Unsupervised Text Style Transfer with Deep Generative Models

We present a general framework for unsupervised text style transfer with deep generative models. The framework models each sentence-label pair in the non-parallel corpus as partially observed from a complete quadruplet which additionally contains two latent codes representing the content and style, respectively. These codes are learned by exploiting dependencies inside the observed data. Then a sentence is transferred by manipulating them. Our framework is able to unify previous embedding and prototype methods as two special forms. It also provides a principled perspective to explain previously proposed techniques in the field such as aligned encoder and adversarial training. We further conduct experiments on three benchmarks. Both automatic and human evaluation results show that our methods achieve better or competitive results compared to several strong baselines

The axis of CXCR4/SDF-1 plays a role in colon cancer cell adhesion through regulation of the AKT and IGF1R signalling pathways

Background/aim: Colorectal cancer (CRC) is the third most common cancer in the world. The high mortality of this tumor is mainly due to its invasive properties, as it forms metastases in multiple organs, preferentially in the liver. There has evidence showing that C-X-C chemokine receptor type 4 (CXCR-4) and its ligand, stromal cell-derived factor-1 (SDF-1), plays an important role in cancer progression and metastasis. However, the molecular mechanism underling the CRCR4-mediated CRC metastasis has not been well characterized. In this study, we aimed to investigate the roles of CXCR4 in colorectal cancer using the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9)-based genomic editing technique. Materials and methods: We knocked-down CXCR4 using specific guide-RNA linked CRISPR/Cas9 in HT115 and COLO201 colon cancer cell lines which exhibited high levels of endogenous CXCR4 gene expression. Stable HT115 cells with CXCR4 knock-down were established by CRISPR plasmid transfection and validation was confirmed using T7 endonuclease 1 (T7EN1), flow cytometry (FACS) and western blotting assays. Results: Knock-down of CXCR4 did not decrease proliferation of HT115 cells, but decreased the adhesion potential of cells to the human umbilical vein endothelial cells (HUVEC) and extracellular matrix. We further demonstrated that the AKT and type 1 insulin-like growth factor receptor (IGF1R) signalling pathways may be involved in the alteration of adhesion in CRC cells when CXCR4 is knocked down. Conclusion: Our data suggest that CXCR4 plays a key role in colorectal cancer progression via the mediation of tumor cell adhesion. The Axis of CXCR4/SDF-1 Plays a Role in Colon Cancer Cell Adhesion Through... | Request PDF. Available from: https://www.researchgate.net/publication/319179295_The_Axis_of_CXCR4SDF-1_Plays_a_Role_in_Colon_Cancer_Cell_Adhesion_Through_Regulation_of_the_AKT_and_IGF1R_Signalling_Pathways [accessed Jan 08 2018]

Interpreting Sentiment Composition with Latent Semantic Tree

As the key to sentiment analysis, sentiment composition considers the classification of a constituent via classifications of its contained sub-constituents and rules operated on them. Such compositionality has been widely studied previously in the form of hierarchical trees including untagged and sentiment ones, which are intrinsically suboptimal in our view. To address this, we propose semantic tree, a new tree form capable of interpreting the sentiment composition in a principled way. Semantic tree is a derivation of a context-free grammar (CFG) describing the specific composition rules on difference semantic roles, which is designed carefully following previous linguistic conclusions. However, semantic tree is a latent variable since there is no its annotation in regular datasets. Thus, in our method, it is marginalized out via inside algorithm and learned to optimize the classification performance. Quantitative and qualitative results demonstrate that our method not only achieves better or competitive results compared to baselines in the setting of regular and domain adaptation classification, and also generates plausible tree explanations.Comment: Findings of ACL202

Differential expression of CCN family members CYR611, CTGF and NOV in gastric cancer and their association with disease progression

CCN is an acronym for cysteine-rich protein 61 (CYR61), connective tissue growth factor (CTGF) and nephroblastoma overexpressed (NOV). Aberrations of certain CCN members including CYR61, CTGF, Wnt1-inducible signalling pathway protein (WISP)-1 and -3 have been reported in gastric cancer. The present study aimed to examine the clinical relevance of NOV along with CYR61 and CTGF in gastric cancer by analysing their transcript levels. CYR61, CTGF and NOV transcript expression in 324 gastric cancer samples with paired adjacent normal gastric tissues were determined using real-time quantitative PCR and the results were statistically analysed against patient clinicopathological data using SPSS software. NOV mRNA levels in gastric cancer tissues were significantly elevated when compared with levels in their paired adjacent non-cancerous tissues. Local advanced tumours with invasive expansion (T3 and T4) expressed higher levels of NOV (p=0.013) compared with the less invasive tumours (T1 and T2). CYR61 transcript levels were also significantly increased in gastric cancers compared with levels in the adjacent non cancerous tissues. Kaplan-Meier survival curves revealed that patients with CYR61-low transcript levels had longer overall survival (OS) (p=0.018) and disease-free survival (DFS) (p=0.015). NOV overexpression promoted the in vitro proliferation of AGS cells while the knockdown resulted in a reduced proliferation of HGC27 cells. A similar effect was observed for the invasion of these two gastric cancer cell lines. NOV expression was increased in gastric cancer which was associated with local invasion and distant metastases. Taken together, the expression of NOV and CYR61 was increased in gastric cancer. The elevated expression of CYR61 was associated with poorer survival. NOV promoted proliferation and invasion of gastric cancer cells. Further investigations may highlight their predictive and therapeutic potential in gastric cancer.Cancer Research Wales; Chinese Medical Research Scholarship of Cardiff UniversitySCI(E)[email protected]; [email protected]

EphB2 represents an independent prognostic marker in patients with gastric cancer and promotes tumour cell aggressiveness

Dysregulated expression of ephrin type-B receptor 2 (EphB2) has been linked with development and progression of solid tumours. In the current study we attempted to investigate the clinical relevance in GC and the effect of EphB2 expression on gastric cancer (GC) cells. EphB2 protein levels in GC and benign gastric tissues were determined using immunohistochemistry. EphB2 transcript expression in a GC cohort with GC tissue samples (n=171) and paired adjacent normal gastric tissues (n=97) was determined using qPCR. The EphB2 expression was over-activated using a CRISPR activator for the investigation of its cellular function. The expression levels of the EphB2 protein in the tumour tissues of tissue arrays were higher than the benign non-cancerous gastric tissues (P<0.05). EphB2 mRNA expression in GC tissues was also significantly elevated when compared with adjacent non-cancerous tissues (P<0.01). EphB2 activation promoted the migration and invasion abilities of the GC cell lines (P<0.01, respectively). In contrast, EphB2 activation significantly decreased the adhesion in GC cells (P<0.0001, respectively). The enrichment analysis of the correlated genes in a GC cohort indicates that EphB2 may function through mediating the cytokine-cytokine interaction, JAK-STAT and TP53 signaling pathways. In conclusion, EphB2 represents as a novel independent prognostic marker in GC. And activation of the EphB2 gene expression elevated the levels of migration and invasion, but suppressed adhesion of GC cells, indicating that EphB2 may act as a tumour promotor in GC. Our findings thus provide fundamental evidence for the consideration of the therapeutic potential of targeting EphB2 in GC

Emerging role of CCN family proteins in tumorigenesis and cancer metastasis (Review)

The CCN family of proteins comprises the members CCN1, CCN2, CCN3, CCN4, CCN5 and CCN6. They share four evolutionarily conserved functional domains, and usually interact with various cytokines to elicit different biological functions including cell proliferation, adhesion, invasion, migration, embryonic development, angiogenesis, wound healing, fibrosis and inflammation through a variety of signalling pathways. In the past two decades, emerging functions for the CCN proteins (CCNs) have been identified in various types of cancer. Perturbed expression of CCNs has been observed in a variety of malignancies. The aberrant expression of certain CCNs is associated with disease progression and poor prognosis. Insight into the detailed mechanisms involved in CCN-mediated regulation may be useful in understanding their roles and functions in tumorigenesis and cancer metastasis. In this review, we briefly introduced the functions of CCNs, especially in cancer

MTA1 is up-regulated in colorectal cancer and is inversely correlated with lymphatic metastasis

Background: Metastasis-associated protein 1 (MTA1) plays an important role in tumourigenesis and progression of certain cancer types. In the current study, we analyzed the relationship between MTA1 expression and disease progression of colorectal cancer (CRC). Materials and Methods: CRC tissues (n=93) and adjacent normal colorectal tissues (n=70) were analyzed by quantitative real-time polymerase chain reaction. MTA1 knockdown was established in RKO and HT115 cells using MTA1 siRNA. Results: The expression of MTA1 was significantly increased in CRC tissues compared to paired normal colorectal tissues, but decreased expression of MTA1 was correlated with poor prognosis (higher lymph node involvement stage, TNM stage, local invasion and recurrence) that was associated with increased expression of VEGFC and -D and the receptor VEGFR3. Conclusion: MTA1 is up-regulated in CRC. MTA1 expression is inversely associated with lymphatic metastases and the expression of VEGFC, VEGFD and VEGFR3

Development of Organo-Dispersible Graphene Oxide via Pseudo-Surface Modification for Thermally Conductive Green Polymer Composites

Graphene has attracted lots of researchers attention because of its remarkable conductivity in both electrically and thermally. However, it has poor dispersibility in organic solvents which limited its applications. Polymers with aromatic end group which act as an intercalator were prepared by ring-opening polymerization with ε-caprolactone by utilizing 1-naphthalene methanol (1-NM) as an initiator. These intercalators will exist between graphene oxide (GO) sheets to prevent aggregation via interactions. The attachment of 1-NM on polymer chains was supported by ultraviolet–visible spectra, size exclusion chromatography profiles, and 1H nuclear magnetic resonance spectra. Exfoliated structured functionalized GO (fGO)/polycaprolactone (PCL) (synthesized fGO) nanocomposites that dispersed well in acetone, chloroform, N,N-dimethylformamide, dimethyl sulfoxide, tetrahydrofuran, and toluene were successfully synthesized. This agreed well with the enlarged interlayer spacing in the optimized fGO as compared to that of GO from density functional theory simulations using the DMol3 module that implemented in the Materials Studio 6.0. Furthermore, its potential to be applied as green electronics in electronics, aerospace, and automotive industries was presented, by trailering the thermal conductivity enhancement from the incorporation of fGO/PCL with commercialized biodegradable polymers, PCL, and poly[(R)-3-hydroxybutyric acid]

Reduced NOV expression correlates with disease progression in colorectal cancer and is associated with survival, invasion and chemoresistance of cancer cells

Aberrant expression of nephroblastoma overexpressed (NOV) has been evident in certain malignancies. In the current study, we aim to investigate the role played by NOV in colorectal cancer (CRC). NOV expression was determined in a cohort of 359 CRC tissues and 174 normal colorectal tissues. Its impact on CRC cells was investigated using in vitro NOV knockdown and overexpression models. NOV transcripts were reduced in the CRC tumours compared with the paired adjacent normal colorectal tissues (p < 0.01) and was associated with distant metastases. NOV knockdown resulted in increased cell proliferation and invasion of RKO cells, whilst an opposite effect was seen in the HT115 NOV over expressing cells. A positive association between Caspase-3/-8 and NOV was seen in NOV knockdown and overexpression cell lines which contributed to the survival of serum deprived CRC cells. Further investigation showed that NOV regulated proliferation, survival and invasion through the JNK pathway. NOV knockdown in RKO cells reduced the responsiveness to 5-Fluorouracil treatment, whilst overexpression in HT115 cells exhibited a contrasting effect. Taken together, NOV is reduced in CRC tumours and this is associated with disease progression. NOV inhibits the proliferation and invasion of CRC cells in vitro. Inhibition of proliferation is mediated by a regulation of Caspase-3/-8, via the JNK pathway, which has potential for predicting and preventing chemoresistance