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Shiga toxin-producing Escherichia coli (STEC) causes diarrhea and hemorrhagic colitis with life-threatening complications, such as hemolytic uremic syndrome. The aim of this study was to assess the molecular epidemiologic features of non-O157 STEC strains from different resources in China and illustrate the role of animal reservoirs or animal-derived foodstuffs in human STEC infections. A collection of 301 non-O157 STEC isolates from domestic and wild animals (i.e., cattle, goat, pig, yak, pika, and antelope), raw meats (i.e., beef, pork, mutton, chicken, and duck), diarrheal patients, and healthy carriers in different regions of China were selected in this study. Of the 301 analyzed STEC isolates, 67 serogroups, and 118 serotypes were identified; this included some predominant serogroups associated with human disease, such as O26, O45, O103, O111, and O121. Eighteen different combinations of stx subtypes were found. Eleven isolates carried the intimin gene eae, 93 isolates contained ehxA, and 73 isolates carried astA. The prevalence of other putative adhesion genes saa, paa, efa1, and toxB was 28.90% (87), 6.98% (21), 2.31% (7), and 1% (3), respectively. The phylogenetic distribution of isolates was analyzed by multilocus sequence typing (MLST). Ninety-four sequence types were assigned across the 301 isolates. A subset of isolates recovered from yak and pika residing in the similar wild environments, Qinghai-Tibetan plateau, showed similar genetic profiles and more tendencies to cluster together. Isolates from goat and mutton exhibited close genetic relatedness with those from human-derived isolates, providing evidence that transmission may have occurred locally within intraspecies or interspecies, and importantly, from animal reservoirs, or raw meats to humans. Comparing isolates in this study with highly virulent strains by MLST, along with serotyping and virulence profiles, it is conceivable that some of isolates from goat, yak, or raw meats may have potential to cause human diseases.

Metastasis is the major cause for high mortality of lung cancer with the underlying mechanisms poorly understood. The scaffolding protein neural precursor cell expressed, developmentally down-regulated 9 (NEDD9) has been identified as a prometastasis gene in several types of cancers including melanoma and breast cancer. However, the exact role and related mechanism of NEDD9 in regulating lung cancer metastasis still remain largely unknown. Here, we demonstrate that NEDD9 knockdown significantly inhibits migration, invasion and metastasis of lung cancer cells in vitro and in vivo. The pro-metastasis role of Nedd9 in lung cancer is further supported by studies in mice models of spontaneous cancer metastasis. Moreover, we find that NEDD9 promotes lung cancer cell migration and invasion through the induction of epithelial-mesenchymal transition (EMT) potentially via focal adhesion kinase activation. More importantly, NEDD9 expression inversely correlates with Ecadherin expression in human lung cancer specimens, consistent with the findings from in vitro studies. Taken together, this study highlights that NEDD9 is an important mediator promotes lung cancer metastasis via EMT.Lung cancer is a deadly disease with high mortality and its 5-year survival rate is approximately 15% globally. Metastasis, frequently observed in patients initially diagnosed with lung cancer, remains as an important factor in contribution to high mortality of lung cancer.1 Despite great efforts in last decades, the molecular mechanisms involved in lung cancer metastasis process still remain far from being fully understood.Recent studies have shown that NEDD9 (Neural precursor cell expressed, developmentally down-regulated 9, also known as HEF1), a scaffolding protein without known catalytic activity, is important for pro-metastasis behavior in several types of solid tumors. 2,3 In melanoma, NEDD9 is frequently up-regulated by gene allele amplification and activates FAK (focal adhesion kinase) to promote cell invasion and metastasis.2 NEDD9 complexes with DOCK3 and regulates the activation of Rac which are essential for promoting the mesenchymal-type movement of melanoma cells. 4 In glioblastoma, NEDD9 works as an effector of FAK to promote tumor cell aggression.5 Interestingly, Nedd9 2/2 mice displayed much less mammary tumor formation as well as lung metastasis, which is potentially due to the reduction of Fak and Src activation.6 Consistently, we have recently found that NEDD9 is transcriptionally regulated by CRTC1/CREB complex in LKB1-deficient lung cancer and significantly contributes to tumor progression via the promotion of tumor differentiation status.7 However, the roles of NEDD9 in lung