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Articles by L Cao
Total Records ( 3 ) for L Cao
  J Meng , W Xie , L Cao , C Hu and Z. Zhen

Hepatoma-derived growth factor (HDGF), a nuclear protein with both mitogenic and angiogenic activity, has been reported to be mainly involved in tumorigenesis and the progression of non-small cell lung cancer. In this study, the HDGF expression was knocked down by specific-shRNA with lentivirus expression vector targeting HDGF in lung squamous cell carcinoma 520 cells. HDGF knocked down by shRNA suppressed the cell proliferation significantly both in vitro and in vivo as indicated by MTT, plate clone and transplanted tumor model assays. In addition, the knocked-down expression of HDGF also inhibited cell migration and invasion as shown in transwell and Boyden experiments. We concluded that HDGF acts as an oncogene participating in the pathogenesis of squamous cell lung cancer, and HDGF may be a key therapeutic target for non-small cell lung cancer.

  B Peng , L Cao , W Wang , L Xian , D Jiang , J Zhao , Z Zhang , X Wang and L. Yu

Matrix metalloproteinase (MMP) 1 and MMP3 are enzymes that degrade the extracellular matrix and have been implicated to play an important role in cancer development. Many studies have been carried out on the association between polymorphisms of MMP1 –1607 1G>2G and MMP3 –1171 5A>6A and cancer risk. However, results from these studies remain inconclusive. Here, we performed a meta-analysis of >38 000 subjects to better assess the purported associations. For MMP1, –1607 2G/2G genotype carriers were found to have an increased risk of colorectal cancer [2G/2G versus 2G/1G + 1G/1G, odds ratio (OR) = 1.48, 95% confidence interval (CI) (1.26–1.74), Pheterogeneity = 0.066, I2 = 49.3%], head and neck cancer [2G/2G versus 2G/1G + 1G/1G, OR = 1.61, 95% CI (1.26–2.07), Pheterogeneity = 0.002, I2 = 64.7%] and renal cancer [2G/2G versus 2G/1G + 1G/1G, OR = 1.82, 95% CI (1.38–2.39), Pheterogeneity = 0.589, I2 = 0.0%] risk. For MMP3, no association was found between –1171 5A>6A polymorphism and cancer risk in the overall group [6A versus 5A, OR = 1.00, 95% CI (0.95–1.05), Pheterogeneity = 0.124, I2 = 24.9%] and individual cancer subgroups, but stratified analysis by smoking status showed that this polymorphism had different effects on smokers and non-smokers under recessive genetic model. In summary, our study suggests that MMP1 –1607 2G may be associated with an increased cancer risk for certain types of cancers, MMP3 –1171 5A>6A may not be a major risk factor for cancer, but it may be modified by certain environmental factors. Future studies with larger sample sizes are warranted to further evaluate these associations in more detail.

  B Peng , L Cao , X Ma , W Wang , D Wang and L. Yu

Matrix metalloproteinase (MMP) 2, MMP7 and MMP9 are important members of the MMP family. Four polymorphisms in the promoter region of these MMPs, which are MMP2 –1306 C>T, MMP2 –735 C>T, MMP7 –181 A>G and MMP9 –1562 C>T, have been reported to be functional and may contribute to genetic susceptibility to cancers. However, the associations between these polymorphisms and cancer risk remain inconclusive due to conflicting results from different case–control studies. To better evaluate the role of these polymorphisms in cancer development, we conducted a meta-analysis that included 51 studies, with more than 40 000 subjects. The results showed that under dominant genetic model, MMP2 –1306 T was associated with lower susceptibility to lung cancer [odds ratio (OR) = 0.50, 95% confidence interval (CI) 0.43–0.59, Pheterogeneity = 0.147, I2 = 44.1%], head and neck cancer (OR = 0.53, 95% CI 0.41–0.69, Pheterogeneity = 0.974, I2 = 0.0%) and oesophageal cancer (OR = 0.67, 95% CI 0.55–0.80, Pheterogeneity = 0.593, I2 = 0.0%); MMP2-735T was associated with lower risk in lung cancer (OR = 0.65, 95%CI 0.53–0.79, Pheterogeneity = 0.42, I2 = 0.0%) and oesophageal cancer (OR = 0.84, 95% CI 0.70–0.99, Pheterogeneity = 0.206, I2 = 37.4%); MMP7 –181 AG and GG genotype carriers had an increased gastric cancer risk (OR = 1.90, 95% CI 1.43–2.51, Pheterogeneity = 0.992, I2 = 0.0%) and MMP9 –1562 C>T was not associated with cancer risk in the whole group analysis (OR = 0.99, 95% CI 0.91–1.08, Pheterogeneity = 0.419, I2 = 3.0%) and subgroup analyses. In all, our meta-analysis suggests that MMP2 –1306 C>T, MMP2 –735 C>T and MMP7 –181 A>G may play allele-specific roles in cancer development, while MMP9 –1562 C>T may not be a major risk factor for most cancer types. Large case–control studies should be performed to clarify the possible roles of these four polymorphisms in different kinds of cancer in more detail.

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