A Soluble Form of B Cell Maturation Antigen, a Receptor for the Tumor Necrosis Factor Family Member April, Inhibits Tumor Cell Growth

Rennert, Paul D.; Schneider, Pascal; Cachero, Teresa G.; Thompson, Jeffrey S.; Trabach, Luciana; Hertig, Sylvie; Holler, Nils; Qian, Fang; Mullen, Colleen; Strauch, Kathy; Browning, Jeffrey L.; Ambrose, Christine; Tschopp, Jürg

doi:10.1084/jem.192.11.1677

Cited by 242 publications

(215 citation statements)

References 17 publications

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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%

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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Section: Discussionmentioning

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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“…1,2,[6][7][8][9][10] In BLyS deficient mice, the number of B cells, serum IgG and IgM levels were decreased, and B cell development was blocked at the transitional T1 stage. 11 BLyS and a proliferation-inducing ligand (APRIL) bind to B cell maturation antigen (BCMA) and transmembrane activator and CAML-interactor (TACI), 4,12,13 which belong to the tumor necrosis factor receptor superfamily and are mainly expressed in B cells. [14][15][16][17] The intracellular domains of BCMA and TACI associate with TNFreceptor-associated factors (TRAFs), leading to activation of NF-kB.…”

Section: Introductionmentioning

confidence: 99%

Analysis on the association of human BLYS (BAFF, TNFSF13B) polymorphisms with systemic lupus erythematosus and rheumatoid arthritis

et al. 2002

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Recent studies indicated a substantial role of BLyS (BAFF, TNFSF13B) in the pathogenesis of systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) in humans and in animal models. This study was conducted to screen for polymorphisms of human BLYS, and to examine whether they are involved in the genetic susceptibility to human SLE and RA. A systematic polymorphism screening was performed in the coding region, 5 0 and 3 0 untranslated regions, and promoter region of human BLYS. Association of the detected polymorphisms with SLE and RA was analyzed in 221 Japanese patients with RA, 156 with SLE, and 227 healthy individuals, using the case-control approach. Four single nucleotide polymorphisms (SNPs) in the promoter, one SNP in intron 1, and one rare nonsynonymous substitution (Ala105Thr) in the coding region were detected. The BLYS SNPs were found to form three common haplotypes. Significant association with the susceptibility to SLE or RA was not observed. However, a tendency for the increase of À871T/T genotype was observed in SLE patients with anti-Sm antibody (P ¼ 0.082). BLYS mRNA level was significantly elevated in the monocytes from individuals carrying À871T (P ¼ 0.010). In addition, although statistically not significant, 105Thr allele was slightly increased in patients with RA compared with controls (P ¼ 0.058). Characterizing the functional and clinical significance of these new SNPs requires further study.

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“…In addition, APRIL interacts with proteoglycans, which are structurally unrelated to TNF receptors, and are likely to be the initially unidentified APRILspecific binding partner that was predicted to exist several years ago (K Ingold et al, unpublished; [6]). This interaction involves acidic sulfated glycosaminoglycan (GAG) sidechains of proteoglycans and basic amino acid residues, which are present in APRIL, but not in BAFF, and is independent from the interaction site for TACI and BCMA (K Ingold et al, unpublished; Figure 2).…”

Section: The Interactions Of Baff and April With Their Receptors And mentioning

confidence: 99%

The role of APRIL and BAFF in lymphocyte activation

Schneider

2005

Current Opinion in Immunology

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A Soluble Form of B Cell Maturation Antigen, a Receptor for the Tumor Necrosis Factor Family Member April, Inhibits Tumor Cell Growth

Cited by 242 publications

References 17 publications

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

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

Analysis on the association of human BLYS (BAFF, TNFSF13B) polymorphisms with systemic lupus erythematosus and rheumatoid arthritis

The role of APRIL and BAFF in lymphocyte activation

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