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Non-small cell lung cancer (NSCLC) ranks the first in incidence and mortality among malignant tumors in China. Molecular targeted therapies such as gefitinib, an oral inhibitor of the epidermal growth factor receptor tyrosine kinase, have shown significant benefits in patients with advanced NSCLC. However, most patients have unsatisfactory outcomes due to the development of drug resistance, and there is an urgent need to better understand the pathways involved in the resistance mechanisms. In this study, we found that HMGB1 is highly expressed in drug-resistant cells and confers to gefitinib resistance in NSCLC cells via activating autophagy process. Gefitinib upregulates HMGB1 expression in time-dependent and dose-dependent manners in human NSCLC cells. RNA interference-mediated knockdown of HMGB1 reduces PC9GR cell viability, induces apoptosis, and partially restores gefitinib sensitivity. Mechanistic analyses indicate that elevated HMGB1 expression contributes to gefitinib resistance by inducing autophagy. Thus, our results suggest that HMGB1 is an autophagy regulator and plays a key role in gefitinib resistance of NSCLC.

The bulletin board system (BBS) significantly changed the production and transmission of knowledge in China's information technology (IT). Launched in 1991, Chinese FidoNet (CFido) provided a virtual space for hobbyists to explore technology-for-fun and aggregated many future Chinese digital entrepreneurs, enabling them to experiment with business models and pursue open-source software with Chinese characters. CFido's short history (1991–1998) also encapsulates the fast-changing dynamic between knowledge and its social context. CFido participants first perceived the BBS as a utopian "pure land" where grassroots intellectuals could develop software and digital technologies, free from outside interests and interventions. Yet the beginning of government control of cyberspace, the boom of the IT industry and e-commerce, and the transition from the dial-up BBS to the Internet led the CFidoers to diverging positions about amateurs and ultimately brought CFido to an end. [ABSTRACT FROM AUTHOR]

The random laser from sheared dye-doped polymer-dispersed liquid crystal (DDPDLC) is investigated. As the emission intensity weakens, the threshold of random laser from DDPDLC increases from 2.0 mJ/pulse to 4.0 mJ/pulse, and the degree of polarization (DOP) increases from 0.1 to 0.78, obviously when the shear distance increases from 0 mm to 4 mm. As the liquid crystal droplets are gradually oriented in the shear direction caused by alignment direction of polymer chain and anisotropy of droplet shape, the scattering intensity perpendicular to the shear direction gradually decreases and that parallel to the shear direction gradually increases. The anisotropic absorption of the laser dye also plays a certain role as the shear distance is 0 mm. The controllable intensity and polarization degree of random laser have a huge potential for sensing applications.

Neuropathic pain is a debilitating clinical condition with few efficacious treatments, warranting development of novel therapeutics. Ozone is widely used as an alternative therapy for many different pain conditions, with exact mechanisms still elusive. In this study, we found that a single peri-sciatic nerve injection of ozone decreased mechanical allodynia and thermal hyperalgesia, and normalized the phosphorylation of protein kinase C γ, N-methyl-D-aspartate receptor, and extracellular signal-regulated kinase in a chronic constriction injury (CCI) model in rat sciatic nerve. Meanwhile, ozone significantly suppressed CCI-induced activation of spinal microglia. More importantly, the anti-nociceptive effect of ozone depended on the activation of 5'-adenosine monophosphate (AMP)-activated protein kinase (AMPK), which was proved by the fact that the phosphorylated AMPK level increased during the ozone therapy and AMPK antagonist abolished the effect of ozone in vivo and in vitro. In addition, direct injection of AMPK agonist could replicate the anti-nociceptive effect of ozone in CCI rats. In conclusion, our observations indicate that peri-sciatic nerve injection of ozone activates AMPK to attenuate CCI-induced neuropathic pain., (© The Author (2016). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, IBCB, SIBS, CAS. All rights reserved.)

Background: RhoB is a member of the Rho small GTPase family that regulates cytoskeletal dynamics and vesicle trafficking. The RhoB homologs, RhoA and RhoC, have been shown to promote cancer progression and metastasis. In contrast, the functions of RhoB in human cancers are context dependent. Although expression of RhoB inversely correlates with disease progression in several epithelial cancers, recent data suggest that RhoB may support malignant phenotypes in certain cancer types., Methods: We assessed RhoB protein levels in glioma surgical specimens and patient-derived xenografts. The roles of RhoB in glioblastoma were determined by loss-of-function and gain-of-function assays in vitro and in vivo. The impact on p53 and STAT3 signaling was investigated., Results: RhoB expression was similar in tumor specimens compared with normal neural tissues obtained from epilepsy surgery. RhoB was expressed in the vast majority of xenograft tumors and spheroid cultures. Knockdown of RhoB induced cell-cycle arrest and apoptosis and compromised in vivo tumorigenic potential. However, overexpression of wild-type RhoB or a constitutively active mutant (RhoB-V14) did not significantly affect cell growth, which suggests that RhoB is not a rate-limiting oncogenic factor and is consistent with the scarcity of RhoB mutations in human cancer. Knockdown of RhoB reduced basal STAT3 activity and impaired cytokine-induced STAT3 activation. In glioblastoma tumors retaining wild-type p53, depletion of RhoB also activated p53 and induced expression of p21(CIP1) (/WAF1)., Conclusions: Our data suggest that RhoB belongs to an emerging class of "nononcogene addiction" factors that are essential for maintenance of malignant phenotypes in human cancers., (© The Author(s) 2014. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)