Downregulation of nuclear expression of the p33ING1b inhibitor of growth protein in invasive carcinoma of the breast

Nouman, G S; Anderson, James; Crosier, S; Shrimankar, J; Lunec, Joseph; Angus, Brian

doi:10.1136/jcp.56.7.507

Cited by 42 publications

(38 citation statements)

References 20 publications

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“…ING1b expression was down-regulated in the gastric adenocarcinoma cell lines SGC-7901, MKN28, and MKN45 compared with the normal by nucleus-to-cytoplasm translocation in cancer cells [11,22]. Based on these results, it can be concluded that decreased expression of p33 ING1b is a common phenomenon in gastric adenocarcinoma, and this alteration might contribute to the development of gastric adenocarcinoma.…”

Section: P33mentioning

confidence: 62%

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Adenovirus-mediated expression of p33ING1b induces apoptosis and inhibits proliferation in gastric adenocarcinoma cells in vitro

Purbey

Huang

et al. 2012

Gastric Cancer

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Background Inhibitor of growth 1b (ING1b) is considered to be a class II tumor suppressor gene. Although reduced expression of p33ING1b has been reported in many human malignancies, including gastric cancers, the effect of p33ING1b on gastric cancer cells has yet to be investigated. Methods Expression of p33ING1b in gastric adenocarcinoma tissues and their adjacent non-malignant gastric mucosa, as well as in gastric adenocarcinoma cell lines and normal gastric epithelial cells, was detected by using Western blotting. Recombinant adenoviruses were prepared to mediate the ectopic expression of p33 ING1b(Ad-ING1b) and green fluorescent protein (GFP)(Ad-GFP) in the gastric adenocarcinoma cell lines, SGC-7901, MKN28, and MKN45 and the normal gastric epithelial cell line GES-1. Alterations in the proliferation and apoptosis of the cells after adenoviral infection were determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry, respectively, and cell cycle distribution was analyzed in a fluorescenceactivated cell sorter. Results Western blotting confirmed the reduced expression of p33ING1b in gastric adenocarcinoma tissues and gastric adenocarcinoma cell lines. The ectopic expression of p33ING1b mediated by Ad-ING1b resulted in decreased growth, increased apoptosis, and cell cycle arrest at the G1 phase in both benign and malignant gastric epithelial cells regardless of their p53 status. Addition of a p53 inhibitor, pifithrin-a, did not abolish the pro-apoptotic and cell cyclearresting effects of p33ING1b in p53 wild-type cells. Conclusions Down-regulation of p33ING1b might play an important role in the development of gastric adenocarcinoma. Targeted local expression of p33ING1b may offer a promising alternative therapeutic measure for gastric cancer.

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Section: P33mentioning

confidence: 62%

“…Based on reports of malignancies in the stomach [7], esophagus [8], brain [9], breast [10], blood [11,12], lung [13], liver [14], head and neck [15], lymphoid system [16], thyroid [17], and ovary [18], it can be deduced that the expression of p33…”

Section: Introductionmentioning

confidence: 99%

Adenovirus-mediated expression of p33ING1b induces apoptosis and inhibits proliferation in gastric adenocarcinoma cells in vitro

Purbey

Huang

et al. 2012

Gastric Cancer

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“…Most of these studies used primers for mRNA expression analysis An interesting finding is that one group showed the downregulation of nuclear expression of the p33ING1b protein in invasive carcinoma of the breast, acute lymphoblastic leukemia, and melanocytic lesions [55][56][57] . Reduced nuclear expression of p33ING1b both in intensity and in the proportion of cells stained was associated with enhanced cytoplasmic p33ING1b expression in a subset of cases.…”

Section: Deregulation Of Ing Family Genes In Tumorsmentioning

confidence: 99%

Inhibitor of Growth (ING) Family: An Emerging Molecular Target for Cancer Therapy

Gündüz

Beder

et al. 2008

J. Hard Tissue Biology.

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ING1 gene, the founding member of the ING tumor suppressor family, was originally identified through subtractive hybridization between normal mammary epithelial cells and breast cancer cell lines, and subsequent in vivo selection of genetic suppressor element that displayed oncogenic features. Soon after identification of ING1, four additional members of the ING family (ING2-5) were cloned and all the gene products contain a highly conserved plant homeodomain (PHD) finger motif in the carboxy (C)-terminal end, that plays important role for their function. Furthermore, ING family members contain nuclear localization signals and N-terminal sequences important in the interaction with histone acetyltransferase (HAT) and histone deacetyltransferase (HDAC) that regulate gene promoter activity within chromatin. Although exact functions of ING family genes have not been clarified, the gene products are involved in transcriptional regulation, apoptosis, cell cyle, angiogenesis and DNA repair through p53-dependent and -independent pathways. Chromosomal deletion and decreased expression of each ING family member gene in various cancer types strongly suggested products of these genes as tumor suppressor factors. Rare mutation but frequent allelic loss and epigenetic changes have been shown in ING family genes, suggesting them as a class II tumor suppressor gene. This review summarizes the known biological functions of the ING tumor suppressors and signaling related pathways.

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“…To date, inactivation and/or decreased expression of p33 ING1b have been reported in various types of cancer, including head and neck squamous cell, breast, lung, stomach, blood and brain malignancies (7,(12)(13)(14)(15)(16). To the best of our knowledge, although there are a few studies of p33…”

Section: Previous Studies Have Shown That P33mentioning

confidence: 98%

Cytoplasmic expression of p33ING1b is correlated with tumorigenesis and progression of human esophageal squamous cell carcinoma

et al. 2012

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Abstract. p33ING1b , a newly discovered candidate tumor suppressor gene and a nuclear protein, belongs to the inhibitor of growth gene family. Previous studies have shown that p33ING1b is involved in the restriction of cell growth and proliferation, apoptosis, tumor anchorage-independent growth, cellular senescence, maintenance of genomic stability and modulation of cell cycle checkpoints. Loss of nuclear p33ING1b has been observed in melanoma, seminoma, papillary thyroid carcinoma, oral squamous cell carcinoma, breast ductal cancer and acute lymphoblastic leukemia. Inactivation and/or decreased expression of p33ING1b have been reported in various types of cancer, including head and neck squamous cell, breast, lung, stomach, blood and brain malignancies. Since little is known about the clinicopathological significance of p33 ING1b in esophageal squamous cell carcinoma (ESCC), this study aimed to investigate the association of p33ING1b expression with clinicopathological variables and particularly interesting new cysteine-histidine rich protein (PINCH) in patients with ESCC. p33ING1b expression was examined by immunohistochemistry in 20 normal esophageal mucosa and in 64 ESCC specimens. The results revealed that the positive expression of p33 ING1b protein in normal squamous cells was localized in the nucleus alone and the positive rate was 95%, while in ESCCs, the positive expression was mainly in the cytoplasm, together with nuclear expression, and the positive rate was 36% (P<0.0001). Furthermore, the cases with lymph node metastasis showed a higher frequency of positive cytoplasmic expression than those without metastasis (P=0.001). The cytoplasmic expression of p33ING1b was positively related to PINCH expression (P<0.0001) in ESCC, and the cases positive for both proteins had a high lymph node metastasis rate (P=0.001). In conclusion, p33ING1b cellular compartmental shift from the nucleus to the cytoplasm may cause loss of normal cellular function and play a central role in the tumorigenesis and metastasis of ESCC.

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Downregulation of nuclear expression of the p33ING1b inhibitor of growth protein in invasive carcinoma of the breast

Cited by 42 publications

References 20 publications

Adenovirus-mediated expression of p33ING1b induces apoptosis and inhibits proliferation in gastric adenocarcinoma cells in vitro

Adenovirus-mediated expression of p33ING1b induces apoptosis and inhibits proliferation in gastric adenocarcinoma cells in vitro

Inhibitor of Growth (ING) Family: An Emerging Molecular Target for Cancer Therapy

Cytoplasmic expression of p33ING1b is correlated with tumorigenesis and progression of human esophageal squamous cell carcinoma

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