Publications by authors named "Donghua Wu"

The aim of the present study was to report a clinical survey of hereditary multiple exostoses (HME) in a large Chinese pedigree, and the identification of a novel deletion mutation of exostosin glycosyltransferase 2 () gene. A patient with multiple exostoses with huge cartilage‑capped tumors in scapula, knees and ankles received surgery in Department of Orthopedics (Shanghai Changhai Hospital). A total of 20 family members were recruited to the study, with seven members (five male; two female) diagnosed as HME.

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Metastasis is the leading cause of death in patients with advanced non-small cell lung cancer (NSCLC), and epithelial-mesenchymal transition (EMT) is a crucial event in the metastasis of NSCLC. Our previous works demonstrated that NgBR promoted EMT in NSCLC. However, the molecular mechanism was unclear.

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is a fast-growing, large tree and one of the largest North American hardwood trees. In this study, the complete chloroplast (cp) genome sequence of is characterized. The whole cp genome was assembled to 156,867 bp, including a large single copy (LSC) region of 85,534 bp, a small single copy (SSC) region of 16,513 bp and a pair of inverted repeats (IRs) region of 27,410 bp.

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Background: Our previous study demonstrated that aldolase A (ALDOA) is overexpressed in clinical human lung squamous cell carcinoma and that ALDOA promotes epithelial-mesenchymal transition and tumorigenesis. The present study aimed to explore the function of ALDOA in the modulation of non-small cell lung cancer (NSCLC) proliferation and cell cycle progression and the potential mechanism.

Methods: ALDOA was knocked down by short hairpin RNA in H520 and H1299 cells.

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Nogo-B receptor (NgBR) is a specific receptor of Nogo-B that regulates vascular remodeling and angiogenesis. Previously, we found that NgBR promotes the membrane translocation and activation of Ras in breast cancer cells and enhances the chemoresistance of hepatocellular carcinoma cells to 5-fluorouracil. However, the role of NgBR in lung cancer has not yet been elucidated.

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RIOK3 was initially characterized as a homolog of Aspergillus nidulans sudD and showed down-regulation at the invasive front of malignant melanomas, but the molecular mechanism remains elusive. Here, we report that overexpression of RIOK3 inhibits TNFalpha-induced NF-kappaB activation, but down-regulation of endogenous RIOK3 expression by siRNA potentiates it. A yeast two-hybrid experiment revealed that RIOK3 interacted with caspase-10, and further, a GST pull-down assay and endogenous coimmunoprecipitation validated the interaction.

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Background: To screen the differential expression genes of KANLAITE in anti-tumor metastasis.

Methods: mRNA was extracted and purified from the lung of the mouse with LA795 lung metastasis, hybridized respectively on 4 096-gene chip. cDNA microarray was scanned for the fluorescent signals and analyzing difference expression.

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