ROGDI was a novel gene isolated from primary human renal epithelial cells. The gene located on chromosome 16p13.3 and the size of coding region is 864 bp which encodes 287 amino acids. Our previous studies revealed that the expression of human ROGDI gene is elevated in several cancer cell lines. Overexpression of ROGDI increases proliferation in the HEK293T and Hep3B human cell lines, as indicated by cell growth curves. On the other hand, according to indirect immunofluorescence, some ROGDI expressed in the nucleus. Therefore, we suggest that it may involve in regulation of cell cycle. In support of this, flow cytometry studies using HeLa cells demonstrate that ROGDI decreases the overall population of cells in G1 phase of the cell cycle. Furthermore, cells overexpressing ROGDI demonstrate an increase in the incorporation of BrdU and in WST-1 activity, respectively, indicating that both DNA synthesis and mitochondrial enzyme activity are enhanced. Taken together, ROGDI appears to be a positive regulator of cell cycle progression.

ROGDI is a novel gene which locates on human chromosome 16p13.3 and has unknown function. The length of ROGDI coding region is 864 bp which encodes 287 amino acids. According to our previous studies, overexpression of ROGDI increased proliferation in several human cell lines. CDK2 is a member of cyclin-dependent kinases (CDKs) which plays a key role in regulation of G1/S cell cycle transition and is activated during G1 and S phases. In this studies, we found that expression of CDK2 and cyclin A were up-regulated following overexpression of ROGDI in HEK293T. On the other hand, down-regulation of CDK2 and cyclin A was observed following silencing of ROGDI. In addition, the interaction between ROGDI and CDK2 was evidenced by using immunoprecipitation. Meanwhile, we observed co-localization of ROGDI and CDK2 in the nucleus. We also exploited a drug, olomoucine, known to selectively inhibit CDK2. The result demonstrated that ROGDI-enhanced cell proliferation was dependent on CDK2 activity. Flow cytometry profiles of depletion of ROGDI displayed G1/S phase arrest as well as up-reguated the expression of p53 and p21. Taken together, we suggest that ROGDI may be a positive regulator of cell cycle and its action is CDK2-depedent.

According to GenBank, ROGDI is located on chromosome 16p13.3 and the size of its coding region is 864 bp which encodes 287 amino acids. It is a novel gene which has unknown function. By bioinformatic analysis, the product of this gene was predicted as a hydrophilic protein containing leucine zipper domain. Some transcription factors utilize their leucine zipper structures as function domains. A full-length coding region cDNA of this gene was cloned in our laboratory. After the ROGDI gene was transfected into HEK293T cells, cell clones with different ROGDI protein expression levels were selected and classified into groups of high, middle and low. According to the results of foci formation assay, growth curve, anchorage indepentdent growth assay and MTS assay, it is found that clones with higher ROGDI protein level could enhance faster proliferation rate of HEK293T cells. Thus ROGDI may be a positive regulator of cell cycle and may play a role in cell proliferation.

ROGDI was a novel gene with unknown function, located on human chromosome 16p13.3. The coding region of the gene is 864 bp that encodes 287 amino acids. According to GenBank database, ROGDI contains leucine zipper domain. Previous studies in our laboratory showed that ROGDI increases cell proliferation in cell lines. In addition, overexpression of ROGDI induces p53 and p27 mRNA levels in human glioma cell line T98G and U251. In this study, we use two hepatocellular carcinoma cell lines, Hep G2 and Hep 3B, which contains wild-type and deleted tumor suppressor protein p53 respectively to investigate the expression of p53 and the response of anticancer drugs treatment in ROGDI overexpression cells. In addition, we compare the relation between the cell apoptosis the expression of p53 and ROGDI. Hence, we found that expression of p53 and ROGDI influences the cell response to anticancer drugs and induces apoptosis.

ROGDI is a novel gene which has unknown function. According to GenBank, the gene is located on chromosome 16p13.3 and the size of coding region is 864 bp which encodes 287 amino acids. It was a novel gene isolated from primary human renal epithelial cells in NEDO human cDNA sequencing project (AK026039). The definition of its reference sequence (RefSeq NM_024589) described as Homo sapiens rogdi homolog (Drosophila), ROGDI. By bioinformatic analysis, the gene was predicted as a hydrophilic protein with leucine zipper domain and located in cytoplasm. A partial cDNA of this gene was cloned in our laboratory. For further study of the biological function of the gene, the coding region of this gene was cloned into pGEX-6p and pET-28a vector and expressed in E. coli BL21 (DE3). The fusion protein was partially purified for preparation of polyclonal antibody. Northern blot analysis revealed that the gene was not expressed in all tissues. From the results of RT-PCR and western blot analysis, it can be concluded that the products, both mRNA and protein, of this gene were found in many cancer cell lines, but protein level expression of the gene was much less in normal cell lines. By immunocytochemistry analysis and subcellular localization analysis of GFP-tagged ROGDI, the gene was expressed both in the nucleus and cytoplasm, but expressed more in the nucleus than cytoplasm. In addition, ROGDI was up-regulated in early stages of liver fibrosis of TAA-treated mouse livers. This novel gene may play roles in tumorigenesis and liver fibrosis.

ROGDI, a novel gene, locates on human¡¦s chromosome 16p13.3. According to Gene Ontology Annotation database, ROGDI is related to hemopoiesis and positive regulation of cell proliferation. In order to investigate the function of this novel gene in pulmonary fibrosis, fibrotic models in vivo and in vitro were created. Mice which received single intra-tracheal bleomycin injection were sacrificed on various intervals. Rogdi and other pro-fibrotic mediators, including CCL2 and TGF-£]1, were up-regulated in the early phase(< 10 days). On contrary, the anti-fibrotic mediators IL-10, IFN-£^ and heme oxygenase(HO)-1 were up-regulated in the late phase(> 10 days). The precursor microRNA 21 (miR-21) was up-regulated as the fibrotic severity increased. The human embryonic fibroblasts(WI-38 cells) showed fibrogenic phenotype and up-regulation of precursor miR-21 and ROGDI after bleomycin treatment. Human embryonic fibroblasts transfected by coding sequence of ROGDI showed up-regulated precursor miR-21 and £\-SMA compared to those transfected by empty vectors after bleomycin treatment. Two signaling molecules related to positive regulation of cell proliferation, Akt and Erk, showed over-expressed after ROGDI transfection and bleomycin treatment compared to those with empty vector transfection. Our results imply that ROGDI is up-regulated in pulmonary fibrosis and turns fibroblasts into fibrogenic phenotype through positive regulation of miR-21. The increase of precursor, but not primary miR-21, after ROGDI transfection and bleomycin treatment indicates that ROGDI may regulate the TGF-£] signaling pathway in human embryonic fibroblasts. Our results support that ROGDI is a novel gene for pulmonary fibrosis and warrants for further investigation. £[

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