Involvement of programmed cell death 4 in transforming growth factor-β1-induced apoptosis in human hepatocellular carcinoma

Zhang, Hao; Ozaki, Iwata; Mizuta, Toshihiko; Hamajima, Hiroshi; Yasutake, Tsutomu; Eguchi, Yuichiro; Ideguchi, H; Yamamoto, Kyosuke; Matsuhashi, Sachiko

doi:10.1038/sj.onc.1209634

Cited by 230 publications

(187 citation statements)

References 43 publications

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“…An anti-PDCD4 antibody was prepared by immunizing rabbits with a synthetic peptide corresponding to the N-terminal amino acid sequence (13). Anti-β-catenin, anti-Ecadherin, anti-Akt, anti-p44/42 MAP kinase and anti-β-actin antibodies were purchased from Cell Signaling Technology (Beverly, MA).…”

Section: Methodsmentioning

confidence: 99%

“…Homologs in mice (MA-3/TIS) (4,5), chickens (6,7) and rats (DUG) (8) have also been reported. 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).…”

Section: Introductionmentioning

confidence: 99%

“…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%

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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: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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show abstract

“…Pdcd4 was initially shown to suppress tumor development in an in vitro mouse keratinocyte model of tumor promotion (Cmarik et al, 1999). More recently, decreased expression of Pdcd4 has been implicated in the development and progression of human lung, colon, liver and breast cancer (Chen et al, 2003;Afonja et al, 2004;Zhang et al, 2006;Mudduluru et al, 2007). Pdcd4 expression is controlled by multiple mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Pdcd4 directly binds the coding region of c-myb mRNA and suppresses its translation

et al. 2011

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Pdcd4 is a novel tumor suppressor protein that functions in the nucleus and the cytoplasm, and appears to be involved in the regulation of transcription and translation. In the cytoplasm, Pdcd4 has been implicated in the suppression of translation of mRNAs containing structured 5 0 -untranslated regions; however, the mechanisms that recruit Pdcd4 to specific target mRNAs and the identities of these mRNAs are mostly unknown. In this study, we have identified c-myb mRNA as the first natural translational target mRNA of Pdcd4. We have found that translational suppression of c-myb mRNA by Pdcd4 is dependent on sequences located within the c-myb-coding region. Furthermore, we have found that the N-terminal domain of Pdcd4 has an important role in targeting Pdcd4 to c-myb RNA by mediating preferential RNA binding to the Pdcd4-responsive region of c-myb mRNA. Overall, our work demonstrates for the first time that Pdcd4 is directly involved in translational suppression of a natural mRNA and provides the first evidence for a key role of the RNA-binding domain in targeting Pdcd4 to a specific mRNA.

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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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Involvement of programmed cell death 4 in transforming growth factor-β1-induced apoptosis in human hepatocellular carcinoma

Cited by 230 publications

References 43 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

Pdcd4 directly binds the coding region of c-myb mRNA and suppresses its translation

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

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