Decreased annexin I expression in prostatic adenocarcinoma and in high‐grade prostatic intraepithelial neoplasia

Patton, Kurt T.; Chen, H. M.; Joseph, Loren; Yang, Ximing J.

doi:10.1111/j.1365-2559.2005.02300.x

Cited by 52 publications

(36 citation statements)

References 14 publications

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“…Annexin I is involved in many biological functions such as cell differentiation[36], anti-inflammation[37], apoptosis[38], and cell growth[39], and acts as a stress protein[40]. Decrease or loss of annexin I expression in a number of cancer types including breast[41], prostate[42,43], lymphoma[44], esophageal[42,45] and bladder[4] cancers has been reported recently, indicating annexin I may serve as a useful marker of cancer development and progression. Annexin I was also reported to be degraded in bronchoalveolar lavage fluid from patients with cystic fibrosis, and is therefore considered to be related to lung inflammation[46].…”

Section: Discussionmentioning

confidence: 99%

Effects of green tea extract on lung cancer A549 cells: Proteomic identification of proteins associated with cell migration

Yang

Jin

et al. 2009

Proteomics

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Green tea polyphenols exhibit multiple antitumor activities, and the mechanisms of action are not completely understood. Previously, we reported that green tea extract (GTE)-induced actin remolding is associated with increased cell adhesion and decreased motility in A549 lung cancer cells. To identify the cellular targets responsible for green tea-induced actin remodeling, we performed 2-DE LC-MS/MS of A549 cells before and after GTE exposure. We have identified 14 protein spots that changed in expression (!2-fold) after GTE treatment. These proteins are involved in calcium-binding, cytoskeleton and motility, metabolism, detoxification, or gene regulation. In particular we found upregulation of several genes that modulate actin remodeling and cell migration, including lamin A/C. Our data indicated that GTE-induced lamin A/C upregulation appears to be at the transcriptional level and the increased expression results in the decrease in cell motility, as confirmed by siRNA. The result of the study demonstrates that GTE alters the levels of many proteins involved in growth, motility and apoptosis of A549 cells and their identification may explain the multiple antitumor activities of GTE.

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Section: Discussionmentioning

confidence: 99%

Effects of green tea extract on lung cancer A549 cells: Proteomic identification of proteins associated with cell migration

Yang

Jin

et al. 2009

Proteomics

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“…A great deal of controversy still exists regarding the expression of ANXA1 in different types of cancers. Several studies have shown that the expression of ANXA1 is down-regulated in cervical, breast, head and neck, or thyroid cancer [16], [17], [18], [19], [20]. On the other hand, there is also some evidence that an increase of ANXA1 expression has occurred in other types of cancer, such as pancreatic, esophageal, and gastric carcinomas [21], [22], [23].…”

Section: Introductionmentioning

confidence: 99%

Sodium Butyrate Induces Growth Inhibition and Apoptosis in Human Prostate Cancer DU145 Cells by Up-Regulation of the Expression of Annexin A1

Gao

Guo

et al. 2013

PLoS ONE

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BackgroundSodium butyrate, a histone deacetylase inhibitor, has emerged as a promising anticancer drug for multiple cancers. Recent studies have indicated that sodium butyrate could inhibit the progression of prostate cancer; however, the exact mechanism is still unclear. The aim of this study was to investigate the mechanism of sodium butyrate action in prostate cancer DU145 cells.MethodsThe inhibitory effects of NaB on cell growth were detected by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrrazolium bromide assay. Cell apoptosis was determined by flow cytometric analysis of DU145 cells stained with annexin V and PI. Hoechst 33258 and fluorescence microscopes were used to observe the nuclear morphology of DU145 cells after treatment with NaB. ANXA1 knockdown cells were established through transfection with ANXA1 siRNA. ANXA1 mRNA levels were measured by qRT-PCR. Bcl-2, Bax, ANXA1, ERK1/2 and pERK1/2 were detected by western blot.ResultsNaB significantly inhibited the growth and induction apoptosis of DU145 and PC3 cells in a dose-dependent manner. Expression of the anti-apoptosis gene Bcl-xl and Bcl-2 in DU145 cells are decreased and expression of the pro-apoptosis gene Bax and Bak increased after NaB treatment. Further studies have demonstrated that NaB up-regulated the expression of ANXA1 and that the tumor inhibition action of NaB was reduced markedly through knockdown of the ANXA1 gene in DU145 cells. Moreover, the siANXA1 cells showed that cell proliferation increased and cell apoptosis was induced by the inactivation of extracellular regulated kinase (ERK).ConclusionOur results support a significant correlation between NaB functions and ANXA1 expression in prostate cancer, and pave the way for further studying the molecular mechanism of NaB actions in cancers.

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“…Together, these studies suggest that dysregulation of annexin A1 loss is important in oesophageal tumour development and progression. Other types of cancer in which the expression of annexin A1 has been shown to be altered include pancreatic adenocarcinoma (Bai et al, 2004), where it was found to show increased expression in the majority of tumours, renal cell carcinoma (Zimmermann et al, 2007), prostate adenocarcinoma (Patton et al, 2005), breast cancer (Shen et al, 2006) and B-cell non-Hodgkin's lymphoma (Vishwanatha et al, 2004).…”

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confidence: 99%

Characterisation and protein expression profiling of annexins in colorectal cancer

Carpenter²,

et al. 2007

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The annexins are family of calcium-regulated phospholipid-binding proteins with diverse roles in cell biology. Individual annexins have been implicated in tumour development and progression, and in this investigation a range of annexins have been studied in colorectal cancer. Annexins A1, A2, A4 and A11 were identified by comparative proteomic analysis to be overexpressed in colorectal cancer. Annexins A1, A2, A4 and A11 were further studied by immunohistochemistry with a colorectal cancer tissue microarray containing primary and metastatic colorectal cancer and also normal colon. There was significant increase in expression in annexins A1 (P ¼ 0.01), A2 (Po0.001), A4 (Po0.001) and A11 (Po0.001) in primary tumours compared with normal colon. There was increasing expression of annexins A2 (P ¼ 0.001), A4 (P ¼ 0.03) and A11 (P ¼ 0.006) with increasing tumour stage. An annexin expression profile was identified by k-means cluster analysis, and the annexin profile was associated with tumour stage (P ¼ 0.01) and also patient survival. Patients in annexin cluster group 1 (low annexin expression) had a better survival (log rank ¼ 5.33, P ¼ 0.02) than patients in cluster group 2 (high annexins A4 and A11 expression). In conclusion, this study has shown that individual annexins are present in colorectal cancer, specific annexins are overexpressed in colorectal cancer and the annexin expression profile is associated with survival.

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Decreased annexin I expression in prostatic adenocarcinoma and in high‐grade prostatic intraepithelial neoplasia

Cited by 52 publications

References 14 publications

Effects of green tea extract on lung cancer A549 cells: Proteomic identification of proteins associated with cell migration

Effects of green tea extract on lung cancer A549 cells: Proteomic identification of proteins associated with cell migration

Sodium Butyrate Induces Growth Inhibition and Apoptosis in Human Prostate Cancer DU145 Cells by Up-Regulation of the Expression of Annexin A1

Characterisation and protein expression profiling of annexins in colorectal cancer

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