APRIL, a new member of the tumor necrosis factor family, modulates death ligand-induced apoptosis

Roth, Wilfried; Wagenknecht, Bettina; Klumpp, Andrea; Naumann, Ulrike; Hahne, Michael; Tschopp, Jürg; Weller, Michael

doi:10.1038/sj.cdd.4400827

Cited by 83 publications

(67 citation statements)

References 33 publications

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“…Our results differ from those of Roth et al (2001), who found that APRIL did not promote glioblastoma cell growth in vitro or in vivo. This discrepancy may be due to the material used: we used defined amounts of pure human recombinant soluble trimeric APRIL, whereas Roth et al studied the proliferation rate of glioblastoma cell lines transfected with a construct encoding APRIL.…”

Section: Discussioncontrasting

confidence: 57%

“…All eight glioblastoma cell lines used in this study produced APRIL transcripts. In a previous study (Roth et al, 2001), APRIL transcripts were detected in five of the 12 glioblastoma cell lines tested. Our panel of glioblastoma cell lines differed from that used in this previous study, with only the U373MG and T98G cell lines common to both studies.…”

Section: Discussionmentioning

confidence: 99%

“…APRIL, which is processed by furin convertase within the cell before its secretion, is detected only in soluble form (Lo´pez-Fraga et al, 2001). Roth et al (2001) reported APRIL to be present in some malignant glioblastoma cell lines, but with no stimulatory effect on cell growth. In this study, we found that APRIL was abnormally produced in eight human malignant glioblastoma cell lines as this protein was not detected in normal human counterpart cells.…”

Section: Introductionmentioning

confidence: 99%

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Abnormal production of the TNF-homologue APRIL increases the proliferation of human malignant glioblastoma cell lines via a specific receptor

et al. 2003

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Section: Discussioncontrasting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Abnormal production of the TNF-homologue APRIL increases the proliferation of human malignant glioblastoma cell lines via a specific receptor

et al. 2003

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“…Indeed, PRIL was also shown to provide a proliferative/survival signal to solid tumor cells. Although only modestly detectable in vitro (Hahne et al, 1998;Roth et al, 2001), this activity has been observed significantly in vivo by overexpressing APRIL in tumor cells (Hahne et al, 1998) or by blocking endogenous PRIL (Rennert et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…APRIL is expressed by a subset of immune cells that also produce B-cell activating factor (BAFF): monocytes, macrophages, (Hahne et al, 1998;Nardelli et al, 2001;He et al, 2004;Chu et al, 2007) as well as in some non-immune cells such as epithelial cells and osteoclasts. Moreover, PRIL is abundantly expressed in a variety of tumor cells and tissues, such as lung carcinomas, melanoma (Roth et al, 2001;Stein et al, 2002), lymphoid malignancies (Nardelli et al, 2001;Deshayes et al, 2004;Kern et al, 2004;Moreaux et al, 2004;Chiu et al, 2007;Pelekanou et al, 2008;Yaccoby et al, 2008) and in particular gastrointestinal tumors including rectum, duodenum, colon, stomach and esophagus (Hahne et al, 1998;Kelly et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Knockdown of a Proliferation-inducing Ligand (PRIL) Suppresses the Proliferation of Gastric Cancer Cells

Cui

Li²,

Wang³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Asian Pacific J Cancer Prev, 13, 633-636 IntroductionGastric cancer (GC), the second most common cause of cancer-related death in the world, can develop in any part of the stomach and spread throughout the stomach and to other organs. There are about 1,000,000 new diagnoses and 800,000 deaths worldwide each year (Kamangar et al., 2006). The 5-year survival rate for curative surgical resection ranges from 30-50% for patients with stage II disease and from 10-25% for patients with stage III disease. The operative mortality rate for patients undergoing curative surgical resection at major academic centers is less than 3% (http://emedicine.medscape.com/ article/278744-overview). In this scenario, understanding the molecular mechanisms underlying the initiation and progression of GC is important for prevention, early diagnosis and identifying novel therapeutic and clinical targets for GC (Li et al., 2009;Yu et al., 2009).A proliferation-inducing ligand (PRIL) (also known as TALL-2, TRDL1, or TNFSF13) is a member of tumor necrosis factor (TNF) family. It was originally identified in cell lines and primary samples from various tumor lesions in 1998 and named for its capacity to stimulate the proliferation of tumor cells (Hahne et al., 1998). In contrast to most TNF family members, APRIL is processed in the Golgi apparatus into the active soluble form by a furin convertase (Lopez-Fraga et al., 2001). APRIL is expressed by a subset of immune cells that also produce B-cell activating factor (BAFF): monocytes, macrophages, Moreover, the cell cycle was arrested at G2/M phase, elucidating the mechanism underlying the inhibitory effect of siRNA on cell proliferation. Conclusions: Our study indicated that PRIL functions in promoting cell growth, and lentivirus-mediated PRIL gene knockdown might be a promising strategy in the treatment of gastric cancer.

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Genomic profiling reveals distinctive molecular relapse patterns in IDH1/2 wild‐type glioblastoma

Riehmer

Gietzelt

Beyer

et al. 2014

Genes Chromosomes & Cancer

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Molecular changes associated with the progression of glioblastoma after standard radiochemotherapy remain poorly understood. We compared genomic profiles of 27 paired primary and recurrent IDH1/2 wild-type glioblastomas by genome-wide array-based comparative genomic hybridization. By bioinformatic analysis, primary and recurrent tumor profiles were normalized and segmented, chromosomal gains and losses identified taking the tumor cell content into account, and difference profiles deduced. Seven of 27 (26%) pairs lacked DNA copy number differences between primary and recurrent tumors (equal pairs). The recurrent tumors in 9/27 (33%) pairs contained all chromosomal imbalances of the primary tumors plus additional ones, suggesting a sequential acquisition of and/or selection for aberrations during progression (sequential pairs). In 11/27 (41%) pairs, the profiles of primary and recurrent tumors were divergent, i.e., the recurrent tumors contained additional aberrations but had lost others, suggesting a polyclonal composition of the primary tumors and considerable clonal evolution (discrepant pairs). Losses on 9p21.3 harboring the CDKN2A/B locus were significantly more common in primary tumors from sequential and discrepant (nonequal) pairs. Nonequal pairs showed ten regions of recurrent genomic differences between primary and recurrent tumors harboring 46 candidate genes associated with tumor recurrence. In particular, copy numbers of genes encoding apoptosis regulators were frequently changed at progression. In summary, approximately 25% of IDH1/2 wild-type glioblastoma pairs have stable genomic imbalances. In contrast, approximately 75% of IDH1/2 wild-type glioblastomas undergo further genomic aberrations and alter their clonal composition upon recurrence impacting their genomic profile, a process possibly facilitated by 9p21.3 loss in the primary tumor. © 2014 Wiley Periodicals, Inc.

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APRIL, a new member of the tumor necrosis factor family, modulates death ligand-induced apoptosis

Abstract: APRIL (a proliferation-inducing ligand)

Cited by 83 publications

References 33 publications

Abnormal production of the TNF-homologue APRIL increases the proliferation of human malignant glioblastoma cell lines via a specific receptor

Abnormal production of the TNF-homologue APRIL increases the proliferation of human malignant glioblastoma cell lines via a specific receptor

Knockdown of a Proliferation-inducing Ligand (PRIL) Suppresses the Proliferation of Gastric Cancer Cells

Genomic profiling reveals distinctive molecular relapse patterns in IDH1/2 wild‐type glioblastoma

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