Clinical significance of CUL4A in human prostate cancer

Liu, Gang; Zhu, Z.; Lang, Fang; Li, Bao; Dian-jun, Gao

doi:10.1007/s13277-015-3580-2

Cited by 3 publications

(3 citation statements)

References 15 publications

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“…These genes include: transcription factor Dp-1 (TFDP1) , cullin 4A ( CUL4A) , and cell division cycle 16 ( CDC16) identified in hepatocellular carcinoma (HCC) [ 7 ], breast cancer [ 8 ], and lung cancer [ 9 ]; and insulin receptor substrate 2 ( IRS2) present in colorectal cancer [ 10 ]. CUL4A overexpression has been reported to be associated with migration, invasion, epithelial-mesenchymal transition and disease progression [ 11 – 13 ]. The role and frequency of gene CN alterations at 13q34 in iCCA has yet to be investigated.…”

Section: Introductionmentioning

confidence: 99%

Recurrent Amplification at 13q34 Targets at CUL4A, IRS2, and TFDP1 As an Independent Adverse Prognosticator in Intrahepatic Cholangiocarcinoma

et al. 2015

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Amplification of genes at 13q34 has been reported to be associated with tumor proliferation and progression in diverse types of cancers. However, its role in intrahepatic cholangiocarcinoma (iCCA) has yet to be explored. We examined two iCCA cell lines and 86 cases of intrahepatic cholangiocarcinoma to analyze copy number of three target genes, including cullin 4A (CUL4A), insulin receptor substrate 2 (IRS2), and transcription factor Dp-1 (TFDP1) at 13q34 by quantitative real-time polymerase chain reaction. The cell lines and all tumor samples were used to test the relationship between copy number (CN) alterations and protein expression by western blotting and immunohistochemical assays, respectively. IRS2 was introduced, and each target gene was silenced in cell lines. The mobility potential of cells was compared in the basal condition and after manipulation using cell migration and invasion assays. CN alterations correlated with protein expression levels. The SNU1079 cell line containing deletions of the target genes demonstrated decreased protein expression levels and significantly lower numbers of migratory and invasive cells, as opposed to the RBE cell line, which does not contain CN alterations. Overexpression of IRS2 by introducing IRS2 in SUN1079 cells increased the mobility potential. In contrast, silencing each target gene showed a trend or statistical significance toward inhibition of migratory and invasive capacities in RBE cells. In tumor samples, the amplification of each of these genes was associated with poor disease-free survival. Twelve cases (13.9%) demonstrated copy numbers > 4 for all three genes tested (CUL4A, IRS2, and TFDP1), and showed a significant difference in disease-free survival by both univariate and multivariate survival analyses (hazard ratio, 2.69; 95% confidence interval, 1.23 to 5.88; P = 0.013). Our data demonstrate that amplification of genes at 13q34 plays an oncogenic role in iCCA featuring adverse disease-free survival, which may provide new directions for targeted therapy.

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Section: Introductionmentioning

confidence: 99%

Recurrent Amplification at 13q34 Targets at CUL4A, IRS2, and TFDP1 As an Independent Adverse Prognosticator in Intrahepatic Cholangiocarcinoma

et al. 2015

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“…35:111-116, doi 10.1007/s13277-013-1013 Jin, B., Dong, P., Li, K. et al (2014) Meta-analysis of the association between GSTT1 null genotype and risk of nasopharyngeal carcinoma in Chinese Tumor Biol. Jiang, Y., Sun, S., Liu, G. et al (2015) Nrdp1 inhibits metastasis of colorectal cancer cells by EGFR-signaling-dependent MMP7 modulation Tumor Biol. 36:1129-1133, doi 10.1007/ s13277-014-2726-y Zhang, Z., Yan, Z., Yuan, Z. et al (2015 Lin, ZY., Song, QQ., Chen, J. et al (2015) Local curative effect of MRI-guided radiofrequency ablation on small hepatocellular carcinoma Tumor Biol.…”

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confidence: 99%

Retraction Note to multiple articles in Tumor Biology

Stigbrand

2017

Tumor Biol.

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“…Previous studies have shown that Cul4A is amplified in malignant pleural mesothelioma , breast , lung cancer and liver cancers . Overexpression of Cul4A has been reported in pituitary adenoma , prostate cancer and osteosarcoma . Cul4A overexpression is associated with tumorigenesis of lung cancer and hepatocellular carcinoma .…”

Section: Introductionmentioning

confidence: 98%

Knockdown of cullin 4A inhibits growth and increases chemosensitivity in lung cancer cells

Hung

Chen

et al. 2016

J Cellular Molecular Medi

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Cullin 4A (Cul4A) has been observed to be overexpressed in various cancers. In this study, the role of Cul4A in the growth and chemosensitivity in lung cancer cells were studied. We showed that Cul4A is overexpressed in lung cancer cells and tissues. Knockdown of the Cul4A expression by shRNA in lung cancer cells resulted in decreased cellular proliferation and growth in lung cancer cells. Increased sensitivity to gemcitabine, a chemotherapy drug, was also noted in those Cul4A knockdown lung cancer cells. Moreover, increased expression of p21, transforming growth factor (TGF)‐β inducible early gene‐1 (TIEG1) and TGF beta‐induced (TGFBI) was observed in lung cancer cells after Cul4A knockdown, which may be partially related to increased chemosensitivity to gemcitabine. G0/G1 cell cycle arrest was also noted after Cul4A knockdown. Notably, decreased tumour growth and increased chemosensitivity to gemcitabine were also noted after Cul4A knockdown in lung cancer xenograft nude mice models. In summary, our study showed that targeting Cul4A with RNAi or other techniques may provide a possible insight to the development of lung cancer therapy in the future.

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Clinical significance of CUL4A in human prostate cancer

Cited by 3 publications

References 15 publications

Recurrent Amplification at 13q34 Targets at CUL4A, IRS2, and TFDP1 As an Independent Adverse Prognosticator in Intrahepatic Cholangiocarcinoma

Recurrent Amplification at 13q34 Targets at CUL4A, IRS2, and TFDP1 As an Independent Adverse Prognosticator in Intrahepatic Cholangiocarcinoma

Retraction Note to multiple articles in Tumor Biology

Knockdown of cullin 4A inhibits growth and increases chemosensitivity in lung cancer cells

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