Search

Biological processes, especially developmental processes, are often dynamic. Previous BodyMap projects for human and mouse have provided researchers with portals to tissue-specific gene expression, but these efforts have not included dynamic gene expression patterns. Over the past few years, substantial progress in our understanding of the molecular mechanisms of protein-coding and long noncoding RNA (lncRNA) genes in development processes has been achieved through numerous time series RNA sequencing (RNA-seq) studies. However, none of the existing databases focuses on these time series data, thus rendering the exploration of dynamic gene expression patterns inconvenient. Here, we present Dynamic BodyMap (Dynamic-BM), a database for temporal gene expression profiles, obtained from 2203 time series of RNA-seq samples, covering >25 tissues from five species. Dynamic-BM has a user-friendly Web interface designed for browsing and searching the dynamic expression pattern of genes from different sources. It is an open resource for efficient data exploration, providing dynamic expression profiles of both protein-coding genes and lncRNAs to facilitate the generation of new hypotheses in developmental biology research. Additionally, Dynamic-BM includes a literature-based knowledgebase for lncRNAs associated with tissue development and a list of manually selected lncRNA candidates that may be involved in tissue development. Dynamic-BM is available at http://bioinfo.ibp.ac.cn/Dynamic-BM. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is the most prevalent liver cancer, characterized by a high rate of recurrence and heterogeneity. Liver cancer stem cells (CSCs) may well contribute to both of these pathological properties, but the mechanism underlying their self‐renewal maintenance is poorly understood. Here, we identified a long noncoding RNA (lncRNA) termed HAND2‐AS1 that is highly expressed in liver CSCs. Human HAND2‐AS1 and its mouse ortholog lncHand2 display a high level of conservation. HAND2‐AS1 is required for the self‐renewal maintenance of liver CSCs to initiate HCC development. Mechanistically, HAND2‐AS1 recruits the INO80 chromatin‐remodeling complex to the promoter of BMPR1A, thereby inducing its expression and leading to the activation of BMP signaling. Importantly, interfering with expression of HAND2‐AS1 by antisense oligonucleotides (ASOs) and BMPR1A by siRNAs has synergistic anti‐tumorigenic effects on humanized HCC models. Moreover, knockout of lncHand2 or Bmpr1a in mouse hepatocytes impairs BMP signaling and suppresses the initiation of liver cancer. Our findings reveal that HAND2‐AS1 promotes the self‐renewal of liver CSCs and drives liver oncogenesis, offering a potential new target for HCC therapy. Synopsis: Cancer stem cells (CSCs) have been reported to contribute to hepatocellular carcinoma (HCC), but the control mechanisms underlying their maintenance are poorly understood. Here, a long noncoding RNA (lncRNA) termed HAND2‐AS1 is identified as conserved control factor for CSC self‐renewal and HCC development. LncRNA HAND2‐AS1 is highly expressed in human liver tumors and CSCs.HAND2‐AS1 deficiency in hepatocytes protects against chemically induced HCC development.HAND2‐AS1 is required for self‐renewal of liver CSCs.HAND2‐AS1 recruits the INO80 complex to the BMPR1A promoter activating BMP signaling.Depletion of HAND2‐AS1 and BMPR1A synergise in anti‐tumor effects in vivo. [ABSTRACT FROM AUTHOR]

• One LncRNA HRCEG inhibits cell proliferation and EMT process in gastric cancer. • HRCEG was significantly connected with gastric cancer related pathways and were also highly involved in the EMT processes. • The expression of HRCEG is regulated by HDAC1. Recently, a number of long noncoding RNAs (lncRNAs) have been reported to play significant roles in human tumorigenesis. However, only few gastric cancer related lncRNAs have been well characterized. Here, we identified one lncRNA HRCEG, whose expression was decreased in the gastric cancer tissues compared with adjacent normal tissues. Overexpression of HRCEG significantly promoted cell apoptosis and inhibited cell proliferation. Importantly, we demonstrated that HRCEG levels inversely correlated with EMT process and HRCEG was regulated by the histone deacetylase 1 (HDAC1) in gastric cancer. These findings suggest that HRCEG might be regulated by HDAC1 to inhibit gastric cancer progress and metastatic capability via EMT pathway. [ABSTRACT FROM AUTHOR]