and Prognostic Impact of 14-3-3 Protein Isoforms Expression in Human Cholangiocarcinoma by Immunohistochemistry

The Clinicopathological and Prognostic Impact of 14-3-3 Protein Isoforms Expression in Human Cholangiocarcinoma by Immunohistochemistry

A‐FABP, a candidate progression marker of human transitional cell carcinoma of the bladder, is differentially regulated by PPAR in urothelial cancer cells

Antioxidative function of L-FABP in L-FABP stably transfected Chang liver cells

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