DIGE-based proteomic analysis identifies nucleophosmin/B23 and nucleolin C23 as over-expressed proteins in relapsed/refractory acute leukemia

Hu, Jianda; Lin, Mao; Liu, Tingbo; Li, Jing; Chen, Buyuan; Chen, Yingyu

doi:10.1016/j.leukres.2011.01.010

Cited by 36 publications

(28 citation statements)

References 33 publications

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“…Data were expressed as the mean ± SEM; *p \ 0.001, versus si-control cell invasion and migration. In accordance with our reports, some studies on tumor biology also testified the significances of C23 in the migration and invasion of cancer cells [25,26].…”

Section: Discussionsupporting

confidence: 91%

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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Section: Discussionsupporting

confidence: 91%

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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“…Yang et al also reported that NPM1 was over-expressed in the gastric cancer drug-resistant SGC7901/ADM cell line, and that the suppression of NPM1 expression in the cell line enhanced adriamycin chemosensitivity (Yang et al 2007). Recently, Hu et al found that NPM1 may be associated with drug resistance and may aid in the prognostic assessment of leukemia cases (Hu et al 2011). These results indicate that the over-expression of NPM1 may have important implications in the bladder cancer pumc-91/ADM cell line.…”

Section: Discussionmentioning

confidence: 93%

Identification of proteins differentially expressed in adriamycin-resistant (pumc-91/ADM) and parental (pumc-91) human bladder cancer cell lines by proteome analysis

Meng

Lei

Zhang

et al. 2012

J Cancer Res Clin Oncol

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“…Hu et al (24) have investigated novel protein changes involved in drug Overexpression of MGAT5 influences the chemosensitivity of MCF-7 cells both in vitro and in vivo. (A) MCF-7 cells were transfected with a pcDNA3.1 expression vector, and Western blot analysis for MGAT5 was assessed.…”

Section: Discussionmentioning

confidence: 99%

Functional roles of glycogene and N‐glycan in multidrug resistance of human breast cancer cells

Xing

et al. 2013

IUBMB Life

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Drug resistance is a major problem in cancer chemotherapy. Aberrant glycosylation has been known to be associated with cancer chemoresistance. Aim of this work is to investigate the alterations of glycogene and N-glycan involved in multidrug resistance (MDR) in human breast cancer cell lines. Using real-time polymerase chain reaction (PCR) for quantification of glycogenes, fluorescein isothiocyanate (FITC)-lectin binding for glycan profiling, and mass spectrometry for N-glycan composition, the expression of glycogenes, glycan profiling, and N-glycan composition differed between drug-resistant MCF/ ADR cells and the parental MCF-7 line. Further analysis of the N-glycan regulation by tunicamycin (TM) application or PNGase F treatment in MCF/ADR cells showed partial inhibition of the N-glycan biosynthesis and increased sensitivity to chemotherapeutic drugs dramatically both in vitro and in vivo. Using an RNA interference strategy, we showed that the downregulation of MGAT5 in MCF/ADR cells could enhance the chemosensitivity to antitumor drugs both in vitro and in vivo. Conversely, a stable high expression of MGAT5 in MCF-7 cells could increase resistance to chemotherapeutic drugs both in vitro and in vivo. In conclusion, the alterations of glycogene and N-glycan in human breast cancer cells correlate with tumor sensitivity to chemotherapeutic drug and have significant implications for the development of new treatment strategies. V C 2013 IUBMB Life, 65(5): 409-422, 2013.

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DIGE-based proteomic analysis identifies nucleophosmin/B23 and nucleolin C23 as over-expressed proteins in relapsed/refractory acute leukemia

Cited by 36 publications

References 33 publications

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

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

Identification of proteins differentially expressed in adriamycin-resistant (pumc-91/ADM) and parental (pumc-91) human bladder cancer cell lines by proteome analysis

Functional roles of glycogene and N‐glycan in multidrug resistance of human breast cancer cells

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