Mol Cancer: The Shanghai Nine-Yuan Fan Group team discovered a new type of LncRNA that accelerates the onset of retinoblastoma and reveals its specific molecular mechanisms.

Long non coding RNA (lncrna) is defined as a transcript with a length of more than 200 nt and lacking protein coding potential. Lncrna involves a wide range of biological processes and can regulate gene expression cis or trans through a variety of mechanisms, such as RNA degradation, chromatin remodeling and histone modification.lncrna has been identified as an important epigenetic regulator and plays an important role in human cancer. However, the regulatory function of lncrna in tumorigenesis remains to be elucidated.because lncrna is essential in maintaining homeostasis, mutations or abnormal expression of some lncrnas may also lead to various diseases, especially in cancer.up to now, abnormal expression of lncrna has been found in many types of cancer, and it has been confirmed that these abnormal expression of lncrna will lead to abnormal proliferation, migration and apoptosis of cells.previously, fan xianqun's team found that lncrna gau1 can recruit transcription elongation factor a1 (tcea1) to the promoter of peptide N-acetylgalactosamine transferase 8 (galnt8), thus up regulating the expression of oncogene and accelerating the tumorigenesis of retinoblastoma.in addition, the upregulation of lncrna pandar was associated with cell growth and apoptosis in retinoblastoma cell lines.however, our knowledge of lncrna in tumors, especially retinoblastoma, is still limited.recently, fan xianqun's team from the Ninth People's Hospital Affiliated to Shanghai Jiaotong University Medical College published a research paper entitled "a new lncrna transcript, rbat1, accelerates tumorigenesis through interacting with hnrnpl and CIS activating E2F3" in molecular cancer.in this study, we found and named a novel lncrna, rbat1, which was slightly and significantly overexpressed in retinoblastoma (RB) and bladder cancer (BCA).experiments in vivo and in vitro showed that rbat1 could promote tumor formation.the team further confirmed that rbat1 promotes tumorigenesis by directly recruiting hnpnpl into the promoter of E2F3 and CIS activating E2F3 expression.this study has found a new biological mechanism of lncrna and provided a potential new target for the diagnosis and treatment of retinoblastoma (RB).retinoblastoma (RB) is the most common primary intraocular malignant tumor in children.it has been proved that retinoblastoma (RB) is related to the loss of double allele, copy number abnormality and epigenetic abnormality of RB1 gene.in this study, the team found that rbat1 is a novel noncoding transcript and one of the most up-regulated lncrnas in retinoblastoma (RB).rbat1 plays a key role in cell proliferation in vitro and in vivo.rbat1 is an important transcription promoter, which can induce the expression of E2F3 in tumor cells. in terms of mechanism, rbat1 directly recruited hnrnpl protein into the promoter region of oncogene E2F3, thus activating E2F3 signal transduction to induce tumor cell proliferation. in treatment, the silencing of rbat1 mediated by antisense oligonucleotide gapmer can inhibit the tumorigenesis in orthotopic xenograft retinoblastoma models derived from retinoblastoma (RB) cell line and retinoblastoma (RB) primary cells. it indicates that targeting rbat1 / E2F3 is a potential therapeutic strategy for retinoblastoma. in general, this study elucidates the potential role of rbat1 in the development of retinoblastoma (RB) and its molecular mechanism in tumor progression. it also indicates that rbat1 may be a potential therapeutic target for retinoblastoma (RB). it is reported that he Xiaoyu, Chai Peiwei and Li Fang are the co first authors of the paper, and fan xianqun, Jia Renbing and Zhang he are the co corresponding authors of the paper. the research was supported by the national health and Family Planning Commission's research program (201402014), the National Natural Science Foundation (NSFC) (8157088481770961), and the dawn project (14sg18) of Shanghai Education Commission and Shanghai Education Development Foundation. paper links: