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lung neoplasms/phosphatase

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Protein tyrosine phosphatase PTPN3 inhibits lung cancer cell proliferation and migration by promoting EGFR endocytic degradation.

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Epidermal growth factor receptor (EGFR) regulates multiple signaling cascades essential for cell proliferation, growth and differentiation. Using a genetic approach, we found that Drosophila FERM and PDZ domain-containing protein tyrosine phosphatase, dPtpmeg, negatively regulates border cell

SHCBP1 regulates apoptosis in lung cancer cells through phosphatase and tensin homolog.

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Src homologous and collagen (SHC) SH2-binding protein 1 (SHCBP1) is a member of the SHC family, and is overexpressed in numerous types of cancer. In addition, apoptosis serves an important role in the development of cancer. The purpose of this study was to examine the effect of SHCBP1 on apoptosis

Upregulation of phosphoserine phosphatase contributes to tumor progression and predicts poor prognosis in non-small cell lung cancer patients.

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Growing evidence indicates that high phosphoserine phosphatase (PSPH) expression is associated with tumor prognosis in many types of cancers. However, the role of PSPH in non-small cell lung cancer (NSCLC) is unclear. The purpose of this study was to investigate the clinical

Molecular analysis of the protein tyrosine phosphatase gamma gene in human lung cancer cell lines.

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The protein tyrosine phosphatase gamma (PTP gamma) gene has recently been suggested as a candidate tumor suppressor gene involved in the oncogenesis of human lung and renal cancers, although no direct evidence for PTP gamma mutations has been demonstrated thus far. We explored the status of PTP

Dual Specificity Phosphatase 6 (DUSP6) Polymorphism Predicts Prognosis of Inoperable Non-Small Cell Lung Cancer after Chemoradiotherapy.

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BACKGROUND Dual-specificity phosphatase 6 (DUSP6) inactivates different target kinases to regulate cell proliferation and differentiation. Altered DUSP6 expressions or gene polymorphisms are associated with human cancer development including non-small cell lung cancer (NSCLC). DNA topoisomerase II

Inhibition of protein phosphatase 5 suppresses non-small cell lung cancer through AMP-activated kinase activation.

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Non-small cell lung cancer (NSCLC) continues to be the top cause of cancer death. To improve the treatment of lung cancer, there is necessity to identify novel oncogenes and investigate their effects on lung carcinogenesis. Protein phosphatase 5 (PP5) has long been known to regulate stress-induced

Chemotherapy agents induce tartrate-resistant acid phosphatase 5a contributing to the symptom distress in lung cancer patients.

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Tartrate-resistant acid phosphatase 5a (TRACP5a) is mainly secreted by activated macrophages in chronic inflammation. Serum TRACP5a is associated with symptom distress in lung cancer patients during chemotherapy. Therefore, this study aimed to investigate whether chemotherapy drugs modulate TRACP5a

Structural and Functional Analyses of an Allosteric EYA2 Phosphatase Inhibitor That Has On-Target Effects in Human Lung Cancer Cells.

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EYA proteins (EYA1-4) are critical developmental transcriptional cofactors that contain an EYA domain (ED) harboring Tyr phosphatase activity. EYA proteins are largely downregulated after embryogenesis but are reexpressed in cancers, and their Tyr phosphatase activity plays an important role in the

Protein phosphatase 2A (PP2A): a key phosphatase in the progression of chronic obstructive pulmonary disease (COPD) to lung cancer.

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Lung cancer (LC) has the highest relative risk of development as a comorbidity of chronic obstructive pulmonary disease (COPD). The molecular mechanisms that mediate chronic inflammation and lung function impairment in COPD have been identified in LC. This suggests the two diseases are more linked
Although luteolin is identified as a potential cancer therapeutic and preventive agent because of its potent cancer cell-killing activity, the molecular mechanisms by which its cancer cell cytotoxicity is achieved have not been well elucidated. In this report, luteolin-induced cellular signaling was
Bone scan (BS) and serum alkaline phosphatase (ALP) concentration are used to detect bone metastasis in malignancy, although whole-body fluoro-D-glucose positron emission tomography computed tomography (FDG PET/CT) is being used increasingly. But BS is still used for the detection of metastatic bone
A new losartan [2-butyl-5-chloro-3-[[4-[2-(2H-tetrazol-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol zinc(II) complex [Zn(Los)Cl], was synthesized and characterized. The crystal structure was determined by x-ray diffraction methods. When aqueous solutions of the ligand and the metal were mixed,
Transforming growth factor β (TGFβ) causes the acquisition of epithelial-mesenchymal transition (EMT). Although the tumor suppressor gene PTEN (phosphatase and tensin homologue deleted from chromosome 10) can negatively regulate many signaling pathways activated by TGFβ, hyperactivation of these

Serum acid phosphatase activities in patients with lung cancer: a biochemical and immunohistochemical analysis of 25 cases.

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A series of 25 cases of lung cancer are presented in which total (TAcP) and nonprostatic serum acid phosphatase (NPAcP) activities were measured. Of these cases, 36% had raised TAcP and NPAcP activities in their serum. However, the serum activities of TAcP and NPAcP did not correlate with either the

[Expression of protein-tyrosine-phosphatase 1B in non-small-cell lung cancer and its prognostic significance].

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OBJECTIVE To explore the protein-tyrosine-phosphatase 1B (PTP1B) expression and its prognostic significance in non-small-cell lung cancer (NSCLC). METHODS Immunohistochemical method of EnVision was applied to investigate the expression of PTP1B in lung specimens from 63 cases with NSCLC and 9 cases
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