Nucleolin antisense oligodeoxynucleotides induce apoptosis and may be used as a potential drug for nasopharyngeal carcinoma therapy

Wu, Ching Hsiang; Chou, Hung‐Wen; Kuo, Ya‐Huei; Lu, Ruei‐Min; Hwang, Yu-Chyi; Wu, Han‐Chung; Lin, Chin‐Tarng

doi:10.3892/or.2011.1476

Cited by 6 publications

(1 citation statement)

References 18 publications

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“…Decreased nucleolin expression also caused a dramatic decrease of tumor size in an intracranial xenograft model. Wu et al 34 showed that antisense phosphorothioate-modified oligodeoxynucleotides (S-ODNs) directed at nucleolin mRNA could trigger the apoptosis of nasopharyngeal carcinoma (NPC) cells and that S-ODN treatment would result in the suppression of NPC growth in tumor xenografts. It was also reported that upon binding of miRNA-494 to nucleolin, nucleolin expression was inhibited and led to an obvious reduction of cancer cell survival.…”

Section: Nucleolin-based Sirna and Microrna Treatmentmentioning

confidence: 99%

Roles of nucleolin

Chen

2016

SMJ

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Nucleolin, a multifunctional protein distributed in the nucleolus, participates in many modulations including rDNA transcription, RNA metabolism, and ribosome assembly. Nucleolin is also found in the cytoplasm and on the cell membrane, and surface nucleolin can bind to various ligands to affect many physiological functions. The expression and localization of nucleolin is often abnormal in cancers, as the differential distribution of nucleolin in cancer can influence the carcinogenesis, proliferation, survival, and metastasis of cancer cells, leading to the cancer progression. Thus, nucleolin may be a novel and promising target for anti-cancer treatment. Here, we describe how nucleolin act functions in cancer development and describe nucleolin-dependent anti-cancer therapies.

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Section: Nucleolin-based Sirna and Microrna Treatmentmentioning

confidence: 99%

Roles of nucleolin

Chen

2016

SMJ

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C23 protein meditates bone morphogenetic protein-2-mediated EMT via up-regulation of Erk1/2 and Akt in gastric cancer

2015

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In our previous study, the epithelial-to-mesenchymal transition (EMT) has been identified to be involved in gastric cancer progression. Notably, nuclear protein C23 and bone morphogenetic protein-2 (BMP2) have been linked into EMT. However, the specific mechanisms underlying BMP2 pathway-mediated EMT are not still unraveled. In this study, we adopted immunohistochemistry and immunoblotting to determine the expression of C23 and BMP2 receptor II (BMPR-II) in 90 gastric cancer samples and cell lines. Subsequently, relevant cell lines were selected to be treated with si-C23 or si-BMPRII and the detection of in vitro assay. Our results revealed that both C23 and BMPRII were aberrantly and constitutively expressed in gastric cancer specimens and cell lines, whose expression was positively associated with metastasis, stage and differentiation, and portended poor survival outcome of gastric cancer patients. In vitro assay validated the increased expression of p-Erk1/2, p-Akt, vimentin, N-cadherin, and MMP2 in BMP2-stimulated MGC803 cells, which was in a dose-dependent manner. By contrast, si-C23 treatment attenuated the BMP2-stimulated expression of p-Erk1/2, p-Akt, vimentin, N-cadherin, and MMP2. Also, the treatment of either si-C23 or si-BMPRII decreased the ability of migration and invasion of MGC803 cells. In conclusion, C23 mediates BMP2-induced EMT progression via the up-regulation of Erk1/2 and Akt signaling pathway in gastric cancer, which indicated both C23 and BMPRII pathway could be recommended as prospective targets or biomarkers to antagonize the progression of gastric cancer.

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