LINC01287 regulates tumorigenesis and invasion via miR-298/MYB in hepatocellular carcinoma.

Recently, it was reported that long non-coding RNAs (lncRNAs) participated in promoting hepatocellular carcinoma (HCC) initiation and progression. Herein, we reported that the expression level of LINC01287 was elevated in HCC cell lines and tissues. LINC01287 down-regulation inhibited HCC cells growth and invasion both in vitro and in vivo. LINC01287 exerted as a ceRNA and negatively regulated miR-298 expression. MYB was identified as a downstream target of miR-298. The miR-298/MYB axis mediated LINC01287's effect on HCC. To the best of our knowledge, our findings provided the first evidence that LINC01287 functioned as an oncogene in HCC. LINC01287 may be a candidate prognostic biomarker and a target for new therapies in HCC patients.

NutriColoring: designing a doodling toolkit to support daily self-reported dietary assessment among office workers.

This study was motivated by a desire to help working-age individuals gain a better understanding of their daily nutritional intakes with a new self-reported dietary assessment method because an unhealthy eating behavior increases the risks of developing chronic diseases. In this study, we present the design and evaluation of NutriColoring, a food diary that leverages doodling on sketches to report and reflect on everyday diet in the working context. Through a 2-week field study involving 18 participants, the usefulness of NutriColoring in facilitating dietary assessment was tested by making comparisons with the typical bullet diary method. Our quantitative results showed that NutriColoring provided users with improved dietary assessment experience and intrinsic motivations, with significantly low task frustration and high enjoyment. Because of the freedom and playfulness in reporting intakes at work, the interview findings showed a high acceptance of employing NutriColoring at work. This article is concluded with a set of implications for the design and development of a Doodling toolkit to support healthy eating behaviors among office workers.

Short and Long-Term Innovations on Dietary Behavior Assessment and Coaching: Present Efforts and Vision of the Pride and Prejudice Consortium.

Overweight, obesity and cardiometabolic diseases are major global health concerns. Lifestyle factors, including diet, have been acknowledged to play a key role in the solution of these health risks. However, as shown by numerous studies, and in clinical practice, it is extremely challenging to quantify dietary behaviors as well as influencing them via dietary interventions. As shown by the limited success of 'one-size-fits-all' nutritional campaigns catered to an entire population or subpopulation, the need for more personalized coaching approaches is evident. New technology-based innovations provide opportunities to further improve the accuracy of dietary assessment and develop approaches to coach individuals towards healthier dietary behaviors. Pride & Prejudice (P&P) is a unique multi-disciplinary consortium consisting of researchers in life, nutrition, ICT, design, behavioral and social sciences from all four Dutch Universities of Technology. P&P focuses on the development and integration of innovative technological techniques such as artificial intelligence (AI), machine learning, conversational agents, behavior change theory and personalized coaching to improve current practices and establish lasting dietary behavior change.

Gold nano-particles (AuNPs) carrying miR-326 targets PDK1/AKT/c-myc axis in hepatocellular carcinoma.

Abnormal expression of microRNAs (miRNAs) contributes to tumour growth and invasion. MiR-326 expression often down-regulates in several kinds of cancer and low expression of miR-326 is linked with poor prognosis in cancer patients. In the present study, we aimed to explore the modulatory mechanism of miR-326 in hepatocellular carcinoma (HCC). miR-326 expression was significantly decreased in HCC cell lines and tissues. miR-326 decreased HCC cell growth by affecting cell-cycle progression and by promoting apoptosis. In addition, miR-326 inhibited HCC cell invasion by decreasing the EMT phenotype. We found that miR-326 functioned as a tumour suppressor by repressing its down-stream target PDK1. C-myc contributed to miR-326 down-regulation through binding at its promoter and inhibited its expression. Based on these results, we conducted a therapeutic experiment by using gold nano-particles (AuNPs) carrying miR-326. Restoration of miR-326 reduced tumour growth in vivo. Our findings suggest that miR-326 may be a candidate prognostic biomarker and a target for new therapies in HCC patients.

LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cells.

BACKGROUND: The long non-coding RNAs (lncRNAs) have participated in the promotion of hepatocellular carcinoma (HCC) initiation and progression. Nevertheless, the biological role and underlying mechanism of LINC01287 in HCC has never been reported. METHODS: The TGCA database was used to explore the abnormal expression of lncRNAs in HCC. Real-time PCR and in situ hybridization assays were used to examine the expression of LINC01287 in HCC tissues. The clinicopathological characteristics of HCC patients in relation to LINC01287 expression were then analyzed. Infection of cells with the si-LINC01287 lentiviral vector was performed to down-regulate LINC01287 expression in HCC cells. MTT and colony formation assays were performed to examine cell growth ability, and FACS analysis was performed to examine the cell cycle and apoptosis. A Boyden assay was used to examine HCC cell invasion ability, and RNA immunoprecipitation tested the interaction between LINC01287 and miR-298. A luciferase reporter assay was used to examine whether STAT3 was a direct target of miR-298, and chromatin immunoprecipitation (ChIP) was used to examine the potential binding of c-jun to the miR-298 promoter. RESULTS: We revealed that the expression of LINC01287 was increased in HCC cell lines, as well as tissues. Knockdown of LINC01287 decreased HCC cell growth and invasion both in vitro and in vivo. LINC01287 can negatively regulate miR-298 expression by acting as a ceRNA. miR-298 directly targeted STAT3 and inhibited its expression. LINC01287 exerted its function via the miR-298/STAT3 axis in HCC. Interestingly, STAT3 elevated LINC01287 expression via c-jun, which bound to the LINC01287 promoter. A feedback loop was also discovered between LINC01287 and the miR-298/STAT3 axis. CONCLUSIONS: Our data indicated that LINC01287 played an oncogenic role in HCC growth and metastasis and that this lncRNA might serve as a novel molecular target for the treatment of HCC.