MCM3 (minichromosome maintenance complex component 3)

Review on MCM3, with data on DNA/RNA, on the protein encoded and where the gene is implicated

ATP2B4 (ATPase, Ca++ transporting, plasma membrane 4)

Review on ATP2B4, with data on DNA/RNA, on the protein encoded and where the gene is implicated

ATP5B (ATP synthase, H+ transporting, mitochondrial F1 complex, beta polypeptide)

Review on ATP5B, with data on DNA/RNA, on the protein encoded and where the gene is implicated

UTS2 (urotensin 2)

Review on UTS2, with data on DNA/RNA, on the protein encoded and where the gene is implicated

SEPT7 (septin 7)

Review on SEPT7, with data on DNA/RNA, on the protein encoded and where the gene is implicated

ARID3A-mediated modulation of TP73 and TP73-AS1 in osteosarcoma cells

Osteosarcoma is the most common primary malignancy arising from bone. Increasing mass of indications suggest that long non-coding RNAs (lncRNAs) play crucial roles in the development of progressions of human cancers including osteosarcoma. Although several lncRNAs have shown to be involved in the molecular pathogenesis of osteosarcoma, identification of novel lncRNAs involved in the osteosarcoma pathobiology remained muchly elusive. Besides, ARID3A is a member of ARID family of DNA binding proteins. ARID3A was also implicated in osteosarcoma pathogenesis. Accordingly, in the present study, we mechanistically investigated the effect of ARID3A on the expression of TP73 and TP73-AS1 in osteosarcoma cells and to determine the relationship between them. For the overexpression of ARID3A in U2-OS cells, pER_xpress_ARID3A expression vector and for the silencing of ARID3A, ARID3A-spesific siRNA was used. Expression levels of ARID3A, TP73 and TP73-AS1 genes were determined by qPCR method. As a result, expression levels of TP73-AS1 were well-correlated with the ARID3A expression levels whereas TP73 expression levels were not well-correlated with ARID3A. In conclusion, our results indicate that ARID3A might be involved in the regulation of TP73-AS1 in osteosarcoma. To our knowledge, this is the first study revealing the role of ARID3A in the regulation of TP73 and TP73-AS1 genes. © 2020 Elsevier Inc

Novel thiosemicarbazone derivative 17B interferes with the cell cycle progression and induce apoptosis through modulating downstream signaling pathways

Thiosemicarbazones (TSCs) are interesting group of chemical compounds that received significant levels of attention due their wide range of pharmacological effects including antibacterial, antiviral, and especially anti-tumor activities. Several thiosemicarbazone derivatives have been extensively reported recently with their anti-tumor properties but designing and developing novel thiosemicarbazone derivatives with more potent chemotherapeutic activities is of great interest for cancer future cancer therapy. Thus, here we aimed to demonstrate as yet undetermined anti-cancer properties of novel thiosemicarbazone derivative 17B. Viability of cells was determined using MTT assay and LDH activities were analyzed using lactate dehydrogenase activity assay. Apoptosis were assayed using Annexin V-FITC and PI double staining method and cell cycle analysis was achieved by using PI staining with fluorescence-activated cell sorting and migration capacities of cells were determined by wound healing assay. As a result, 17B limited cell viability and showed cytotoxic effects in a dose-dependent manner in A549, MCF7 and U2OS cells. In addition, it inhibited progression through cell cycle by interfering with the Gl/S transition and triggered apoptosis by modulating expression levels of pro-apoptotic and anti-apoptotic mediators in MCF7 and U2OS cells. Also, 17B significantly impaired the migration of cancer cells and delayed wound healing in all cells. Consequently, findings of the present study have strongly indicated that 17B might be a novel anti-cancer agent for the treatment of breast cancer and osteosarcoma but not for lung cancer. Our results have provided mechanistic insights into anti-cancer properties of a novel thiosemicarbazone derivative 17B

Long noncoding RNA ERICD interacts with ARID3A via E2F1 and regulates migration and proliferation of osteosarcoma cells

Long noncoding RNA (lncRNA) dysregulation is known to be taking part in majority of cancers, including osteosarcoma. In one of our previous studies, we showed that lncRNA MEG3 is being regulated by microRNA-664a (miR-664a) suppresses the migratory potential of osteosarcoma cells (U-2OS). We now report a novel lncRNA, namely, ERICD, which is linked to the transcription factor AT-rich interaction domain 3A (ARID3A) in U-2OS cells. We show that ARID3A binds to ERICD and indirectly interacts with each other via the E2F transcription factor 1 (E2F1). Furthermore, small interfering RNA (siRNA)-mediated knockdown of ERICD inhibited cell migration, formation of colonies, and proliferation in U-2OS cells. Overexpression of ARID3A inhibited cell migration, colony formation, and proliferation, whereas siRNA-mediated knockdown of ARID3A promoted cell migration, colony formation, and proliferation. Our findings indicate that ARID3A and lncRNA ERICD have plausible tumor suppressive and oncogenic functions, respectively, in osteosarcoma. Our data demonstrate the converse interaction between ARID3A and lncRNA ERICD that target DNA-binding proteins and dysregulation of their expression through E2F1 augments osteosarcoma progression. The cell rescue experiment also indicated E2F1 to be involved in the regulation of ARID3A and ERICD

GFI1 tethers the NuRD complex to open and transcriptionally active chromatin in myeloid progenitors

Growth factor indepdendent 1 (GFI1) is a SNAG-domain, DNA binding transcriptional repressor which controls myeloid differentiation through molecular mechanisms and co-factors that still remain to be clearly identified. Here we show that GFI1 associates with the chromodomain helicase DNA binding protein 4 (CHD4) and other components of the Nucleosome remodeling and deacetylase (NuRD) complex. In granulo-monocytic precursors, GFI1, CHD4 or GFI1/CHD4 complexes occupy sites enriched for histone marks associated with active transcription suggesting that GFI1 recruits the NuRD complex to target genes regulated by active or bivalent promoters and enhancers. GFI1 and GFI1/CHD4 complexes occupy promoters that are either enriched for IRF1 or SPI1 consensus binding sites, respectively. During neutrophil differentiation, chromatin closure and depletion of H3K4me2 occurs at different degrees depending on whether GFI1, CHD4 or both are present, indicating that GFI1 is more efficient in depleting of H3K4me2 and -me1 marks when associated with CHD4. Our data suggest that GFI1/CHD4 complexes regulate histone modifications differentially to enable regulation of target genes affecting immune response, nucleosome organization or cellular metabolic processes and that both the target gene specificity and the activity of GFI1 during myeloid differentiation depends on the presence of chromatin remodeling complexes.ISSN:2399-364

Long noncoding RNA ERICD interacts with ARID3A via E2F1 and regulates migration and proliferation of osteosarcoma cells

Long noncoding RNA (lncRNA) dysregulation is known to be taking part in majority of cancers, including osteosarcoma. In one of our previous studies, we showed that lncRNA MEG3 is being regulated by microRNA-664a (miR-664a) suppresses the migratory potential of osteosarcoma cells (U-2OS). We now report a novel lncRNA, namely, ERICD, which is linked to the transcription factor AT-rich interaction domain 3A (ARID3A) in U-2OS cells. We show that ARID3A binds to ERICD and indirectly interacts with each other via the E2F transcription factor 1 (E2F1). Furthermore, small interfering RNA (siRNA)-mediated knockdown of ERICD inhibited cell migration, formation of colonies, and proliferation in U-2OS cells. Overexpression of ARID3A inhibited cell migration, colony formation, and proliferation, whereas siRNA-mediated knockdown of ARID3A promoted cell migration, colony formation, and proliferation. Our findings indicate that ARID3A and lncRNA ERICD have plausible tumor suppressive and oncogenic functions, respectively, in osteosarcoma. Our data demonstrate the converse interaction between ARID3A and lncRNA ERICD that target DNA-binding proteins and dysregulation of their expression through E2F1 augments osteosarcoma progression. The cell rescue experiment also indicated E2F1 to be involved in the regulation of ARID3A and ERICD