SOX4 expression levels in urothelial bladder carcinoma

Güneş, Sezgin; Yegin, Zeynep; Süllü, Yüksel; Büyükalpelli, Recep; Bağcı, Hasan

doi:10.1016/j.prp.2011.05.005

Cited by 19 publications

(15 citation statements)

References 17 publications

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“…SOX4 is over-expressed in various cancers and was closely correlated with tumor invasion and metastasis [16]–[19]. It is also one of members of EMT-transcriptional inducers [26].…”

Section: Discussionmentioning

confidence: 99%

“…These transcription factors are defined by a conserved signature sequence in the high-mobility group (HMG) DNA-binding domain (DBD) [14], [15]. SOX4 is a 47-kDa protein is highly conserved in vertebrates and its clinical importance has gained increasing attention in recent years, with numerous reports suggesting that SOX4 may contribute to tumor progression [16], [17]. Increased SOX4 expression is found in tumors of the bladder, prostate, and colon, and with non-small-cell lung tumors [18]–[21].…”

Section: Introductionmentioning

confidence: 99%

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Decreased miR-204 in H. pylori-Associated Gastric Cancer Promotes Cancer Cell Proliferation and Invasion by Targeting SOX4

Zhou

Lin

et al. 2014

PLoS ONE

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BackgroundThe molecular mechanism between Helicobacter pylori (H. pylori) infection and gastric cancer remained largely unknown. In this study, we determined the role of miRNA in H. pylori induced gastric cancer.Methods and ResultsWe found that miR-204 was decreased in H. pylori positive tissues by qRT-PCR. Knockdown of miR-204 enhanced the invasion and proliferation ability of gastric cancer cells in vitro. Luciferase assay revealed that SOX4 was target gene of miR-204, which was found up-regulated in H. pylori positive tissues. Down-regulation of miR-204 and over-expression of SOX4 promoted epithelial-mesenchymal transition process.ConclusionTaken together, our findings demonstrated that miR-204 may act as a tumor suppressor in H. pylori induced gastric cancer by targeting SOX4.

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“…SOX4 is over-expressed in various cancers and was closely correlated with tumor invasion and metastasis [16]–[19]. It is also one of members of EMT-transcriptional inducers [26].…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Decreased miR-204 in H. pylori-Associated Gastric Cancer Promotes Cancer Cell Proliferation and Invasion by Targeting SOX4

Zhou

Lin

et al. 2014

PLoS ONE

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“…As the results, the expression of SOX4 was observed in both cell nucleus and cytoplasm of tumor cells in PGC samples (Figure 1A) which was consistent with previous studies [11,12], and varied in intensity and extent of staining in different tumors. SOX4 expression was not detected in the normal epithelium of the gallbladder (Figure 1B).…”

Section: Resultssupporting

confidence: 92%

Clinicopathological significance of SOX4 expression in primary gallbladder carcinoma

Wang

Zhao

et al. 2012

Diagn Pathol

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AimSOX4, as a member of the SRY-related HMG-box (SOX) transcription factor family, has been demonstrated to be involved in tumorigenesis of many human malignancies; however, its role in primary gallbladder carcinoma (PGC) is still largely unknown. The aim of this study was to investigate SOX4 expression in PGC and its prognostic significance.MethodsFrom 1997 to 2006, 136 patients underwent resection for PGC. The median follow-up was 12.8 months. Immunostainings for SOX4 were performed on these archival tissues. The correlation of SOX4 expression with clinicopathological features including survival was analyzed.ResultsSOX4 was expressed in 75.0% (102/136) of PGC but not in the normal epithelium of the gallbladder. In addition, the over-expression of SOX4 was significantly associated with low histologic grade (P = 0.02), low pathologic T stage (P = 0.02), and early clinical stage (P = 0.03). The levels of SOX4 immunostainings in PGC tissues with positive nodal metastasis were also significantly lower than those without (P = 0.01). Moreover, Kaplan-Meier curves showed that SOX4 over-expression was significantly related to better overall (P = 0.008) and disease-free survival (P = 0.01). Furthermore, multivariate analyses showed that SOX4 expression was an independent risk factor for both overall (P = 0.03, hazard ratio, 3.682) and disease-free survival (P = 0.04, hazard ratio, 2.215).ConclusionOur data indicate for the first time that the over-expression of SOX4 in PGC was significantly correlated with favorable clinicopathologic features and was an independent prognostic factor for better overall and disease-free survival in patients. Therefore, SOX4 might be an auxiliary parameter for predicting malignant behavior for PGC.Virtual slidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1534825818694957.

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“…Subsequent studies in recent years suggested that Sox4 might be an important oncogene contributing to tumor progression [8]. For instance, its expression was dramatically elevated in tumors of the prostate, bladder, breast and lung [9,10,11]. Besides, nuclear Sox4 expression was also increased in colon tumor tissues relative to non-tumor colon tissues [12].…”

Section: Introductionmentioning

confidence: 99%

Sox4 Up-Regulates Cyr61 Expression in Colon Cancer Cells

Zhu

Zhang³

2014

Cell Physiol Biochem

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Background/Aims:Genetic changes leading to aberrant activation of oncogenes are viewed as a crucial step in colon cancer. Sox4, a member of Sox (Sry-box) family of transcription factors, plays a critical role in tumorigenesis. Methods: PCR-based microarrays were used to identify potential transcriptional target of Sox4. siRNA was used to knockdown the expression of Sox4. Luciferase and chromatin immunoprecipitation (ChIP) assays were used to test the transcriptional regulations. Results: PCR-based microarrays found that Cyr61, a secreted extracellular matrix-associated signaling protein, was a transcriptional target of Sox4. Overexpression of Sox4 increased, while its knockdown using small interfering RNA (siRNA) reduced Cyr61 expression. A potential Sox4 binding motif located at the proximal Cyr61 promoter was identified. Conclusion: Thus, our results suggest a previously unknown Sox4-Cyr61 molecular network, which may control colon cancer cell proliferation and survival.

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SOX4 expression levels in urothelial bladder carcinoma

Cited by 19 publications

References 17 publications

Decreased miR-204 in H. pylori-Associated Gastric Cancer Promotes Cancer Cell Proliferation and Invasion by Targeting SOX4

Decreased miR-204 in H. pylori-Associated Gastric Cancer Promotes Cancer Cell Proliferation and Invasion by Targeting SOX4

Clinicopathological significance of SOX4 expression in primary gallbladder carcinoma

Sox4 Up-Regulates Cyr61 Expression in Colon Cancer Cells

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