Hepatoma-Derived Growth Factor Is a Novel Prognostic Factor for Patients with Pancreatic Cancer

Uyama, Hirokazu; Tomita, Yoshihiro; Nakamura, Hitomi; Nakamori, Shoji; Zhang, Binglin; Hoshida, Yoshihiko; Enomoto, Hirayuki; Okuda, Yuji; Sakon, Masato; Aozasa, Katsuyuki; Kawase, Ichiro; Hayashi, Norio; Monden, Morito

doi:10.1158/1078-0432.ccr-06-1064

Cited by 91 publications

(70 citation statements)

References 32 publications

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“…The following articles were also excluded: three duplicated publications (Zhou et al, 2007b;Zhou et al, 2010a;Yang et al, 2014); three without data for HR and 95%CI calculations and adequate contact with the investigators could not be established (Natrajan et al, 2006;Mao et al, 2008;Hanada et al, 2013); two with a sample size<50 (Hsu et al, 2012;Tao et al, 2014); two in which HDGF expression was not detected by IHC methods (Savola et al, 2009;Zhang et al, 2010); three uncorrelated. Finally, 26 cohort studies were found eligible for the meta-analysis (Hu et al, 2003;Ren et al, 2004;Iwasaki et al, 2005;Uyama et al, 2006;Yamamoto et al, 2006;Yoshida et al, 2006;Chang et al, 2007;Yamamoto et al, 2007;Zhou et al, 2007a;Hu et al, 2009;Zhou et al, 2010b;Liu et al, 2011;Wang et al, 2011;Zhang et al, 2011;Chen et al, 2012a;Chen et al, 2012b;Lin et al, 2012;Han et al, 2013;Li et al, 2013a;Li et al, 2013b;Li et al, 2013c;Yang et al, 2013;Guo et al, 2014b;Song et al, 2014;Wang et al, 2014;Zhang et al, 2014), containing 32 datasets (29 datasets for OS; 17 datasets for DFS) were qualified to the standard of the meta-analysis. The main characteristics of the selected studies were summari...…”

Section: Study Inclusion and Characteristicsmentioning

confidence: 99%

“…In recent years, elevated levels of hepatoma-derived growth factor (HDGF) have been observed in a variety of malignancies and high levels of HDGF appears to be associated with increased malignancy across cancers, as witnessed by the correlation with adverse characteristics such as poor patient survival (Hu et al, 2003;Ren et al, 2004;Iwasaki et al, 2005;Uyama et al, 2006;Yamamoto et al, 2006;Yoshida et al, 2006;Chang et al, 2007;Yamamoto et al, 2007;Zhou et al, 2007a;Hu et al, 2009;Savola et al, 2009;Zhang et al, 2010;Zhou et al, 2010b;Liu et al, 2011;Wang et al, 2011;Ye et al, 2011;Zhang et al, 2011;Chen et al, 2012a;Chen et al, 2012b;Hsu et al, 2012;Lin et al, 2012;Han et al, 2013;Hanada et al, 2013;Li et al, 2013a;Li et al, 2013b;Li et al, 2013c;Yang et al, 2013;Guo et al, 2014b;Song et al, 2014;Wang et al, 2014;Yang et al, 2014;Zhang et al, 2014). As a multifunctional protein Bao et al, 2014) widely expressed by many types of human cells, HDGF is involved in the regulations of a myriad of cancer cell activities during cancer transformation (Yang et al, 2013), apoptosis , angiogenesis (Ren et al, 2009), and metastasis (Chen et al, 2012a).…”

Section: Introductionmentioning

confidence: 99%

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Prognostic Role of Hepatoma-derived Growth Factor in Solid Tumors of Eastern Asia: a Systematic Review and Meta-Analysis

Bao

Liu²,

Wang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Hepatoma-derived growth factor (HDGF) is a novel jack-of-all-trades in cancer. Here we quantify the prognostic impact of this biomarker and assess how consistent is its expression in solid tumors. A comprehensive search strategy was used to search relevant literature updated on October 3, 2014 in PubMed, EMBASE and WEB of Science. Correlations between HDGF expression and clinicopathological features or cancer prognosis was analyzed. All pooled HRs or ORs were derived from random-effects models. Twenty-six studies, primarily in Eastern Asia, covering 2,803 patients were included in the analysis, all of them published during the past decade. We found that HDGF overexpression was significantly associated with overall survival (

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Section: Study Inclusion and Characteristicsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Prognostic Role of Hepatoma-derived Growth Factor in Solid Tumors of Eastern Asia: a Systematic Review and Meta-Analysis

Bao

Liu²,

Wang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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“…71 HMGB1-RAGE interaction induces proliferation, angiogenesis, invasion, metastasis and chemotherapy-resistance. 71 Similarly, HDGF is overexpressed in many different cancers, including gastrointestinal stromal tumors (GISTs), 72 esophageal carcinoma, 73 pancreatic cancer, 74 hepatocellular carcinoma, 75 non-small cell lung cancer, 76 colorectal cancer 77 and melanoma, 78 and has potent angiogenic, 79 invasive 80 and metastatic potential. 73 Contrasting its role under pathophysiological conditions, such as gliomagenesis, necrosis can also be beneficial for an organism as it constitutes a warning system against toxic exposure.…”

Section: The Two Faces Of Necrosis-a Benefical Adaptive Warning Systementioning

confidence: 99%

What drives intense apoptosis resistance and propensity for necrosis in glioblastoma? A role for Bcl2L12 as a multifunctional cell death regulator

Stegh¹,

Chin²,

Louis³

et al. 2008

Cell Cycle

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Glioblastoma (GBM) is the most common type of primary brain cancer and carries a dismal prognosis primarily due to the emergence of resistance towards extant radiation, conventional and targeted chemotherapies. Although GBM resists therapy-induced apoptosis, tumors show a seemingly paradoxical propensity for florid intratumoral necrogenesis. This necrosis manifests pathologically as microscopic foci or confluent expanses of necrotic tumor. While it is now well recognized that necrosis is an active cell death process and that apoptosis and necrosis death modalities are intertwined on multiple levels, the precise molecular mechanisms and genetic elements underlying these forms of cell death in GBM remain areas of active investigation. In recent oncogenomic studies, we identified a novel GBM oncoprotein, Bcl2-Like 12 (Bcl2L12), which is significantly expressed in the majority of primary GBM tumor specimens and distantly related to canonical Bcl-2 proteins. Due to its distinctive impact on cell death signaling, Bcl2L12 phenocopies pro-necrotic and anti-apoptotic propensities of highgrade glioma: Mechanistically, we determined that unlike prototypic Bcl-2 family members, Bcl2L12 does not safeguard mitochondrial membrane integrity, but instead potently inhibits apoptosis at the level of post-mitochondrial effector caspase-3/7 activation. A combination of enforced expression, RNAi-mediated extinction, co-localization and protein interaction studies revealed that Bcl2L12 inhibits caspases 3 and 7 via distinct mechanisms. Direct physical interaction underlies Bcl2L12's inhibition of caspase-7 processing, whereas Bcl2L12-induced transcriptional upregulation of the small heat shock protein αB-crystallin is instrumental to neutralization of caspase-3 activation. Mirroring the cellular phenotype elicited by energy depletion, genetic or pharmacologic inhibition of post-mitochondrial apoptosis signaling molecules, Bcl2L12 promotes necrogenesis in glial cells in the context of a proapoptotic stimulus establishing that it represents a novel regulator of the balance between apoptosis and necrosis in GBM.

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“…Several findings suggest that HDGF overexpression is associated with aggressive phenotypes of cancer cells, such as proliferation, invasiveness, and metastasis (11)(12)(13)(14)(15). Therefore, HDGF may prove useful as a prognostic factor for patients with hepatocellular carcinoma (16), gastric (17), pancreatic (18) and non-small-cell lung cancers (19), and gastrointestinal stromal tumors (20).…”

Section: Introductionmentioning

confidence: 99%

p53 Negatively Regulates the Hepatoma Growth Factor HDGF

et al. 2011

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Hepatoma-derived growth factor (HDGF) is a secreted heparin-binding growth factor that has been implicated in cancer development and progression. Here, we report that HDGF is a critical target for transcriptional repression by the tumor suppressor p53. Endogenous HDGF expression was decreased in cancer cells with introduction of wild-type p53, which also downregulated HDGF expression after DNA damage. In support of the likelihood that HDGF is a critical driver of cancer cell growth, addition of neutralizing HDGF antibodies to culture media was sufficient to block cell growth, migration, and invasion. Similarly, these effects were elicited by conditioned culture medium from p53-expressing cells, and they could be reversed by the addition of recombinant human HDGF. Interestingly, we found that HDGF was overexpressed also in primary gastric, breast, and lung cancer tissues harboring mutant p53 genes. Mechanistic investigations revealed that p53 repressed HDGF transcription by altering HDAC-dependent chromatin remodeling. Taken together, our results reveal a new pathway in which loss of p53 function contributes to the aggressive pathobiological potential of human cancers by elevating HDGF expression. Cancer Res; 71(22); 7038-47. Ó2011 AACR.

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Hepatoma-Derived Growth Factor Is a Novel Prognostic Factor for Patients with Pancreatic Cancer

Cited by 91 publications

References 32 publications

Prognostic Role of Hepatoma-derived Growth Factor in Solid Tumors of Eastern Asia: a Systematic Review and Meta-Analysis

Prognostic Role of Hepatoma-derived Growth Factor in Solid Tumors of Eastern Asia: a Systematic Review and Meta-Analysis

What drives intense apoptosis resistance and propensity for necrosis in glioblastoma? A role for Bcl2L12 as a multifunctional cell death regulator

p53 Negatively Regulates the Hepatoma Growth Factor HDGF

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