The lncRNA MALAT1 has multiple biological functions, including influencing RNA processing, miRNA sponging, and cancer development. It is acknowledged that miR663a and its targets are inflammation-related genes frequently deregulated in many cancers. The associations between MALAT1 and miR663a and their target genes remain unknown. In this study, it was found that in colon cancer (CC) cells, MALAT1 and miR663a were reciprocally repressed in cDNA array screening and qRT-PCR analysis. However, MALAT1 was significantly upregulated in CC tissues, and miR663a was significantly downregulated relative to the corresponding surgical margin (SM) tissues. An inverse relationship between MALAT1 and miR663a expression was detected among CC tissue samples (n = 172, r = −0.333, p < 0.0001). The RNA-pulldown results showed MALAT1 lncRNA–miR663a binding. The results of luciferase-reporter analysis further revealed that the MALAT1 7038–7059 nt fragment was the miR663a seed sequence. Both miR663a knockdown and MALAT1 activation alone significantly upregulated the expression levels of miR663a targets, including TGFB1, PIK3CD, P53, P21, and JUND, in the CC cell lines HCT116 and SW480. A positive relationship was also observed between the expression levels of MALAT1 and these miR663a targets in the above 172 CC samples and 160 CC samples in publicly available databases. In addition, reciprocal abolishment of the effects of miR663a overexpression and MALAT1 activation on the proliferation, migration, and invasion of cancer cells was also observed, while miR663a upregulation and MALAT1 activation alone inhibited and promoted the behaviors of these CC cell lines, respectively. All these suggested that, as a competing endogenous lncRNA, MALAT1 maybe a dominant protector for the degradation of miR663a targets. miR663a and MALAT1 may consist of a negative feedback loop to determine their roles in CC development.

The risk of venous thrombosis and mortality associated with central catheter (PICC/CICC) for malignant tumor patients is not definite. So, we carried out a systematic review and meta-analysis to evaluate it. Among patients with comparing PICC with CICC, odds ratio (OR) or risk ratio (RR) was calculated with a random effect model meta-analysis. The result of the stratification analysis of 7 studies (PICC vs CICC) supported the theory that CICCs were associated with a decrease in the odds ratio of thrombosis compared with PICCs. 7 of 15 studies provided the information about the compared mortality rate of the patients. The result showed that CICCs were associated with a decrease in the odds ratio of thrombosis compared with PICCs (OR = 0.45, 95% CI:0.32–0.62, p < 0.0001, I2 = 0%,Tau2 = 0.00). Meta-analysis of 8 studies of 2639 patients showed that pharmacological deep vein thrombosis prophylaxis drugs could decrease the risk of mortality of malignant tumor patients with CICCs (RR = 0.58, 95% CI:0.48–0.71, Z = 5.32, p < 0.0001, I2 = 71%). We found that PICCs are associated with a raised risk of deep vein thrombosis, and pharmacological deep vein thrombosis prophylaxis drugs is a beneficial factor in decreasing the incidence of thrombosis, while warfarin may decrease the risk of mortality of malignant tumor patients with CICCs.

An increasing number of studies have demonstrated that microRNAs (miRs) may act as oncogenes or anti-oncogenes in various types of cancer, including colon cancer (CC). However, the clinical and biological significance of miR663a in the prognosis of CC and its underlying molecular mechanisms remain unknown. Using the reverse transcription-quantitative polymerase chain reaction on CC and surgical margin tissue samples from 172 patients with CC, it was identified that miR663a was significantly downregulated in CC (P<0.001), particularly in metastatic CC (P=0.044). miR663a overexpression inhibited the proliferation and migration/invasion of CC cells in vitro, and also tumor growth and metastasis of CC cells in vivo. Additionally, miR663a target genes were analyzed. Inverse changes in tetratricopeptide repeat domain 22 variant 1 (TTC22V1) in response to alterations in miR663a expression were observed. miR663a decreased the reporter activity of the wild-type TTC22V1−3′ untranslated region (UTR), but did not decrease that of a 3′UTR mutant. miR663a completely abolished cell migration/invasion induced by TTC22V1 containing the wild-type 3′UTR sequence, but not that induced by TTC22V1 containing the 3′UTR mutant. An inverse correlation between miR663a and TTC22 mRNA levels was observed in CC tissues. These results suggest that TTC22V1 mRNA is a crucial miR663a target that directly promotes cell migration/invasion. TTC22, which, to the best of our knowledge, has rarely been investigated, is located in the nuclei of epithelial cells in colon stem cell niches at crypt bases, and is significantly downregulated in CC, particularly in non-metastatic CC. High TTC22V1 expression is a significant poor survival factor for patients with CC. Collectively, the results of the present study suggested that TTC22V1 may be a metastasis-associated gene and that the miR663a-TTC22V1 axis inhibited CC metastasis.

Background The MIR663AHG gene encode both miR663AHG and miR663a. While miR663a contributes to the defense of host cells against inflammation and inhibits colon cancer development, the biological function of lncRNA miR663AHG has not been previously reported. Methods The subcellular localization of lncRNA miR663AHG was determined by RNA-FISH. miR663AHG and miR663a were measured by qRT-PCR. The effects of miR663AHG on the growth and metastasis of colon cancer cells were investigated in vitro and in vivo. CRISPR/Cas9, RNA pulldown, and other biological assays were used to explore the underlying mechanism of miR663AHG. Results miR663AHG was mainly distributed in the nucleus of Caco2 and HCT116 cells and the cytoplasm of SW480 cells. The expression level of miR663AHG was positively correlated with the level of miR663a (r = 0.179, P = 0.015) and significantly downregulated in colon cancer tissues relative to paired normal tissues from 119 patients (P < 0.008). Colon cancers with low miR663AHG expression were associated with advanced pTNM stage (P = 0.021), lymph metastasis (P = 0.041), and shorter overall survival (hazard ratio = 2.026; P = 0.021). Experimentally, miR663AHG inhibited colon cancer cell proliferation, migration, and invasion. The growth of xenografts from RKO cells overexpressing miR663AHG was slower than that of xenografts from vector control cells in BALB/c nude mice (P = 0.007). Interestingly, either RNA-interfering or resveratrol-inducing expression changes of miR663AHG or miR663a can trigger negative feedback regulation of transcription of the MIR663AHG gene. Mechanistically, miR663AHG could bind to miR663a and its precursor pre-miR663a, and prevent the degradation of miR663a target mRNAs. Disruption of the negative feedback by knockout of the MIR663AHG promoter, exon-1, and pri-miR663A-coding sequence entirely blocked these effects of miR663AHG. Conclusion miR663AHG functions as a tumor suppressor that inhibits the development of colon cancer through its cis-binding to miR663a/pre-miR663a. The negative feedback loop between miR663AHG and miR663a expression may play dominant roles in maintaining the functions of miR663AHG in colon cancer development.

The existence of native code in Android apps plays an essential role in triggering inconspicuous propagation of secrets and circumventing malware detection. However, the stateof-the-art information-flow analysis tools for Android apps all have limited capabilities of analyzing native code. Due to the complexity of binary-level static analysis, most static analyzers choose to build conservative models for a selected portion of native code. Though the recent inter-language analysis improves the capability of tracking information flow in native code, it is still far from attaining similar effectiveness of the state-ofthe-art information-flow analyzers that focus on non-native Java methods. To overcome the above constraints, we propose a new analysis framework, i.e., µDep, to detect sensitive information flows of the Android apps containing native code. In this framework, we combine a control-flow-based static binary analysis with a mutation-based dynamic analysis to model the tainting behaviors of native code in the apps. Based on the result of the analyses, µDep conducts a stub generation for the related native functions to facilitate the state-of-the-art analyzer, i.e., DroidSafe, with fine-grained tainting behavior summaries of native code. The experimental results show that our framework is competitive on the accuracy and effective in analyzing the information flows in real-world apps and malware compared with the state-of-the-art inter-language static analysis.

In the long history of the pentium, weaving technology carries all the civilization of human production and life.The history of when weaving technology was invented and used by people is still uncertain, and because it cannot be preserved for a long time like stone tools, ceramics and metal products, the records about weaving technology cannot be systematically investigated and verified, but it still cannot hide its shining stars in the history of human civilization. Woven tapestry as traditional fiber art form, the heavy burden of carrying on the past heritage, therefore, this article will begin from tapestry historical evolution, tapestry through the analysis of the research process and form of expression, gradually delve into woven decoration features and technique of expression, mining woven fiber art inspiration, to explore the possibility of more decorative performance semantics.

The MIR663AHG gene encodes both miR663AHG and miR663a. While miR663a contributes to the defense of host cells against inflammation and inhibits colon cancer development, the biological function of lncRNA miR663AHG has not been previously reported. In this study, the subcellular localization of lncRNA miR663AHG was determined by RNA-FISH. miR663AHG and miR663a were measured by qRT-PCR. The effects of miR663AHG on the growth and metastasis of colon cancer cells were investigated in vitro and in vivo. CRISPR/Cas9, RNA pulldown, and other biological assays were used to explore the underlying mechanism of miR663AHG. We found that miR663AHG was mainly distributed in the nucleus of Caco2 and HCT116 cells and the cytoplasm of SW480 cells. The expression level of miR663AHG was positively correlated with the level of miR663a (r = 0.179, P = 0.015) and significantly downregulated in colon cancer tissues relative to paired normal tissues from 119 patients (P < 0.008). Colon cancers with low miR663AHG expression were associated with advanced pTNM stage (P = 0.021), lymph metastasis (P = 0.041), and shorter overall survival (hazard ratio = 2.026; P = 0.021). Experimentally, miR663AHG inhibited colon cancer cell proliferation, migration, and invasion. The growth of xenografts from RKO cells overexpressing miR663AHG was slower than that of xenografts from vector control cells in BALB/c nude mice (P = 0.007). Interestingly, either RNA-interfering or resveratrol-inducing expression changes of miR663AHG or miR663a can trigger negative feedback regulation of transcription of the MIR663AHG gene. Mechanistically, miR663AHG could bind to miR663a and its precursor pre-miR663a, and prevent the degradation of miR663a target mRNAs. Disruption of the negative feedback by knockout of the MIR663AHG promoter, exon-1, and pri-miR663A-coding sequence entirely blocked these effects of miR663AHG, which was restored in cells transfected with miR663a expression vector in rescue experiment. In conclusion, miR663AHG functions as a tumor suppressor that inhibits the development of colon cancer through its cis-binding to miR663a/pre-miR663a. The cross talk between miR663AHG and miR663a expression may play dominant roles in maintaining the functions of miR663AHG in colon cancer development.

This refers to the card type of single-page calendar, the calendar painting in Chinese folk, also known as the calendar, is China's unique art style, has been one hundred years of history, in the thirties of the 20th century when its booming, but later as the Anti-Japanese War, its foundering, become a piece of history, even so, the calendar painting for the development of China's advertisement still has a great role in promoting. This paper studies the origin, development and innovation of the calander painting. The combination of calendar and modern poster advertising design aims to find the inheritable and development of calendar poster, and find a new development angle for modern poster advertising design.In the development process of the calendar painting, it has experienced a combination of Chinese and Western culture, localization and other stages. Poster advertising, also known as posters, is a form of outdoor advertising and has a long history. In the design process of modern poster advertising, the layout, color application and theme selection of the calendar painting have inspiration and reference significance to modern poster design.