Changes in the cellular distribution of Lipocortin-1 (Annexin-1) in C6 glioma cells after exposure to dexamethasone

McLeod, Julie; Goodall, A. Myfanway; Jelic, Petra; Bolton, Christopher

doi:10.1016/0006-2952(95)00234-q

Cited by 22 publications

(18 citation statements)

References 42 publications

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“…This suggests that ANXA1 is inherently an antiproliferative protein up-regulated to counter the overactivation of proliferative signals induced by 17h-E. This is similar to previous studies where ANXA1 was shown to regulate the proliferation of RAW macrophages (11) and mediated steroid-induced growth arrest in lung cancer cells (21). We have shown in this study that ANXA1 siRNAtransfected cells are unable to sustain prolonged ERK1/2 activation after 72 h when treated with high 17h-E doses, suggesting that ANXA1 is required for constitutive ERK1/2 activation observed in cells treated with high 17h-E concentrations over a prolonged period.…”

Section: Discussionsupporting

confidence: 88%

“…Evidence associating ANXA1 expression and function with glucocorticoid treatment is indisputable (21)(22)(23)28). This induction of ANXA1 expression can be blocked by the glucocorticoid receptor antagonist RU486 (29).…”

Section: Discussionmentioning

confidence: 99%

“…This, coupled with the considerable time lag between drug administration and the observable increase in ANXA1 levels, suggests that the induction of ANXA1 expression by 17h-E is a result of gene transcription. In addition, as ANXA1 phosphorylation on Tyr 21 has been proposed to be a prerequisite for its proliferative effects in hepatic cancer cells in vitro and in vivo (15), ANXA1 phosphorylation was also examined in MCF-7 cells using immunoprecipitation of ANXA1 and probing with phosphotyrosine, threonine, and serine antibodies. However, no changes in ANXA1 phosphorylation after 17h-E treatment were observed (data not shown).…”

Section: Effects Of 17b-e On Anxa1 Expressionmentioning

confidence: 99%

“…Its endogenous function is still under debate, but most have focused on its anti-inflammatory actions, shown to mimic those of glucocorticoids (20). ANXA1 is glucocorticoid-inducible (21)(22) through transcriptional activation of the glucocorticoid response element as well as through rapid de novo synthesis (23). Glucocorticoids were not effective in ANXA1-deficient mice in two models of acute inflammation, suggesting that ANXA1 could be the endogenous protein mediating the anti-inflammatory actions of glucocorticoids (24).…”

Section: Introductionmentioning

confidence: 99%

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Annexin-1 Regulates Growth Arrest Induced by High Levels of Estrogen in MCF-7 Breast Cancer Cells

Ang¹,

Nguyen²,

Sim³

et al. 2009

Molecular Cancer Research

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Effects Of 17b-e On Anxa1 Expressionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Annexin-1 Regulates Growth Arrest Induced by High Levels of Estrogen in MCF-7 Breast Cancer Cells

Ang¹,

Nguyen²,

Sim³

et al. 2009

Molecular Cancer Research

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“…49 Involvement of AnxI in cell surface changes induced by steroids has been demonstrated in C6 rat astrocytoma cells. 50,51 AnxI is also involved in the regulation of prostaglandins and nitric oxide. 52,53 Previous associations of AnxI with tumor progression were found with 2D electrophoresis in studies that showed its differential expression in chemoresistant gastric carcinoma cell lines, 54 a cell line established from a metastasis compared to primary squamous carcinoma of the larynx, 55 and in tissue containing metastasized breast carcinoma cells compared to normal tissue.…”

mentioning

confidence: 99%

Proteomic characterization of harvested pseudopodia with differential gel electrophoresis and specific antibodies

Beckner

Chen

et al. 2005

Laboratory Investigation

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Malignant gliomas (astrocytomas) are lethal tumors that invade the brain. Invasive cell migration is initiated by extension of pseudopodia into interstitial spaces. In this study, U87 glioma cells formed pseudopodia in vitro as cells pushed through 3 lm pores of polycarbonate membranes. Harvesting pseudopodia in a novel two-step method provided material for proteomic analysis. Differences in the protein profiles of pseudopodia and whole cells were found using differential gel electrophoresis (DIGE) and immunoblotting. Proteins from twodimensional (2D) gels with M R 's of 20-100 kDa and pI's of 3.0-10.0 were identified by peptide mass fingerprinting analysis using mass spectrometry. For DIGE, lysates of pseudopodia and whole cells were each labeled with electrophilic forms of fluorescent dyes, Cy3 or Cy5, and analyzed as mixtures. Analysis was repeated with reciprocal labeling. Differences in protein distributions were detected by manual inspection and computer analysis. Topographical digital maps of the scanned gels were used for algorithmic spot matching, normalization of background, quantifying spot differences, and elimination of artifacts. Pseudopodial proteins in Coomassie-stained 2D gels included isoforms of glycolytic enzymes as the largest group, seven of 24 proteins. Peptide mass fingerprint analysis of DIGE gels demonstrated increased isoforms of annexin (Anx) I, AnxII, enolase, pyruvate kinase, and aldolase, and decreased mitochondrial manganese superoxide dismutase and transketolase in pseudopodia. Specific antibodies showed restricted immunoreactivity of the hepatocyte growth factor (HGF) a chain to pseudopodia, indicating localization of its active form. Met (the HGF receptor), actin, and total AnxI were increased in pseudopodial lysates on immunoblots. Increased constituents of the pseudopodial proteome in glioma cells, identified in this study as actin, HGF, Met, and isoforms of AnxI, AnxII, and several glycolytic enzymes, represent therapeutic targets to consider for suppression of tumor invasion.

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Hormones, Adrenal‐Cortical

Avery

Woolfrey

2000

Kirk-Othmer Encyclopedia of Chemical Technology

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Adrenal‐cortical hormones, following the introduction of cortisone and hydrocortisone nearly a half‐century ago, have continued to be the drug of choice in treatment of afflictions ranging from skin rash to severe acute inflammatory disorders and are now included in many other therapeutic regimes. The adrenal cortex releases both mineralocorticoids and glucocorticoids; the latter influence carbohydrate and protein metabolism, and the former regulate sodium reabsorption in the kidney. Moreover, corticosteroids and their metabolites were early noted to possess powerful antiinflammatory and immunomodulatory properties, leading to a massive increase in research in the area of steroid synthesis and physiology, imparting great impetus to the development of synthetic steroids. These exhibited activities far greater than those of the natural hormones, thereby opening the way to development of many more active antiinflammatory agents. Corticosteroids are commonly used as topicals for the suppression of symptoms, including inflammation. Though they are rarely considered curative, many diseases respond well symptomatically to treatment with them, eg, liver disease, acute spinal cord injury, organ transplants, GI diseases, and dermatologic diseases, among others. Mineralocorticoid therapy is less common. Progesterone is the key intermediate in both mineralocorticoid and glucocorticoid biosynthesis. Cortisol and aldosterone are results of oxidations of progesterone. The major metabolic transformations of the adrenal cortical hormones generally follow the metabolism of cortisol. The effects of adrenal‐cortical steroids are thought to result from their interaction with intracellular receptors; these are the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR). The primary structure of the GR has been identified as a 795 residue protein; a significant amount of 3‐D structure elucidation of the GR has been made. The process by which adrenocortical steroids impart their action is based on the action of the steroid on a receptor (GR or MR). The use of glucocorticoids leads to antiinflammatory effects by first controlling gene expression, which subsequently leads to the synthesis and/or suppression of inflammation regulatory proteins. Microorganisms are available which transform progesterone and cortisone into steroids. These steroids surpass their parent hormones in antirheumatic and antillergic activity and produce lower levels of side effects. When tested in patients with rheumatoid arthritis, fludrocortisone acetate proved to be 10 times more potent than hydrocortisone acetate. Triamcinolone possesses high glucocorticoid and antiinflammatory activity and is almost entirely devoid of salt‐retaining activity. 2α‐Methyl‐9α‐fluorocortisol has been reported to show enhanced glucocorticoid activity and greatly enhanced mineralocorticoid activity, surpassing aldosterone in sodium‐retaining and potassium‐excreting potency. Hyperaldosteronism is accompanied by elevation of blood pressure and can be treated with an aldosterone antagonist, eg, spironolactone. Antagonists of glucocorticoid and mineralocorticoid activity have found increased use in the treatment of hypertension. The most clinically useful GR antagonist is RU‐486.

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Changes in the cellular distribution of Lipocortin-1 (Annexin-1) in C6 glioma cells after exposure to dexamethasone

Cited by 22 publications

References 42 publications

Annexin-1 Regulates Growth Arrest Induced by High Levels of Estrogen in MCF-7 Breast Cancer Cells

Annexin-1 Regulates Growth Arrest Induced by High Levels of Estrogen in MCF-7 Breast Cancer Cells

Proteomic characterization of harvested pseudopodia with differential gel electrophoresis and specific antibodies

Hormones, Adrenal‐Cortical

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