Serum APRIL, a potential tumor marker in pancreatic cancer

Wang, Feng; Lin, Chen; Ding, Weifeng; Wang, Guihua; Wu, Yueping; Wang, Jingchun; Luo, Leilei; Cong, Hui; Wang, Yueguo; Ju, Shaoqing; Shao, Jianghua; Wang, Huimin

doi:10.1515/cclm.2011.608

Cited by 26 publications

(22 citation statements)

References 19 publications

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“…In the present study, we found that levels of the serum marker of acute inflammation (CRP) and an inflammatory mediator (TNFSF13) were significantly higher in patients with PDAC-DM than in those without diabetes and in pancreatitis patients. Though the serum levels of CRP and TNFSF13 in patients with PDAC-DM were not directly compared with those of healthy individuals in our study, the serum CRP and TNFSF13 levels in patients with chronic pancreatitis were shown to be slightly higher and the same as those of healthy individuals, respectively [18][19][20]. Our data demonstrated similar levels of CRP mRNA expression in tissues from patients with and without PDAC-DM, and in patients with chronic pancreatitis, excluding the possibility that PDAC lesions are the source of the elevated CRP in the serum of patients with PDAC-DM.…”

Section: Discussioncontrasting

confidence: 61%

Analysis of global gene expression profiles suggests a role of acute inflammation in type 3C diabetes mellitus caused by pancreatic ductal adenocarcinoma

Gao

Zhou

et al. 2015

Diabetologia

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Aims/hypothesis Pancreatic ductal adenocarcinoma (PDAC) can cause type 3C diabetes, known as PDAC-associated diabetes mellitus (PDAC-DM), but the mechanism is unknown. This study aimed to reveal the mechanism. Methods PDAC lesions from patients with or without PDAC-DM (n=4 in each group) were individually profiled for 23,512 mRNAs with microarrays. Bioinformatic analysis and in vivo and in vitro assays were then conducted. Results We determined that 2,778 genes were differentially expressed; over-representation of ten genes was validated with quantitative RT-PCR. The analysis of gene ontology showed that the differentially expressed secretory genes were related mainly to inflammation. High levels of a marker of inflammation (C-reactive protein [CRP]) and an inflammatory mediator (TNF super-family member 13 [TNFSF13]) were found in the serum of patients with PDAC-DM. After surgical resection of PDAC lesions, CRP and TNFSF13 levels significantly decreased (p<0.01). Furthermore, we found that the levels of TNFSF13 in PDAC lesions and TNFSF13 and CRP in serum were significantly correlated with the diabetic status of patients with PDAC-DM (p<0.01). Assays in vivo showed that after exposure to an inhibitor of inflammation (celecoxib), the fasting blood glucose level in the mouse model of PDACWenchao Gao, Yu Zhou and Qingyan Li contributed equally to this work Electronic supplementary material The online version of this article

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Section: Discussioncontrasting

confidence: 61%

Analysis of global gene expression profiles suggests a role of acute inflammation in type 3C diabetes mellitus caused by pancreatic ductal adenocarcinoma

Gao

Zhou

et al. 2015

Diabetologia

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“…Although APRIL has low or no expression in various normal cells, previous studies have shown that it is overexpressed in many malignancies, such as colorectal cancer [13], pancreatic cancer [26], and gastric cancer [27], suggesting that APRIL plays an important role in the carcinogenesis of these tumors. Moreover, APRIL also owns an ability to stimulate tumor cell proliferation and survival in vitro and in vivo by interaction with the intracellular environment.…”

Section: Discussionmentioning

confidence: 99%

miR-383 inhibits hepatocellular carcinoma cell proliferation via targeting APRIL

Chen¹,

Guan²,

Gu³

et al. 2015

Tumor Biol.

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Mounting evidence has shown that microRNAs (miRNAs), a class of small non-coding RNAs, are frequently deregulated in human malignancies and have pivotal roles in diverse biological processes including cancer cell proliferation. Herein, we investigated the expression pattern of miR-383 in 64 hepatocellular carcinoma (HCC) tissues and 4 HCC cell lines and found that miR-383 was downregulated in HCC tissues and cell lines. Moreover, miR-383 expression in HCC was significantly correlated with tumor size and tumor-node-metastasis (TNM) stage. Kaplan-Meier analysis showed that decreased miR-383 expression was associated with poor overall survival of HCC patients. In addition, Cox regression analysis indicated that miR-383 was an independent prognostic factor for HCC patients. Then, functional studies demonstrated that ectopic miR-383 expression could significantly suppress the in vitro proliferation of HCC cells, as well as induce cell cycle arrest and cell apoptosis. Luciferase reporter assay further identified that a proliferation-inducing ligand (APRIL), a member in the tumor necrosis factor (TNF) superfamily, was a novel target gene for miR-383. Subsequent investigation revealed that miR-383 expression was inversely correlated with APRIL messenger RNA (mRNA) expression in HCC tissues. Besides, recombinant human APRIL (rhAPRIL) could rescue HCC cell proliferation inhibited by miR-383. Taken together, our present study provided the first evidence that miR-383 was decreased in HCC and associated with tumor progression and prognosis of HCC patients. Furthermore, our findings confirmed that miR-383 might inhibit HCC cell proliferation partially via downregulating APRIL expression. Thus, this study might provide a promising strategy by targeting with the miR-383-APRIL axis in the treatment of HCC.

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“…This marker, representing A Proliferation Inducing Ligand (APRIL) is a member of the Tumor Necrosis Factor (TNF) super family. It essentially is over expressed [12] in pancreatic cancer but only weakly if not at all in the normal pancreatic glandular tissue. The marker was found to be increased in patients with pancreatic cancer which proved to show positive correlation with CEA and CA19.9 levels in the serum The sensitivity of April alone in diagnosing the presence of malignancy was 70.1% when compared with that of CEA alone (56.7%) and similarly somewhat better than CA 19.9 alone.…”

Section: Origin Of the Diagnostic/therapeutic Tumor Markers Expressedmentioning

confidence: 97%

“…The marker was found to be increased in patients with pancreatic cancer which proved to show positive correlation with CEA and CA19.9 levels in the serum The sensitivity of April alone in diagnosing the presence of malignancy was 70.1% when compared with that of CEA alone (56.7%) and similarly somewhat better than CA 19.9 alone. The sensitivity increased when APRIL was used in combination with CA19.9 reaching a level of 88.1% [12].…”

Section: Origin Of the Diagnostic/therapeutic Tumor Markers Expressedmentioning

confidence: 99%

The Clinical Detection of Pancreatic Carcinoma: A Comparison of the Standard Biomarkers to that of a Newer Class of Biomarkers used for both Diagnosis and Therapy

Arlen¹,

Arlen²,

X³

et al. 2012

Pancreat Disord Ther

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Serum APRIL, a potential tumor marker in pancreatic cancer

Abstract: Our results indicate that serum APRIL, as a potential biomarker, has a positive diagnosis and prognosis value for pancreatic cancer. Moreover, the combination assay of APRIL and CA19-9 is highly sensitive to pancreatic cancer.

Cited by 26 publications

References 19 publications

Analysis of global gene expression profiles suggests a role of acute inflammation in type 3C diabetes mellitus caused by pancreatic ductal adenocarcinoma

Analysis of global gene expression profiles suggests a role of acute inflammation in type 3C diabetes mellitus caused by pancreatic ductal adenocarcinoma

miR-383 inhibits hepatocellular carcinoma cell proliferation via targeting APRIL

The Clinical Detection of Pancreatic Carcinoma: A Comparison of the Standard Biomarkers to that of a Newer Class of Biomarkers used for both Diagnosis and Therapy

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