CCA-1 Secure Updatable Encryption with Adaptive Security

Updatable encryption (UE) enables a cloud server to update ciphertexts using client-generated tokens. There are two types of UE: ciphertext-independent (c-i) and ciphertext-dependent (c-d). In terms of construction and efficiency, c-i UE utilizes a single token to update all ciphertexts. The update mechanism relies mainly on the homomorphic properties of exponentiation, which limits the efficiency of encryption and updating. Although c-d UE may seem inconvenient as it requires downloading parts of the ciphertexts during token generation, it allows for easy implementation of the Dec-then-Enc structure. This methodology significantly simplifies the construction of the update mechanism. Notably, the c-d UE scheme proposed by Boneh et al. (ASIACRYPT’20) has been reported to be 200 times faster than prior UE schemes based on DDH hardness, which is the case for most existing c-i UE schemes. Furthermore, c-d UE ensures a high level of security as the token does not reveal any information about the key, which is difficult for c-i UE to achieve. However, previous security studies on c-d UE only addressed selective security; the studies for adaptive security remain an open problem. In this study, we make three significant contributions to ciphertextdependent updatable encryption (c-d UE). Firstly, we provide stronger security notions compared to previous work, which capture adaptive security and also consider the adversary’s decryption capabilities under the adaptive corruption setting. Secondly, we propose a new c-d UE scheme that achieves the proposed security notions. The token generation technique significantly differs from the previous Dec-then-Enc structure, while still preventing key leakages. At last, we introduce a packing technique that enables the simultaneous encryption and updating of multiple messages within a single ciphertext. This technique helps alleviate the cost of c-d UE by reducing the need to download partial ciphertexts during token generation

Cripto-1 overexpression is involved in the tumorigenesis of nasopharyngeal carcinoma

<p>Abstract</p> <p>Background</p> <p>Human Cripto-1, a member of the EGF-CFC family, is indispensable for early embryonic development. Cripto-1 plays an important oncogenic role during tumorigenesis and is overexpressed in a wide range of epithelial carcinomas, yet little is known about Cripto-1 in nasopharyngeal carcinoma (NPC). The aim of this study was to analyze the roles of Cripto-1 in the progression and clinical characteristics in NPC clinical samples and cell lines.</p> <p>Methods</p> <p>The expression of Cripto-1 at mRNA level was detected by the reverse transcription-polymerase chain reaction (RT-PCR) and real time RT-PCR, and western blot was used to examine the protein expression. Cripto-1 expression and its clinical characteristics were investigated by performing immunohistochemical analysis on a total of 37 NPC clinical tissue samples. Lentiviral vectors were constructed to get an efficient expression of anti-Cripto-1 siRNA in CNE-2 and C666-1 cells, with invalid RNAi sequence as control. After the inhibition of the endogenous Cripto-1, the growth, cell cycle and invasion of cells were detected by MTT, FACS and Boyden chamber assay respectively. Moreover, <it>in vivo</it>, the proliferation of the tumor cells was evaluated in xenotransplant nude mice model with whole-body visualizing instrument.</p> <p>Results</p> <p>The results of real-time RT-PCR and western blot showed that the expression level of Cripto-1 was markedly higher in NPC cell lines than that in the immortalized nasopharyngeal epithelial cell at both mRNA and protein levels. RT-PCR of 17 NPC tissues showed a high expression rate in 76.5% (13/17) cases. In an immunohistochemical study, Cripto-1 was found to express in 54.1% (20/37) cases of NPC. In addition, Cripto-1 overexpression was significantly associated with N classification (<it>p </it>= 0.034), distant metastasis (<it>p </it>= 0.036), and clinical stage (<it>p = </it>0.007). Inhibition of endogenous Cripto-1 by lentivirus-mediated RNAi silencing technique suppressed NPC cell growth and invasion <it>in vitro</it>. <it>In vivo</it>, the average weight (<it>p </it>= 0.026) and volume (<it>p </it>= 0.044) of tumor in CNE-2/GFP⁺/Cripto-1^-xenotransplant mice group were significantly lower than those in the control group. The Ki67 index was obviously lower in Cripto-1 RNAi treated tumors (<it>p </it>< 0.01).</p> <p>Conclusion</p> <p>Data of this study suggest that Cripto-1 overexpression is connected with the tumorigenesis and progression of NPC, lentivector-mediated RNAi might be feasible for the inhibition of the growth and invasion of NPC.</p

Increased expression of MMP9 is correlated with poor prognosis of nasopharyngeal carcinoma

<p>Abstract</p> <p>Introduction</p> <p>The aim of the present study was to analyze the expression of matrix metalloproteinase 9 (<it>MMP9</it>) in nasopharyngeal carcinoma (NPC) and its correlation with clinicopathologic features, including the survival of patients with NPC.</p> <p>Methods</p> <p>Using real-time PCR, we detected the mRNA expression of <it>MMP9 </it>in normal nasopharyngeal tissues and nasopharyngeal carcinoma (NPC) tissues. Using immunohistochemistry analysis, we analyzed <it>MMP9 </it>protein expression in clinicopathologically characterized 164 NPC cases (116 male and 48 female) with age ranging from 17 to 80 years (median = 48.4 years) and 32 normal nasopharyngeal tissues. Cases with greater than or equal to 6 and less than 6 of the score value of cytoplasmic <it>MMP9 </it>immunostaining were regarded as high expression and low expression, respectively. The relationship between the expression levels of <it>MMP9 </it>and clinical features was analyzed.</p> <p>Results</p> <p>The expression level of <it>MMP9 </it>mRNA was markedly greater in NPC tissues than that in the nasopharyngeal tissues. Immunohistochemical analysis revealed that the protein expression of <it>MMP9 </it>detected in NPC tissues was higher than that in the nasopharyngeal tissues (<it>P </it>= 0.004). In addition, high levels of <it>MMP9 </it>protein were positively correlated with the status of lymph node metastasis (N classification) (<it>P </it>= 0.002) and clinical stage (<it>P </it>< 0.001) of NPC patients. Patients with higher <it>MMP9 </it>expression had a significantly shorter overall survival time than did patients with low <it>MMP9 </it>expression. Multivariate analysis suggested that the level of <it>MMP9 </it>expression was an independent prognostic indicator (<it>P </it>= 0.008) for the survival of patients with NPC.</p> <p>Conclusion</p> <p>High level of <it>MMP9 </it>expression is a potential unfavorable prognostic factor for patients with NPC.</p

Over-expression of eukaryotic translation initiation factor 4 gamma 1 correlates with tumor progression and poor prognosis in nasopharyngeal carcinoma

<p>Abstract</p> <p>Background</p> <p>The aim of the present study was to analyze the expression of eukaryotic translation initiation factor 4 gamma 1 (<it>EIF4G1</it>) in nasopharyngeal carcinoma (NPC) and its correlation with clinicopathologic features, including patients' survival time.</p> <p>Methods</p> <p>Using real-time PCR, we detected the expression of <it>EIF4G1 </it>in normal nasopharyngeal tissues, immortalized nasopharyngeal epithelial cell lines NP69, NPC tissues and cell lines. <it>EIF4G1 </it>protein expression in NPC tissues was examined using immunohistochemistry. Survival analysis was performed using Kaplan-Meier method. The effect of <it>EIF4G1 </it>on cell invasion and tumorigenesis were investigated.</p> <p>Results</p> <p>The expression levels of <it>EIF4G1 </it>mRNA were significantly greater in NPC tissues and cell lines than those in the normal nasopharyngeal tissues and NP69 cells (<it>P </it>< 0.001). Immunohistochemical analysis revealed that the expression of <it>EIF4G1 </it>protein was higher in NPC tissues than that in the nasopharyngeal tissues (<it>P </it>< 0.001). In addition, the levels of <it>EIF4G1 </it>protein in tumors were positively correlated with tumor T classification (<it>P </it>= 0.039), lymph node involvement (N classification, <it>P </it>= 0.008), and the clinical stages (<it>P </it>= 0.003) of NPC patients. Patients with higher <it>EIF4G</it>1 expression had shorter overall survival time (<it>P </it>= 0.019). Multivariate analysis showed that <it>EIF4G1 </it>expression was an independent prognostic indicator for the overall survival of NPC patients. Using shRNA to knock down the expression of <it>EIF4G1 </it>not only markedly inhibited cell cycle progression, proliferation, migration, invasion, and colony formation, but also dramatically suppressed <it>in vivo </it>xenograft tumor growth.</p> <p>Conclusion</p> <p>Our data suggest that <it>EIF4G1 </it>can serve as a biomarker for the prognosis of NPC patients.</p

DT-CP: a double-TTPs based contract-signing protocol with lower computational cost

This paper characterizes a contract signing protocol with high efficiency in Internet of Things. Recent studies show that existing contract-signing protocols can achieve abuse-freeness and resist inference attack, but cannot meet the high-efficiency and convenience requirement of the future Internet of things applications. To solve this problem, we propose a novel contract-signing protocol. Our proposed protocol includes two main parts: 1) we use the partial public key of the sender, instead of the zero-knowledge protocol, to verify the intermediate result; 2) we employ two independent Trusted Third Parties (TTPs) to prevent the honest-but-curious TTP. Our analysis shows that our double TTP protocol can not only result in lower computational cost, but also can achieve abuse-freeness with trapdoor commitment scheme. In a word, our proposed scheme performs better than the state of the art in terms of four metrics: encryption time, number of exponentiations, data to be exchanged and exchange steps in one round contract-signing

Transcriptional patterns, biomarkers and pathways characterizing nasopharyngeal carcinoma of Southern China

<p>Abstract</p> <p>Background</p> <p>The pathogenesis of nasopharyngeal carcinoma (NPC) is a complicated process involving genetic predisposition, Epstein-Bar Virus infection, and genetic alterations. Although some oncogenes and tumor suppressor genes have been previously reported in NPC, a complete understanding of the pathogenesis of NPC in the context of global gene expression, transcriptional pathways and biomarker assessment remains to be elucidated.</p> <p>Methods</p> <p>Total RNA from 32 pathologically-confirmed cases of poorly-differentiated NPC was divided into pools inclusive of four consecutive specimens and each pool (T1 to T8) was co-hybridized with pooled RNA from 24 normal non-cancerous nasopharyngeal tissues (NP) to a human 8K cDNA array platform. The reliability of microarray data was validated for selected genes by semi-quantitative RT-PCR and immunohistochemistry.</p> <p>Results</p> <p>Stringent statistical filtering parameters identified 435 genes to be up-regulated and 257 genes to be down-regulated in NPC compared to NP. Seven up-regulated genes including CYC1, MIF, LAMB3, TUBB2, UBE2C and TRAP1 had been previously proposed as candidate common cancer biomarkers based on a previous extensive comparison among various cancers and normal tissues which did not, however, include NPC or NP. In addition, nine known oncogenes and tumor suppressor genes, MIF, BIRC5, PTTG1, ATM, FOXO1A, TGFBR2, PRKAR1A, KLF5 and PDCD4 were identified through the microarray literature-based annotation search engine MILANO, suggesting these genes may be specifically involved in the promotion of the malignant conversion of nasopharyngeal epithelium. Finally, we found that these differentially expressed genes were involved in apoptosis, MAPK, VEGF and B cell receptor signaling pathways and other functions associated with cell growth, signal transduction and immune system activation.</p> <p>Conclusion</p> <p>This study identified potential candidate biomarkers, oncogenes/tumor suppressor genes involved in several pathways relevant to the oncogenesis of NPC. This information may facilitate the determination of diagnostic and therapeutic targets for NPC as well as provide insights about the molecular pathogenesis of NPC.</p

A regulatory mutant on TRIM26 conferring the risk of nasopharyngeal carcinoma by inducing low immune response.

The major histocompatibility complex (MHC) is most closely associated with nasopharyngeal carcinoma (NPC), but the complexity of its genome structure has proven challenging for the discovery of causal MHC loci or genes. We conducted a targeted MHC sequencing in 40 Cantonese NPC patients followed by a two-stage replication in 1065 NPC cases and 2137 controls of Southern Chinese descendent. Quantitative RT-PCR analysis (qRT-PCR) was used to detect gene expression status in 108 NPC and 43 noncancerous nasopharyngeal (NP) samples. Luciferase reporter assay and chromatin immunoprecipitation (ChIP) were used to assess the transcription factor binding site. We discovered that a novel SNP rs117565607_A at TRIM26 displayed the strongest association (OR = 1.909, Pcombined = 2.750 × 10-19 ). We also observed that TRIM26 was significantly downregulated in NPC tissue samples with genotype AA/AT than TT. Immunohistochemistry (IHC) test also found the TRIM26 protein expression in NPC tissue samples with the genotype AA/AT was lower than TT. According to computational prediction, rs117565607 locus was a binding site for the transcription factor Yin Yang 1 (YY1). We observed that the luciferase activity of YY1 which is binding to the A allele of rs117565607 was suppressed. ChIP data showed that YY1 was binding with T not A allele. Significance analysis of microarray suggested that TRIM26 downregulation was related to low immune response in NPC. We have identified a novel gene TRIM26 and a novel SNP rs117565607_A associated with NPC risk by regulating transcriptional process and established a new functional link between TRIM26 downregulation and low immune response in NPC

Melanoma NOS1 expression promotes dysfunctional IFN signaling.

In multiple forms of cancer, constitutive activation of type I IFN signaling is a critical consequence of immune surveillance against cancer; however, PBMCs isolated from cancer patients exhibit depressed STAT1 phosphorylation in response to IFN-α, suggesting IFN signaling dysfunction. Here, we demonstrated in a coculture system that melanoma cells differentially impairs the IFN-α response in PBMCs and that the inhibitory potential of a particular melanoma cell correlates with NOS1 expression. Comparison of gene transcription and array comparative genomic hybridization (aCGH) between melanoma cells from different patients indicated that suppression of IFN-α signaling correlates with an amplification of the NOS1 locus within segment 12q22-24. Evaluation of NOS1 levels in melanomas and IFN responsiveness of purified PBMCs from patients indicated a negative correlation between NOS1 expression in melanomas and the responsiveness of PBMCs to IFN-α. Furthermore, in an explorative study, NOS1 expression in melanoma metastases was negatively associated with patient response to adoptive T cell therapy. This study provides a link between cancer cell phenotype and IFN signal dysfunction in circulating immune cells

Potential Tumor Suppressor NESG1 as an Unfavorable Prognosis Factor in Nasopharyngeal Carcinoma

BACKGROUND:Recently we identified nasopharyngeal epithelium specific protein 1 (NESG1) as a potential tumor suppressor in nasopharyngeal carcinoma (NPC). The purpose of this study is to investigate the involvement of NESG1 in tumor progression and prognosis of human NPC. METHODOLOGY/PRINCIPAL FINDINGS:NESG1 protein expression in NPC was examined. Survival analysis was performed using Kaplan-Meier method. The effect of NESG1 on cell proliferation, migration, and invasion were also investigated. RESULTS:NESG1 expression was downregulated in atypical hyperplasia and NPC samples compared to normal and squamous nasopharynx tissues. Reduced protein expression was negatively associated with the status of NPC progression. Patients with lower NESG1 expression had a shorter overall survival and disease-free time than did patients with higher NESG1 expression. Multivariate analysis suggested NESG1 expression as an independent prognostic indicator for NPC patient survival. Proliferation, migration, and invasion ability were significantly increased in cell lines following lentiviral-mediated shRNA suppression of NESG1 expression. Microarray analysis indicated that NESG1 participated in multiple pathways, including MAPK signaling and cell cycle regulation. Finally, DNA methylation microarray examination revealed a lack of hypermethylation at the NESG1 promoter, suggesting other mechanisms are involved in suppressing NESG1 expression in NPC. CONCLUSION:Our studies are the first to demonstrate that decreased NESG1 expression is an unfavorable prognostic factor for NPC