Transcriptional coactivator with PDZ-binding motif (TAZ) is a transcriptional coactivator involved in the differentiation of stem cell as well as the development of multiple organs. Recently, TAZ has also been identified as a major component of the novel Hippo-LATS tumor suppressor pathway and to function as an oncogene in breast cancer. We show for the first time that TAZ is an oncogene in non-small cell lung cancer (NSCLC). Our results show that TAZ is overexpressed in NSCLC cells and that lentivirus-mediated overexpression of TAZ in HBE135 immortalized human bronchial epithelial cells causes increased cell proliferation and transformation, which can be restored back to its original levels by knockdown of TAZ. In addition, short-hairpin RNA (shRNA)-mediated knockdown of TAZ expression in NSCLC cells suppresses their proliferation and anchorage-independent growth in vitro, and tumor growth in mice in vivo, which can be reversed by re-introduction of shRNA-resistant TAZ into TAZ-knockdown NSCLC cells. These results indicate that TAZ is an oncogene and has an important role in tumorigenicity of NSCLC cells. Therefore, TAZ may present a novel target for the future diagnosis, prognosis and therapy of lung cancer.

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Oxidative stress injury is one important factor in intestinal mucosal barrier damage. Expression of heat shock protein (HSP)70 is an endogenous mechanism by which living cells adapt to stress. This study was undertaken to investigate the protective effects of HSP70 on intestinal oxidative stress. Two hundred and forty broilers were injected intraperitoneally with HSP70 inducer l-(1)-glutamine or with the inhibitor quercetin. Twenty-four hours later, they were heat stressed for 0, 2, 3, 5, and 10 h, respectively, at 36 ± 1°C. The l-(1)-glutamine significantly increased HSP70 expression (P < 0.001). At 2 h or 3 h of heat stress, the HSP70 expression obviously elevated (P < 0.001). Levels of corticosterone and the heterophil:lymphocyte ratio significantly increased when HSP70 expression was inhibited (P < 0.0001). Serum corticosterone was negatively correlated with the HSP70 expression at 3 h of heat stress (P = 0.0015; R = -0.6537). Heat shock protein 70 significantly protected the integrity of the intestinal mucosa from heat stress, with significantly decreased lactic dehydrogenase when HSP70 expression was enhanced (P < 0.001). In addition, heat-stress time significantly affected the lactic dehydrogenase release (P < 0.001). Furthermore, HSP70 significantly elevated antioxidant enzyme activities (such as superoxide dismutase, glutathione peroxidase, and total antioxidant capacity) and inhibited lipid peroxidation to relieve intestinal mucosal oxidative injury (P < 0.001). These results suggest that HSP70 is capable of protecting the intestinal mucosa from heat-stress injury by improving antioxidant capacity of broilers and inhibiting the lipid peroxidation production.

The short-term results of the current study suggest that LAG with D2 lymph node dissection is a safe and feasible procedure in treating patients with locally AGC in experienced centers.