Frequent loss of PDCD4 expression in human glioma: Possible role in the tumorigenesis of glioma

Gao, Fei; Zhang, Pin; Chui-xian, Zhou; Li, Jianfeng; Wang, Qun; Zhu, Faliang; Ma, Chao; Sun, Wei; Zhang, Lining

doi:10.3892/or.17.1.123

Cited by 63 publications

(89 citation statements)

References 21 publications

(27 reference statements)

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“…The expression of the gene is modulated by many factors, including interleukins (9), retinoid (10), 12-O-tetradecanoylphorbol 13 acetate (TPA) (11,12), transforming growth factor (TGF)-β1 (13), growth factors (14,15), topoisomerase inhibitors (5) and the transcription factor myb (6,7), and is up-regulated in association with apoptosis (4,13). PDCD4 expression has been shown to be suppressed in many tumor tissues, such as lung cancers (16), pancreatic cancers (17), hepatocellular carcinomas (13), colon cancers (18), skin carcinomas (15), breast cancers (19) and glioma tissues (20). The PDCD4 protein levels are often not correlated with the mRNA levels in certain tumor tissues (16,20), indicating that PDCD4 expression is controlled at both the transcription and post-transcription levels.…”

Section: Introductionmentioning

confidence: 99%

“…PDCD4 expression has been shown to be suppressed in many tumor tissues, such as lung cancers (16), pancreatic cancers (17), hepatocellular carcinomas (13), colon cancers (18), skin carcinomas (15), breast cancers (19) and glioma tissues (20). The PDCD4 protein levels are often not correlated with the mRNA levels in certain tumor tissues (16,20), indicating that PDCD4 expression is controlled at both the transcription and post-transcription levels. Recently, it was reported that microRNA-21 targets PDCD4/Pdcd4 mRNA, thereby regulating PDCD4 expression (reviewed in refs.…”

Section: Introductionmentioning

confidence: 99%

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Expression patterns of the tumor suppressor PDCD4 and correlation with β-catenin expression in gastric cancers

Kakimoto

Shiraishi²,

Iwakiri³

et al. 2011

Oncol Rep

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Abstract. The expression patterns of PDCD4, a tumor suppressor, and β-catenin were immunohistologically investigated in gastric carcinoma tissues. In normal gastric tissues, PDCD4 was strongly expressed in the cell nuclei, but weakly expressed in the cytoplasm. In gastric adenocarcinoma tissues, nuclear PDCD4 expression was decreased, while cytoplasmic PDCD4 expression was unchanged or somewhat increased. In gastric signet ring cell carcinoma tissues, PDCD4 expression patterns were different from the expression patterns of the adenocarcinoma tissues, and PDCD4 was localized in the nuclei of the carcinoma cells as a belt in the middle of the epithelial layer. The nuclear localization of PDCD4 in the adenocarcinoma tissues was correlated with the membrane localization of β-catenin, the activation of which stimulates invasion of colon cancer cells. PDCD4 expression was correlated with β-catenin expression in gastric carcinoma cell lines, but not with E-cadherin, as the binding partner in the cell membrane.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Expression patterns of the tumor suppressor PDCD4 and correlation with β-catenin expression in gastric cancers

Kakimoto

Shiraishi²,

Iwakiri³

et al. 2011

Oncol Rep

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“…These findings indicate PDCD4 has tumor suppressor activity. Loss of PDCD4 expression has been found in several types of human cancer cell lines [14], primary lung cancer [15], primary pancreatic cancer [16], hepatocarcinoma [17], colon carcinoma [18], and gliomas [19]. Recently, Wen et al [20] reported that compared to normal breast epithelial cells, PDCD4 expression is only slightly decreased in ductal carcinoma in situ samples, but is markedly decreased in invasive ductal carcinoma samples.…”

Section: Introductionmentioning

confidence: 99%

Programmed Cell Death 4 inhibits breast cancer cell invasion by increasing Tissue Inhibitor of Metalloproteinases-2 expression

Nieves-Alicea

Colburn

Simeone

et al. 2008

Breast Cancer Res Treat

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High levels of the cyclooxygenase-2 (COX-2) protein have been associated with invasion and metastasis of breast tumors. Both prostaglandin E 2 (PGE 2 ) and interleukin-8 (IL-8) have been shown to mediate the invasive activity of COX-2 in breast cancer cells. Here we expand these studies to determine how COX-2 uses PGE 2 and IL-8 to induce breast cancer cell invasion. We demonstrated that PGE 2 and IL-8 decreased the expression of the tumor suppressor protein Programmed Cell Death 4 (PDCD4). We hypothesized that suppression of PDCD4 expression is vital to the invasive activity of PGE 2 and IL-8. In MCF-7 cells overexpressing PDCD4 (MCF-7/PDCD4), PGE 2 and IL-8 failed to induce invasion, in contrast to the parental MCF-7 cells, thus indicating that PDCD4 blocks breast cancer cell invasion. MCF-7/PDCD4 cells produced higher levels of the Tissue Inhibitor of Metalloproteinases-2 (TIMP-2) than the parental cells. Silencing TIMP-2 mRNA in MCF-7/PDCD4 cells reversed the anti-invasive effects of PDCD4, allowing PGE 2 and IL-8 to induce the invasion of these cells. Here we report the novel findings that suppression of PDCD4 expression is vital for the invasive activity of COX-2 mediated by PGE 2 and IL-8, and that PDCD4 increases TIMP-2 expression to inhibit breast cancer cell invasion.

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“…Loss of PDCD4 expression is closely associated with the progression of a number of tumors, including glioblastomas (7), and kidney, ovarian and lung cancer (8)(9)(10). Low PDCD4 expression levels correlate with poor outcomes in patients with glioblastoma multiforme (11).…”

Section: Introductionmentioning

confidence: 99%

Suppression of PDCD4 mediated by the long non-coding RNA HOTAIR inhibits the proliferation and invasion of glioma cells

Chen¹,

Bian²,

Zhao³

et al. 2016

Oncology Letters

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Abstract. Programmed cell death protein 4 (PDCD4) has recently been demonstrated to be implicated in translation and transcription, and the regulation of cell growth. However, the mechanisms underlying PDCD4 function in glioma cells remain to be elucidated. The current study investigated the function and regulation of PDCD4 and the results demonstrated that the expression of PDCD4 was significantly reduced in glioma cells compared with normal cells. When PDCD4 was overexpressed in glioma cells, the proliferation rate and invasive capability of the cells greatly decreased, suggesting that PDCD4 functions as a tumor suppressor in this cell type. In addition, the histone modification status of the PDCD4 gene was analyzed, and chromatin immunoprecipitation assay identified a high density of histone 3 lysine 27 trimethylation on the promoter of PDCD4, which was associated with the long non-coding RNA, homeobox transcript antisense RNA (HOTAIR). The expression of HOTAIR was significantly increased in glioma cells compared with normal cells, and it exerted its function in a polycomb repressive complex 2-dependent manner. These results may provide novel approaches to therapeutically target PDCD4 and HOTAIR in patients with gliomas. IntroductionHuman gliomas are the most prevalent malignant neoplasms of the central nervous system, with an annual incidence of ~5/100,000 worldwide (1). Despite the use of aggressive surgery in combination with chemotherapy, biological therapy and radiotherapy, gliomas continue to be therapeutically challenging (2). For patients with glioblastoma, the relative 5-year survival rate is <5% (3). Novel therapies for the treatment of glioma are warranted; recent advances in the understanding of the molecular and biological nature of this disease may facilitate the development of successful therapeutics (4).PDCD4 protein was initially determined to be overexpressed during apoptosis, which subsequently suppresses tumorigenesis (5,6). Loss of PDCD4 expression is closely associated with the progression of a number of tumors, including glioblastomas (7), and kidney, ovarian and lung cancer (8-10). Low PDCD4 expression levels correlate with poor outcomes in patients with glioblastoma multiforme (11). The frequent loss of PDCD4 in glioblastoma multiforme is partly due to epigenetic silencing secondary to 5' cytosine-phosphate-guanine island methylation (12), in addition to overexpression of microRNA (miRNA)-21, which targets PDCD4 mRNA for degradation (13). Although several studies have examined PDCD4 in glioma, the detailed molecular mechanisms underlying the role of PDCD4 in glioma remain poorly understood.Long non-coding RNAs (lncRNAs) are non-protein coding transcripts longer than 200 nucleotides, which are involved in various important events, including transcriptional, epigenetic and post-transcriptional regulation (14,15). A previous study profiled the lncRNA homeobox transcript antisense RNA (HOTAIR), and the results demonstrated that HOTAIR was closely correlated with poor prognosis, molecular ...

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Frequent loss of PDCD4 expression in human glioma: Possible role in the tumorigenesis of glioma

Cited by 63 publications

References 21 publications

Expression patterns of the tumor suppressor PDCD4 and correlation with β-catenin expression in gastric cancers

Expression patterns of the tumor suppressor PDCD4 and correlation with β-catenin expression in gastric cancers

Programmed Cell Death 4 inhibits breast cancer cell invasion by increasing Tissue Inhibitor of Metalloproteinases-2 expression

Suppression of PDCD4 mediated by the long non-coding RNA HOTAIR inhibits the proliferation and invasion of glioma cells

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