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Articles by Q Gao
Total Records ( 3 ) for Q Gao
  D Ouyang , X He , L Xu , X Wang , Q Gao and H. Guo

The major histocompatibility complex class I allele Mamu-B*17 of rhesus macaques is an elite controller of simian immunodeficiency virus (SIV) infection whereas Mamu-B*01 has no inhibitory effect on SIV replication. The mechanism is still elusive. In this study, the so-called ‘missing G’ in the leading peptide sequence of Mamu-B*1703 allele was artificially inserted back through PCR amplification, and the new sequence was renamed as Mamu-B*1703(+G). The plasmids harboring Mamu-B*1703, Mamu-B*1703(+G) and Mamu-B*0101 cDNA sequence fused to EGFP gene were transfected into K562 and Cos-7 cells, respectively. Our data showed that these plasmids had similar transfection efficiencies and expression potentials in K562 cells, but the surface density of Mamu-B*1703 complexes, which was slightly influenced by the artificial change of the leading peptide length, was much higher than that of Mamu-B*0101 molecules. These results might partially account for the differential effects of Mamu-B*17 and Mamu-B*01 alleles on SIV replication in rhesus macaques.

  Z Han , Z Hong , C Chen , Q Gao , D Luo , Y Fang , Y Cao , T Zhu , X Jiang , Q Ma , W Li , L Han , D Wang , G Xu , S Wang , L Meng , J Zhou and D. Ma

Tumor cells acquire the ability to proliferate uncontrollably, resist apoptosis, sustain angiogenesis and evade immune surveillance. Signal transducer and activator of transcription (STAT) 3 regulates all of these processes in a surprisingly large number of human cancers. Consequently, the STAT3 protein is emerging as an ideal target for cancer therapy. This paper reports the generation of an oncolytic adenovirus (M4), which selectively blocks STAT3 signaling in tumor cells as a novel therapeutic strategy. M4 selectively replicated in tumor cells and expressed high levels of antisense STAT3 complementary DNA during the late phase of the viral infection in a replication-dependent manner. The viral progeny yield of M4 in tumor cells was much higher than that of the parent adenoviral mutants, Ad5/dE1A. M4 effectively silenced STAT3 and its target genes in tumor cells while sparing normal cells and exhibited potent antitumoral efficacy in vitro and in vivo. Systemic administration of M4 significantly inhibited tumor growth in an orthotopic gastric carcinoma mouse model, eliminated abdominal cavity metastases and prolonged survival time. In summary, M4 has low toxicity and great potential as a therapeutic agent for different types of cancers.

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