Oct-3/4 Expression Reflects Tumor Progression and Regulates Motility of Bladder Cancer Cells

Chang, Chao Ching; Shieh, Gia Shing; Wu, Pensée; Lin, Chia-Cheng; Shiau, Ai‐Li; Wu, Chao

doi:10.1158/0008-5472.can-08-0094

Cited by 148 publications

(146 citation statements)

References 46 publications

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“…Tumors with intense Oct4 expression were associated with further disease progression, a greater degree of metastasis and shorter cancer-related survival compared with those with moderate and low Oct4 expression (32), as revealed in our study. Nanog and Sox2 are another two key regulators in the process of pluripotency maintenance (33,34).…”

Section: Discussionsupporting

confidence: 83%

TCF3 inhibits F9 embryonal carcinoma growth by the down-regulation of Oct4

Lin

Zhao²,

Yin³

et al. 2011

Oncol Rep

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Abstract. T-cell factor 3 (TCF3), a downstream effector of Wnt signaling in embryonic stem (ES) cells, plays an important role in pluripotent self-renewal and proliferation. Loss of TCF3 delays the differentiation of mouse ES cells. The purpose of this study was to investigate the effect of TCF3 on embryonal carcinoma (EC). The mouse F9 EC cell line and a tumor-bearing mouse model were used to evaluate the anti-EC tumor effects of TCF3 in vitro and in vivo, respectively. The overexpression of TCF3 significantly inhibited proliferation, colony-forming and migration in F9 EC cells by approximately 30, 45 and 30%, respectively. The in vivo mouse model showed that the overexpression of TCF3 significantly reduced tumor volume (36.4%) and tumor weight (34.8%), malignancy progression and local infiltration and prolonged the life span of tumor-bearing mice. Overexpression of TCF3 significantly down-regulated Oct4 expression in the F9 EC cells. The results indicate that TCF3 is an inhibitor of the malignant phenotypes of embryonal carcinoma through the regulation of Oct4 expression.

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Section: Discussionsupporting

confidence: 83%

TCF3 inhibits F9 embryonal carcinoma growth by the down-regulation of Oct4

Lin

Zhao²,

Yin³

et al. 2011

Oncol Rep

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“…Three pluripotency-related transcription factors, Oct 3/4, Nanog and Sox-2, form a core regulatory network that coordinates to determine the self-renewal and differentiation of ESCs. These ESC self-renewal molecules may also contribute to tumorigenesis (24). The dysregulated expression of Oct 3/4, Nanog and Sox-2 has been shown in numerous types of tumors and it is possible that this may contribute to the neoplastic process and play a role in cancer development.…”

Section: Discussionmentioning

confidence: 99%

Expression of the pluripotency markers Oct3/4, Nanog and Sox2 in human breast cancer cell lines

et al. 2012

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Abstract. Previous studies have demonstrated that pluripotency-associated transcription factors, such as Oct3/4, Nanog and Sox2, play a crucial role in the development and malignant progression of various types of tumors. Breast cancer is the most frequent cancer among females, being a heterogeneous disease, with distinct morphologies, metastatic behavior and therapeutic responses. The expression of Oct3/4, Nanog and Sox2 in 3 human breast cancer cell lines, MCF7, T-47D and MDA-MB-231, was determined. The expression of Oct3/4, Nanog and Sox2 mRNA was determined by reverse transcription polymerase chain reaction (RT-PCR) and protein expression was detected by immunocytohistochemistry. RT-PCR revealed that all three human breast cancer cell lines tested expressed evident Oct3/4, Nanog and Sox-2 mRNA at various levels. Higher levels of Oct3/4 were identified in MCF7 and MDA-MB-231 cells compared with T-47D cells. Higher levels of Nanog were observed in MCF7 and T-47D cells compared with MDA-MB-231 cells and the highest expression of Sox-2 was detected in MCF7 cells. The nuclear localization of Oct3/4, Nanog and Sox-2 was confirmed by immunostaining. Oct3/4, Nanog and Sox2 were expressed in human breast cancer cell lines. Further studies are required to characterize the role of Oct3/4, Nanog and Sox2 in human breast cancer.

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“…Cancer stem cells (CSCs) or tumor-initiating cells are subpopulation of undifferentiated tumorigenic cells within the tumors that represent unique characteristics such as tumor-initiation, self-renewal, and the ability of proliferation which are responsible for tumor progression, relapse, metastasis and also tumor heterogeneity resulting from differentiation (Heppner, 1984;Reya et al, 2001;Clarke et al, 2006;Jordan et al, 2006;Dwyer et al, 2007;Chang et al, 2008;Bentivegna et al, 2010;Bohl et al, 2011;Ho et al, 2012;Madjd et al, 2013). CSCs also mediate tumor resistance to common treatments such as chemotherapy and radiation (Bao et al, 2006;Li et al, 2008;Bentivegna et al, 2010;Ho et al, 2012;Madjd et al, 2013).…”

Section: Introductionmentioning

confidence: 99%