BackgroundChemoresistance has long been recognized as a major obstacle in cancer therapy. Clarifying the underlying mechanism of chemoresistance would result in novel strategies to improve patient’s response to chemotherapeutics.MethodslncRNA expression levels in gastric cancer (GC) cells was detected by quantitative real-time PCR (qPCR). MALAT1 shRNAs and overexpression vector were transfected into GC cells to down-regulate or up-regulate MALAT1 expression. In vitro and in vivo assays were performed to investigate the functional role of MALAT1 in autophagy associated chemoresistance.ResultsWe showed that chemoresistant GC cells had higher levels of MALAT1 and increased autophagy compared with parental cells. Silencing of MALAT1 inhibited chemo-induced autophagy, whereas MALAT1 promoted autophagy in gastric cancer cells. Knockdown of MALAT1 sensitized GC cells to chemotherapeutics. MALAT1 acts as a competing endogenous RNA for miR-23b-3p and attenuates the inhibitory effect of miR-23b-3p on ATG12, leading to chemo-induced autophagy and chemoresistance in GC cells.ConclusionsTaken together, our study revealed a novel mechanism of lncRNA-regulated autophagy-related chemoresistance in GC, casting new lights on the understanding of chemoresistance.Electronic supplementary materialThe online version of this article (10.1186/s12943-017-0743-3) contains supplementary material, which is available to authorized users.

Gastric cancer (GC) remains a threat to public health with high incidence and mortality worldwide. Increasing evidence demonstrates that long non‐coding RNAs (lncRNAs) play critical regulatory roles in cancer biology, including GC. Previous profiling study showed that lncRNA linc00261 was aberrantly expressed in GC. However, the role of linc00261 in GC progression and the precise molecular mechanism remain unknown. In this study, we report that linc00261 was significantly down‐regulated in GC tissues and the expression level of linc00261 negatively correlated with advanced tumour status and clinical stage as well as poor prognostic outcome. In vitro functional assays indicate that ectopic expression of linc00261 suppressed cell invasion by inhibiting the epithelial–mesenchymal transition (EMT). By RNA pull‐down and mass spectrum experiments, we identified Slug as an RNA‐binding protein that binds to linc00261. We confirmed that linc00261 down‐regulated Slug by decreasing the stability of Slug proteins and that the tumour‐suppressive function of linc00261 can be neutralized by Slug. linc00261 may promote the degradation of Slug via enhancing the interaction between GSK3β and Slug. Moreover, linc00216 overexpression repressed lung metastasis in vivo. Together, our findings suggest that linc00261 acts a tumour suppressor in GC by decreasing the stability of Slug proteins and suppressing EMT. By clarifying the mechanisms underlying GC progression, these findings may facilitate the development of novel therapeutic strategies for GC.

Efficiently estimating properties of large and strongly coupled quantum systems is a central focus in many-body physics and quantum information theory. While quantum computers promise speedups for many such tasks, near-term devices are prone to noise that will generally reduce the accuracy of such estimates. Here we show how to mitigate errors in the shadow estimation protocol recently proposed by Huang, Kueng and Preskill. By adding an experimentally friendly calibration stage to the standard shadow estimation scheme, our robust shadow estimation algorithm can obtain an unbiased estimate of the classical shadow of a quantum system and hence extract many useful properties in a sample-efficient and noise-resilient manner given only minimal assumptions on the experimental conditions. We give rigorous bounds on the sample complexity of our protocol and demonstrate its performance with several numerical experiments.

In this paper we initiate the study of entanglement-breaking (EB) superchannels. These are processes that always yield separable maps when acting on one side of a bipartite completely positive (CP) map. EB superchannels are a generalization of the well-known EB channels. We give several equivalent characterizations of EB supermaps and superchannels. Unlike its channel counterpart, we find that not every EB superchannel can be implemented as a measure-and-prepare superchannel. We also demonstrate that many EB superchannels can be superactivated, in the sense that they can output non-separable channels when wired in series.We then introduce the notions of CPTP- and CP-complete images of a superchannel, which capture deterministic and probabilistic channel convertibility, respectively. This allows us to characterize the power of EB superchannels for generating CP maps in different scenarios, and it reveals some fundamental differences between channels and superchannels. Finally, we relax the definition of separable channels to include (p,q)-non-entangling channels, which are bipartite channels that cannot generate entanglement using p- and q-dimensional ancillary systems. By introducing and investigating k-EB maps, we construct examples of (p,q)-EB superchannels that are not fully entanglement breaking. Partial results on the characterization of (p,q)-EB superchannels are also provided.