Chengyuan Ma

Jilin University, Yung-chi, Jilin Sheng, China

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Publications (8)14.93 Total impact

  • Yang Li · Tong Zhou · Chengyuan Ma · Weiwei Song · Jian Zhang · Zhenxiang Yu ·
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    ABSTRACT: To evaluate the potential of ginsenoside metabolite compound K (CK) in enhancing the anti-tumor effects of cisplatin against lung cancer cells, including cell proliferation and apoptosis, and the underlying mechanism. Western blotting and p53 reporter assay were used to assess p53 expression and activity. MTT assay and TUNEL staining were employed to investigate the drug effects on cell growth and apoptosis, respectively. Combination index (CI) was calculated to determine synergism. We found that CK could significantly enhance cisplatin-induced p53 expression and activity in two lung cancer cell lines, H460 and A549. Consequently, synergistic inhibition of cell growth was observed when the cells were co-treated with CK and cisplatin compared to single treatment. In addition, the ability of cisplatin in apoptosis induction was similarly synergized by CK. Furthermore, by using p53-null lung cancer cells, we demonstrate that the synergy was p53 dependent. Conventional chemotherapies are often accompanied by development of drug resistance and severe side effects. Novel discoveries of low toxicity compounds to improve the outcome or enhance the efficacy of chemotherapies are of great interest. In the present study, our data provide the first evidence that CK could be potentially used as an agent to synergize the efficacy of cisplatin in lung cancer.
    Journal of Thoracic Disease 03/2015; 7(3):400-6. DOI:10.3978/j.issn.2072-1439.2015.01.03 · 1.78 Impact Factor
  • Yang Li · Chengyuan Ma · Xu Shi · Zhongmei Wen · Dan Li · Munan Sun · Hui Ding ·
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    ABSTRACT: Multiple drug resistance (MDR) is considered a major challenge in the clinical treatment of non-small cell lung cancer (NSCLC). Both nitric oxide synthase (iNOS) and Wnt signaling pathway participate in the regulation of drug resistance, but the interaction between them remains unclear. In the present study, we detected the activation of Wnt/β-catenin signaling in iNOS-induced drug-resistant lung cancer cells, and compared the effect of canonical and noncanonical Wnt pathway on the level of iNOS. Moreover, we investigated the expression of Wnt/β-catenin signaling downstream factors and its main inhibitors. The results indicated iNOS-induced drug resistance was possibly mediated by glutathione S-transferase-π (GST-π) and topoisomerase IIα (TOPO IIα), but not P-glycoprotein (P-gp), and this process was closely associated with the activation of canonical Wnt/β-catenin signaling, but less with noncanonical pathways. The mechanism of iNOS promoting Wnt/β-catenin pathway was mainly dependent on the inverse regulation of Dickkopf-1 (DKK-1) and secreted frizzled-related protein-1 (SFRP-1). Clarifying the relationship between iNOS and Wnt signaling may provide insight into a better understanding of the mechanism of drug resistance development in NSCLC.
    Oncology Reports 07/2014; 32(4). DOI:10.3892/or.2014.3351 · 2.30 Impact Factor
  • Ming Qian · Donghua Qian · Hongyu Jing · Yang Li · Chengyuan Ma · Yanmin Zhou ·
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    ABSTRACT: The aim of the present study was to evaluate the potency of epidermal growth factor receptor (EGFR) pathway inhibition achieved by combining cetuximab (CET), an anti-EGFR monoclonal antibody, and celecoxib (CXB), a cyclooxygenase-2 (COX-2) inhibitor, in oral squamous cell carcinoma (OSCC) in vitro and in vivo. The OSCC cell line, HSC3, was treated with CET (0-400 µg/ml), CXB (0-40 µM), or a combination of both at a range of concentrations. Cell proliferation, apoptosis, migration and invasion were determined to assess the anticancer effects in vitro. The in vivo effects of CET and CXB on tumor cell growth were examined using an OSCC xenograft nude mouse model. In addition, downstream protein expression levels of EGFR, p-EGFR, PI3K, p-PI3K, AKT and p-Akt were evaluated by western blot analysis. It was found that the combination of low concentrations of CET and CXB significantly suppressed the proliferation, migration and invasion of the HSC3 tumor cells and decreased PEG2 production and VEGF expression in vitro, and inhibited tumor growth in vivo compared to the action of either agent alone. The results also showed that this combination significantly induced apoptosis and increased caspase-3 and caspase-8 activity compared to the action of either agent alone (P<0.01). Furthermore, the combination treatment significantly reduced the expression of p-EGFR, p-PI3K and p-Akt in the HSC3 cell line, which may contribute to the inhibition of tumor growth. Taken together, our findings revealed that the additive combination of CET and CXB is a potential drug candidate for the treatment of OSCC.
    Oncology Reports 07/2014; 32(4). DOI:10.3892/or.2014.3334 · 2.30 Impact Factor
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    ABSTRACT: A disintegrin and metalloprotease (ADAM) 17 has been implicated in the tumor progression of various types of solid tumor; however, little is known about its role in non-small cell lung carcinoma (NSCLC). The present study evaluated whether the downregulation of ADAM17 affects cell proliferation, the cell cycle, cell migration and cell invasion in NSCLC. A recombinant lentiviral small hairpin RNA (shRNA) expression vector carrying ADAM17 was constructed and then infected into A549 cells, a human NSCLC cell line. Cell proliferation, cell cycle progression, cell migration and cell invasion were determined following the downregulation of ADAM17 by siRNA. It was revealed that downregulation of ADAM17 expression using an RNA silencing approach in A549 tumor cells significantly suppressed cell proliferation and invasion in vitro, and tumor growth in vivo. These data suggested that ADAM17 is an important regulator of the tumorigenic properties of human NSCLC and may be used as a potential anticancer therapeutic target in NSCLC.
    Molecular Medicine Reports 03/2014; 9(5). DOI:10.3892/mmr.2014.2029 · 1.55 Impact Factor
  • Yang Li · Chengyuan Ma · Ming Qian · Zhongmei Wen · Hongyu Jing · Donghua Qian ·
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    ABSTRACT: Non-small cell lung cancer (NSCLC) is a lethal disease due to the absence of effective diagnostic biomarkers and therapeutic targets. Therefore, novel molecular targets are critically needed to formulate new approaches for this devastating disease. In the present study, using quantitive real-time PCR and immunohistochemistry. we initially found that expression of the ribosome assembly factor NIN/RPN12 binding protein (NOB1) was elevated in the majority of NSCLC tissues when compared to that in the normal lung tissue counterparts, and its expression level was correlated with key pathological characteristics including tumor differentiation, stage and metastasis. Then, the recombinant lentiviral shRNA expression vector carrying NOB1 was constructed and infected into the human NSCLC A549 cell line. Cell proliferation, cell apoptosis, cell cycle distribution and colony formation ability in A549 cells were assessed following downregulation of NOB1 by siRNA. In addition, tumor growth ability in nude mice was evaluated to define the function of NOB1 in cell transformation and tumorigenesis. It was found that downregulation of NOB1 expression using the RNA silencing approach in A549 tumor cells significantly suppressed the proliferation and colony formation ability, and induced tumor apoptosis in vitro. Tumor growth was also suppressed in vivo. These data suggest that NOB1 is an important regulator of the tumorigenic properties of human NSCLC and may be used as a new promising diagnostic biomarker and a potential anticancer therapeutic target for NSCLC.
    Oncology Reports 01/2014; 31(3). DOI:10.3892/or.2014.2991 · 2.30 Impact Factor
  • Chengyuan Ma · Yang Li · Xianfeng Zhang · Gang Zhao · Haiyang Xu ·
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    ABSTRACT: To investigate the levels of vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) proteins in patients with glioma, in order to determine if either protein has prognostic value. The presence of VEGF and MMP-9 proteins in paraffin-embedded tumour specimens from patients with glioma was detected using immunohistochemistry. The correlation between the levels of VEGF and MMP-9 proteins and tumour grade was analysed. A total of 32 patients with low-grade gliomas (World Health Organization [WHO] grade II) and 48 patients with high-grade gliomas (WHO grades III-IV) participated in the study. Positive immunohistochemical staining of VEGF and MMP-9 proteins was detected in 58/80 (72.5%) and 60/80 (75.0%) of patients, respectively. The level of VEGF immunostaining was significantly positively correlated with the level of MMP-9 immunostaining (r = 0.78). Significantly more high-grade gliomas (grades III-IV) demonstrated positive VEGF and MMP-9 immunostaining compared with the low grade gliomas (grades I-II). These data suggest that VEGF and MMP-9 play an important role in the malignant behaviour of gliomas.
    The Journal of international medical research 01/2014; 42(1). DOI:10.1177/0300060513481924 · 1.44 Impact Factor
  • Yang Li · Chengyuan Ma · Ming Qian · Zhongmei Wen · Hongyu Jing · Donghua Qian ·
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    ABSTRACT: Butein is a flavonoid isolated from the bark of Rhus verniciflua Stokes and the flowers of Butea monosperma, and is known to be a potential therapeutic drug for treating inflammation and cancer. Cyclooxygenase (COX) converts arachidonic acid to prostanoids, and increased expression of its isoform, COX‑2, has been observed in lung cancer tissue. The aim of the present study was to investigate expression alteration of COX‑2 in A549 lung cancer cells following butein treatment at the mRNA and protein levels by quantitative polymerase chain reaction and western blotting, respectively. It was observed that COX‑2 mRNA and protein levels were significantly downregulated in the butein treatment group in comparison with the control group (P<0.05). In addition, the effects of butein on proliferation and apoptosis were evaluated. The data demonstrated that butein induces cell‑cycle arrest and apoptosis in human lung cancer cells. These results indicated that butein may be a promising candidate drug for lung cancer treatment.
    Molecular Medicine Reports 12/2013; 9(2). DOI:10.3892/mmr.2013.1850 · 1.55 Impact Factor
  • Chengyuan Ma · Yang Li · Zhixin Li · Haiyan Huang · Kan Xu · Haiyang Xu · Jieying Bai · Xiao Li · Gang Zhao ·
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    ABSTRACT: Aberrant epidermal growth factor receptor (EGFR) signaling is a common feature of multiple tumor types, including glioblastoma (GBM). As such, EGFR has emerged as an attractive target for antitumor therapy. In the present study, we sought to develop an immunotoxin capable of specifically targeting EGFR-expressing cells and mediating inhibition of cell growth and cell killing. The Luffin P1 (LP1) ribosome inactivating protein was chosen to generate a fusion protein, antiEGFR/LP1, based upon its potent protein synthesis inhibition and small size (5 kDa). LP1 was fused to the C-terminus of an anti-EGFR single-chain antibody (scFv). The recombinant antiEGFR/LP1 protein was expressed in Escherichia coli, and refolded and purified on an immobilized Ni(2+)-affinity chromatography column. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting analysis revealed that antiEGFR/LP1 was sufficiently expressed. Confocal microscopy and flow cytometry demonstrated that antiEGFR/LP1 bound specifically to EGFR-positive cells (U251), as almost no binding to EGFR-negative (Jurkat cells) was observed under identical time and dosage conditions. Finally, the MTT cell viability assay showed that antiEGFR/LP1 elicited obvious cytotoxicity toward EGFR-positive tumor cells. Collectively, these results suggest that antiEGFR/LP1 is biologically active and specific toward EGFR-positive tumor cells and may represent an effective EGFR-targeted cancer therapy.
    Protein Expression and Purification 02/2012; 83(1):1-7. DOI:10.1016/j.pep.2012.02.011 · 1.70 Impact Factor