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

Lin, Guimiao; Zhao, Lijuan; Yin, Feng; Lan, Rongfeng; Li, Lianbo; Zhang, Xiaoming; Zhang, Hui; Yang, Baoxue

doi:10.3892/or.2011.1376

Cited by 7 publications

(11 citation statements)

References 40 publications

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“…Total proteins from both tumor tissues were extracted according to the previous study [27]. Protein samples (30 ug) were then separated by SDS-PAGE and transferred onto a PVDF membrane (Millipore, Bedford, MA, USA).…”

Section: Methodsmentioning

confidence: 99%

Tumor suppressor gene RBM5 delivered by attenuated Salmonella inhibits lung adenocarcinoma through diverse apoptotic signaling pathways

et al. 2013

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BackgroundRBM5 (RNA-binding motif protein 5, also named H37/LUCA-15) gene from chromosome 3p21.3 has been demonstrated to be a tumor suppressor. Current researches in vitro confirm that RBM5 can suppress the growth of lung adenocarcinoma cells by inducing apoptosis. There is still no effective model in vivo, however, that thoroughly investigates the effect and molecular mechanism of RBM5 on lung adenocarcinoma.MethodWe established the transplanted tumor model on BALB/c nude mice using the A549 cell line. The mice were treated with the recombinant plasmids carried by attenuated Salmonella to induce the overexpression of RBM5 in tumor tissues. RBM5 overexpression was confirmed by immunohistochemistry staining. H&E staining was performed to observe the histological performance on plasmids-treated A549 xenografts. Apoptosis was assessed by TUNEL staining with a TUNEL detection kit. Apoptosis-regulated genes were detected by Western blot.ResultsWe successful established the lung adenocarcinoma animal model in vivo. The growth of tumor xenografts was significantly retarded on the mice treated with pcDNA3.1-RBM5 carried by attenuated Salmonella compared to that on mice treated with pcDNA3.1. Overexpression of RBM5 enhanced the apoptosis in tumor xenografts. Furthermore, the expression of Bcl-2 protein was decreased significantly, while the expression of BAX, TNF-α, cleaved caspase-3, cleaved caspase-8, cleaved caspase-9 and cleaved PARP proteins was significantly increased in the pcDNA3.1-RBM5-treated mice as compared to that in the control mice.ConclusionsIn this study, we established a novel animal model to determine RBM5 function in vivo, and concluded that RBM5 inhibited tumor growth in mice by inducing apoptosis. The study suggests that although RBM5’s involvement in the death receptor-mediated apoptotic pathway is still to be investigated, RBM5-mediated growth suppression, at least in part, employs regulation of the mitochondrial apoptotic pathways.

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Section: Methodsmentioning

confidence: 99%

Tumor suppressor gene RBM5 delivered by attenuated Salmonella inhibits lung adenocarcinoma through diverse apoptotic signaling pathways

et al. 2013

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“…Total cellular proteins from both lung tissues and A549 cells were extracted according to the previous study [22]. Protein samples (50 ug) were then separated by SDS-PAGE and transferred onto a PVDF membrane (Millipore, Bedford, MA).…”

Section: Methodsmentioning

confidence: 99%

“…The second antibody was a goat anti-rabbit IgG-HRP from Santa Cruz Biotechnology (CA, USA). Western blot was carried out as previously described [22]. The protein bands were visualized by SuperSignal West Pico Chemiluminescent Substrate (Pierce, Rockford, IL, USA), and the membranes were subjected to X-ray autoradiography.…”

Section: Methodsmentioning

confidence: 99%

“…These tumor-bearing mice were then divided randomly into two groups (six mice per group): (1) PcDNA3.1 as the control group; (2) pcDNA3.1-RBM5 as the RBM5 group. Plasmids were carried by bioengineered attenuated strains of Salmonella enterica serovar typhimurium using electrotransfection as previously described [22,23]. Briefly, plasmids were electrotransfected into Salmonella typhi Ty21a competent cells before use.…”

Section: Methodsmentioning

confidence: 99%

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The tumor suppressor gene RBM5 inhibits lung adenocarcinoma cell growth and induces apoptosis

et al. 2012

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BackgroundThe loss of tumor suppressor gene (TSG) function is a critical step in the pathogenesis of human lung cancer. RBM5 (RNA-binding motif protein 5, also named H37/LUCA-15) gene from chromosome 3p21.3 demonstrated tumor suppressor activity. However, the role of RBM5 played in the occurrence and development of lung cancer is still not well understood.MethodPaired non-tumor and tumor tissues were obtained from 30 adenocarcinomas. The expression of RBM5 mRNA and protein was examined by RT-PCR and Western blot. A549 cell line was used to determine the apoptotic function of RBM5 in vitro. A549 cells were transiently transfected with pcDNA3.1-RBM5. AnnexinV analysis was performed by flow cytometry. Expression of Bcl-2, cleaved caspase-3, caspase-9 and PAPP proteins in A549 lung cancer cells and the A549 xenograft BALB/c nude mice model was determined by Western blot. Tumor suppressor activity of RBM5 was also examined in the A549 xenograft model treated with pcDNA3.1-RBM5 plasmid carried by attenuated Salmonella typhi Ty21a.ResultThe expression of RBM5 mRNA and protein was decreased significantly in adenocarcinoma tissues compared to that in the non-tumor tissues. In addition, as compared to the vector control, a significant growth inhibition of A549 lung cancer cells was observed when transfected with pcDNA3.1-RBM5 as determined by cell proliferation assay. We also found that overexpression of RBM5 induced both early and late apoptosis in A549 cells using AnnexinV/PI staining as determined by flow cytometry. Furthermore, the expression of Bcl-2 protein was decreased, whereas the expression of cleaved caspase-3, caspase-9 and PARP proteins was significantly increased in the RBM5 transfected cells; similarly, expression of decreased Bcl-2 and increased cleaved caspase-3 proteins was also examined in the A549 xenograft model. More importantly, we showed that accumulative and stable overexpression of RBM5 in the A549 xenograft BALB/c nude mice model significantly inhibited the tumor growth rate in vivo as compared to that in the control.ConclusionOur study demonstrates that RBM5 can inhibit the growth of lung cancer cells and induce apoptosis both in vitro and in vivo, which suggests that RBM5 might be used as a potential biomarker or target for lung cancer diagnosis and chemotherapy. Moreover, we propose a novel animal model set up in BALB/c nude mice treated with attenuated Salmonella as a vector carrying plasmids to determine RBM5 function in vivo.

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“…Nevertheless, canonical Wnt signaling is linked to Oct4 and pluripotency as evident by the fact that the downregulation of Oct4 expression occurs when T-cell factor 3, Tcf3, serving as a transcriptional repressor in the absence of β -catenin, is overexpressed in F9 cells (Figure 2) [169]. This supports what was described earlier where Wnt is induced and Axin, a negative regulator of canonical Wnt signaling, declines in RA-treated F9 and P19 cells [88, 91–93, 170].…”

Section: Pluripotency Factors and Signaling Crosstalkmentioning

confidence: 99%

Mechanisms Regulating Stemness and Differentiation in Embryonal Carcinoma Cells

Kelly

Gatie

2017

Stem Cells International

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Just over ten years have passed since the seminal Takahashi-Yamanaka paper, and while most attention nowadays is on induced, embryonic, and cancer stem cells, much of the pioneering work arose from studies with embryonal carcinoma cells (ECCs) derived from teratocarcinomas. This original work was broad in scope, but eventually led the way for us to focus on the components involved in the gene regulation of stemness and differentiation. As the name implies, ECCs are malignant in nature, yet maintain the ability to differentiate into the 3 germ layers and extraembryonic tissues, as well as behave normally when reintroduced into a healthy blastocyst. Retinoic acid signaling has been thoroughly interrogated in ECCs, especially in the F9 and P19 murine cell models, and while we have touched on this aspect, this review purposely highlights how some key transcription factors regulate pluripotency and cell stemness prior to this signaling. Another major focus is on the epigenetic regulation of ECCs and stem cells, and, towards that end, this review closes on what we see as a new frontier in combating aging and human disease, namely, how cellular metabolism shapes the epigenetic landscape and hence the pluripotency of all stem cells.

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

Cited by 7 publications

References 40 publications

Tumor suppressor gene RBM5 delivered by attenuated Salmonella inhibits lung adenocarcinoma through diverse apoptotic signaling pathways

Tumor suppressor gene RBM5 delivered by attenuated Salmonella inhibits lung adenocarcinoma through diverse apoptotic signaling pathways

The tumor suppressor gene RBM5 inhibits lung adenocarcinoma cell growth and induces apoptosis

Mechanisms Regulating Stemness and Differentiation in Embryonal Carcinoma Cells

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