BackgroundMAPT-AS1, a long non-coding RNA, has not been reported in any previous research about its function in cancers. In this study, we investigated the role of MAPT-AS1 in the progression and paclitaxel resistance in breast cancer, and the regulation between MAPT-AS1 and its natural comparable sense transcripts MAPT.MethodsWe analysed the breast cancer patients’ clinical information and explored the function of MAPT-AS1 by gain- and loss-of function assays in vitro and in vivo. The regulation between MAPT-AS1 and MAPT was confirmed by gene expression analysis and rescue assays. To verify the hypothesis that MAPT-AS1 and MAPT might form a duplex structure, we performed RT-PCR assays on RNA after α-amanitin treatment.ResultsBy analysing the breast cancer patients’ clinical information from the TCGA database, we found that ER-negative patients with younger age (< 60), larger tumors (≥ 2 cm), metastatic lymph nodes and stages (III–IV) had higher expression of MAPT-AS1. MAPT-AS1 is correlated with the cell growth, invasiveness and paclitaxel resistance by regulating its natural comparable sense transcripts MAPT in ER-negative breast cancer cells. The result revealed that MAPT-AS1 overexpression could partially protect the MAPT mRNA from degradation, while MAPT-AS1 knockdown decreased the stability of MAPT mRNA. Meanwhile, MAPT knockdown decreased the expression of MAPT-AS1 mRNA. MAPT-AS1 expressed coordinately with MAPT in breast tumor tissues.ConclusionOur study is the first to report a novel lncRNA MAPT-AS1 in human cancer. ER-negative patients with younger age (< 60), larger tumors (≥ 2 cm), metastatic lymph nodes and stages (III–IV) had higher expression of MAPT-AS1. MAPT-AS1 is correlated with the cell growth, invasiveness and paclitaxel resistance in ER-negative breast cancer cells through antisense pairing with MAPT. MAPT-AS1 may serve as a potential therapeutic target in ER-negative breast cancers.Electronic supplementary materialThe online version of this article (10.1186/s13578-018-0207-5) contains supplementary material, which is available to authorized users.

This study investigated the efficacy of an open-label placebo (OLP) treatment for menopausal hot flushes. Women with at least five moderate or severe hot flushes per day were allocated to receive four weeks of OLP for twice a day or no-treatment. Intention-to-treat analyses included n = 100 women. In comparison to no-treatment, OLP reduced the log-transformed hot flush composite score (frequency × intensity) (mean difference in change: − 0.32, 95% CI [− 0.43; − 0.21], p < 0.001, Cohen’s d = 0.86), hot flush frequency (− 1.12 [− 1.81; − 0.43], p = 0.02, Cohen’s d = 0.51), and improved overall menopause-related quality of life (− 2.53 [− 4.17; − 0.89], p = 0.02, Cohen’s d = 0.49). Twelve (24%) (vs. three [6%]) patients had 50% lesser hot flushes. Problem rating of hot flushes and subdomains of quality of life did not improve. After four weeks, the OLP group was further divided via randomization to continue or discontinue the treatment. Benefits were maintained at week 8 (log-transformed score: − 0.04 [− 0.06; 0.14], p = 0.45). There was no difference between taking placebos for 8 or 4 weeks (log-transformed score: 0.04 [− 0.17; 0.25], p = 0.73). Results indicate that open-label placebos may be an effective, safe alternative for menopausal hot flushes.

Relevance: Informing patients about potential adverse events as part of the informed consent may facilitate the development of nocebo-driven drug adverse events (nocebo side effects). Objective: To investigate whether informing about the nocebo effect using a short information sheet can reduce nocebo side effects. Methods: A total of N = 44 participants with weekly headaches for at least 6 months were recruited using the cover story of a clinical trial for a headache medicine. In reality, all participants took a placebo pill and were randomized to the nocebo information group or the standard leaflet group. Participants were instructed to read the bogus medication leaflet entailing side effects information shortly before pill intake. The nocebo group additionally received an explanation about the nocebo effect as part of the leaflet. Questionnaires were completed at baseline, 2 min, and 4 days after the pill intake. We conducted general linear models with bootstrap sampling. Baseline symptoms were included as a covariate. Results: Most participants (70.5%) reported nocebo side effects at 2 min. Participants who received the nocebo information ( n = 24) reported less nocebo symptoms than the control group ( n = 20) (estimated difference: 3.3, BCa 95% CI [1.14; 5.15], p = 0.01, Cohen’s d = 0.59). Baseline symptoms, perceived sensitivity to medicine, and side effect expectations each moderated the group effect (estimated difference in slope: 0.47, BCa 95% CI [0.19; 0.73], p = 0.001, d = 0.75; 1.07 [0.27; 1.61], p = 0.006, d = 0.73; 1.57 [0.38; 2.76], p = 0.02, d = 0.58). No group differences were found at 4-day follow-up. After revealing the actual aim of the study, 86% of the participants evaluated the nocebo information to be helpful in general. Conclusions: Results provide the first evidence that informing about the nocebo effect can reduce nocebo side effects.