Expression of pS2 in prostate cancer correlates with grade and Chromogranin A expression but not with stage

Ather, M Hammad; Abbas, Farhat; Faruqui, Nuzhat; Israr, Muhammad; Pervez, Shahid

doi:10.1186/1471-2490-4-14

Cited by 12 publications

(12 citation statements)

References 16 publications

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“…TFF1 is a prognostic marker for breast and other cancers (29,30). In agreement with previous studies, we show that the TFF1 is stimulated by estradiol and TPA in MCF-7 cells.…”

Section: Discussionsupporting

confidence: 80%

Chromatin Modification of the Trefoil Factor 1 Gene in Human Breast Cancer Cells by the Ras/Mitogen-Activated Protein Kinase Pathway

Espino

et al. 2006

Cancer Research

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Histone H3 phosphorylation is a downstream response to activation of the Ras/mitogen-activated protein kinase (MAPK) pathway. This modification is thought to have a role in chromatin remodeling and in the initiation of gene transcription. In MCF-7 breast cancer cells, we observed that phosphorylated histone H3 (phospho-H3) at Ser 10 but not Ser 28 increased with phorbol ester (12-O-tetradecanoylphorbol-13-acetate, TPA) treatment. Although phosphorylated extracellular signal-regulated kinase 1/2 levels in these cells cultured under estradiol deplete and replete conditions displayed no change, a significant induction was observed after TPA treatment. Furthermore, whereas both estradiol and TPA increased trefoil factor 1 (TFF1) mRNA levels in these cells, only TPA-induced and not estradiol-induced TFF1 expression was inhibited by the H3 kinase mitogen and stress activated protein kinase (MSK) inhibitor H89 and MAPK kinase inhibitor UO126, showing the involvement of the Ras/ MAPK following TPA induction. Mutation of the activator protein 1 (AP-1) binding site abrogated the TPA-induced transcriptional response of the luciferase reporter gene under the control of the TFF1 promoter, showing the requirement for the AP-1 site. In chromatin immunoprecipitation assays, estradiol treatment resulted in the association of the estrogen receptor-A (ERA) and acetylated H3 with the TFF1 promoter. The levels of phospho-H3 and MSK1 associated with the TFF1 promoter were moderately increased. In the presence of TPA, whereas ERA was not bound to the promoter, a strong association of acetylated and/or phospho-H3, MSK1, and c-Jun was observed. These results show that although both stimuli lead to TFF1 gene activation, estradiol and TPA exert their effects on TFF1 gene expression by different mechanisms.

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“…TFF1 is a prognostic marker for breast and other cancers (29,30). In agreement with previous studies, we show that the TFF1 is stimulated by estradiol and TPA in MCF-7 cells.…”

Section: Discussionsupporting

confidence: 80%

Chromatin Modification of the Trefoil Factor 1 Gene in Human Breast Cancer Cells by the Ras/Mitogen-Activated Protein Kinase Pathway

Espino

et al. 2006

Cancer Research

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“…Commercial goat polyclonal Abs for COX ETC subunits II and III (Santa Cruz Biotechnology), mouse mAbs for COX ETC subunit I, and 17-kDa subunit of complex I (Mitosciences and Molecular Probes, respectively) were used as primary Abs, and respective HRP-conjugated secondary Abs (Sigma-Aldrich) were used for IHC (26). Negative control experiments were performed by using either ␥-globulin as isotype controls (Jackson ImmunoResearch Laboratories) or omission of primary Abs.…”

Section: Immunohistochemistry (Ihc)mentioning

confidence: 99%

Mitochondrial Structural Changes and Dysfunction Are Associated with Experimental Allergic Asthma

Mabalirajan

Dinda

Kumar

et al. 2008

The Journal of Immunology

200

234

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An imbalance between Th1 and Th2 immune response is crucial for the development of pathophysiological features of asthma. A Th2-dominant response produces oxidative stress in the airways, and it is thought to be one of the crucial components of asthma pathogenesis. Although mitochondrion is a crucial organelle to produce endogenous reactive oxygen species, its involvement in this process remains unexplored as yet. We demonstrate in this study that OVA-induced experimental allergic asthma in BALB/c mice is associated with mitochondrial dysfunction, such as reduction of cytochrome c oxidase activity in lung mitochondria, reduction in the expression of subunit III of cytochrome c oxidase in bronchial epithelium, appearance of cytochrome c in the lung cytosol, decreased lung ATP levels, reduction in the expression of 17 kDa of complex I in bronchial epithelium, and mitochondrial ultrastructural changes such as loss of cristae and swelling. However, there was no change in the expression of subunits II and III of cytochrome c oxidase. Interestingly, administration of IL-4 mAb reversed these mitochondrial dysfunction and structural changes. In contrast, IFN-γ mAb administration neither reversed nor further deteriorated the mitochondrial dysfunction and structural changes compared with control asthmatic mice administered with isotypic control Ab, although airway hyperresponsiveness deteriorated further. These results suggest that mitochondrial structural changes and dysfunction are associated with allergic asthma. These findings may help in the development of novel drug molecules targeting mitochondria for the treatment of asthma.

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“…A large number of studies indicate that TFF1 expression is absent or occurs at low levels in nonmalignant pancreatic and prostate tissues. Elevated expression levels of TFF1 are frequently observed in pancreatic and prostate malignancies (19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31), suggesting that TFF1 may be involved in the tumorigenesis of these cancers. These data are not, however, sufficiently convincing because of the lack of strict statistical analysis in some studies and the reduced statistical power in others with small sample sizes.…”

Section: Tff1 Expressionmentioning

confidence: 99%

Trefoil factor 1 acts to suppress senescence induced by oncogene activation during the cellular transformation process

Radiloff

Wakeman²,

Feng³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Senescence is a cellular stress response characterized by persistent cell growth arrest under various stress conditions, including oncogene activation or tumor suppressor loss, which functions as a critical barrier that must be overcome to allow the progression from a precancerous or preinvasive lesion to a malignant tumor. Trefoil factor 1 (TFF1) is a secreted protein involved in maintaining the gastrointestinal epithelium by serving a tumor-suppressive role; however, TFF1 is overexpressed in several types of cancers. Here we report that TFF1 acts as a promoter of tumorigenesis in the context of prostate and pancreatic cancers by suppressing oncogene-induced senescence (OIS). Expression of TFF1 allows human prostate epithelial cells to escape OIS caused by the activated Ras oncogene or by reduced expression of the tumor suppressor PTEN, in part by the involvement of the EGF receptor-mediated pathway and inhibition of the expression of the cell cycle regulator p21. Without intrinsic promitogenic activity TFF1 may act in both autocrine and paracrine manners to enable cells to undergo the initial transformation and expansion against the restrictive microenvironment during early stage tumorigenesis. Taken together, our findings identify TFF1 as a soluble factor designed to act mainly to antagonize the OIS process to accelerate tumorigenesis.

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Expression of pS2 in prostate cancer correlates with grade and Chromogranin A expression but not with stage

Cited by 12 publications

References 16 publications

Chromatin Modification of the Trefoil Factor 1 Gene in Human Breast Cancer Cells by the Ras/Mitogen-Activated Protein Kinase Pathway

Chromatin Modification of the Trefoil Factor 1 Gene in Human Breast Cancer Cells by the Ras/Mitogen-Activated Protein Kinase Pathway

Mitochondrial Structural Changes and Dysfunction Are Associated with Experimental Allergic Asthma

Trefoil factor 1 acts to suppress senescence induced by oncogene activation during the cellular transformation process

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