Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1041302 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR26848077_1.fastq.gz | Fastqsanger.gz |
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Project description:Lip is an anatomical junction between skin and mucosa and the squamous cell carcinoma (SCC) is the most frequent lip cancers. Lip SCC is frequently developed from actinic cheilitis, presented as ulcerative lesions. However, changes in transcriptomes and tumor microenvironment driving oncogenic transformation from actinic cheilitis to lip SCC and determinants of differentiation of lip SCC are largely unknown. This study aimed to investigate differences between lip SCC and its premalignant actinic cheilitis and factors related to tumor differentiation.
2024-10-28 | GSE280136 | GEO
Project description:BACKGROUND & AIMS: C/EBPbeta is involved in numerous process as carcinogenesis but its role is still not clear due to the existence of an active form (LAP) and an inhibitory form (LIP) of this transcription factor. The main goals of the present research were (i) the identification of genes inversely regulated by LAP and LIP i-e the genuine C/EBPbeta molecular signature in the Hep3B human hepatoma cell line (ii) a better understanding of LAP and LIP respective role in hepatic cells survival and proliferation (iii) the search of the C/EBPbeta signature among hepatocellular carcinomas. METHODS: Using Tet-off expression system we engineered Hep3BLAP and Hep3BLIP cells, in which LAP and LIP were over-expressed respectively. Then, using both expression profiling (DNA arrays) and ChIP-on-chip analysis, we identified genes inversely and/or directly regulated by each of the C/EBPbeta isoforms. The expression levels of these genes regulated by LAP/LIP were compared in controls and HCCs patients. RESULTS: We identified 676 genes inversely regulated by LAP and LIP and among these, 45 are direct targets. Using functional studies, we displayed the opposite role of LAP and LIP in staurosporine-induced cell death and the implication of LAP in the repression of Hep3B cells proliferation. Finally we identified a subgroup of HCCs with a deregulation of 165 genes belonging to C/EBPbeta signature and coding for proteins involved in chemoresistance and metastasis formation. CONCLUSIONS: Our study increases knowledge on LAP and LIP functions and provides first evidence that their molecular signature in the HCCs could predict tumor evolution.
2009-02-27 | GSE15010 | GEO
Project description:Two long and one truncated isoforms (termed LAP*, LAP, and LIP, respectively) of the transcription factor CCAAT enhancer binding protein beta (C/EBPβ) are expressed from a single intronless Cebpb gene by alternative translation initiation. Isoform expression is sensitive to mammalian target of rapamycin (mTOR)-mediated activation of the translation initiation machinery and relayed through an upstream open reading frame (uORF) on the C/EBPβ mRNA. The truncated C/EBPβ LIP, initiated by high mTOR activity, has been implied in neoplasia, but it was never shown whether endogenous C/EBPβ LIP may function as an oncogene. In this study, we examined spontaneous tumor formation in C/EBPβ knockin mice that constitutively express only the C/EBPβ LIP isoform from its own locus. Our data show that deregulated C/EBPβ LIP predisposes to oncogenesis in many tissues. Gene expression profiling suggests that C/EBPβ LIP supports a protumorigenic microenvironment, resistance to apoptosis, and alteration of cytokine/chemokine expression. The results imply that enhanced translation reinitiation of C/ EBPβ LIP promotes tumorigenesis. Accordingly, pharmacological restriction of mTOR function might be a therapeutic option in tumorigenesis that involves enhanced expression of the truncated C/EBPβ LIP isoform.
2014-12-16 | GSE53770 | GEO
Project description:Two long and one truncated isoforms (termed LAP*, LAP, and LIP, respectively) of the transcription factor CCAAT enhancer binding protein beta (C/EBPM-NM-2) are expressed from a single intronless Cebpb gene by alternative translation initiation. Isoform expression is sensitive to mammalian target of rapamycin (mTOR)-mediated activation of the translation initiation machinery and relayed through an upstream open reading frame (uORF) on the C/EBPM-NM-2 mRNA. The truncated C/EBPM-NM-2 LIP, initiated by high mTOR activity, has been implied in neoplasia, but it was never shown whether endogenous C/EBPM-NM-2 LIP may function as an oncogene. In this study, we examined spontaneous tumor formation in C/EBPM-NM-2 knockin mice that constitutively express only the C/EBPM-NM-2 LIP isoform from its own locus. Our data show that deregulated C/EBPM-NM-2 LIP predisposes to oncogenesis in many tissues. Gene expression profiling suggests that C/EBPM-NM-2 LIP supports a protumorigenic microenvironment, resistance to apoptosis, and alteration of cytokine/chemokine expression. The results imply that enhanced translation reinitiation of C/ EBPM-NM-2 LIP promotes tumorigenesis. Accordingly, pharmacological restriction of mTOR function might be a therapeutic option in tumorigenesis that involves enhanced expression of the truncated C/EBPM-NM-2 LIP isoform. A cohort of C/EBPb LIP heterozygous (+/L) and wild type (+/+) mice were kept over 25 months and animals showing palpable lymphoma were sacrificed. The lymphoma developed spontaneously. For each genotype, 5 lymphoma were used for RNA preparation and gene expression profiling analysis.
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Project description:summary (1)Objective: To investigate the antileukemic role of Lip-1 in K562 leukemia cells. (2)Methods: We performed CCK-8, flow cytometry, microscopy, western blotting assay, next generation sequencing, PCR assays to evaluate the effect of Lip-1 in K562 leukemia cells. (3)Results: Lip-1 inhibited K562 cell proliferation in a dose- and time-dependent manner. RNA sequencing revealed several pathways that were affected by Lip-1, such as the G1/S transition of the mitotic cell cycle and extrinsic or intrinsic apoptotic signaling pathways. The results of flow cytometry indicated that Lip-1 arrests the cell cycle. K562 cells were characterized by swelling and plasma membrane rupture. The expression of the hallmark of pyroptosis, the cleaved N-terminal GSDME, increased. Endoplasmic reticulum stress and autophagy were involved in Lip-1-induced cell death. (4)Conclusion：Lip-1 induces cell cycle arrest, apoptosis, and secondary pyroptosis in K562 leukemia cells, which provides new hope for the treatment of leukemia.
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Project description:Our histological findings showed that vermillion is present in the lip of Japanese macaque. In addition, the immunostaining pattern of K10 and SPRR3 of the lip of Japanese macaque is similar to that of a human. Thus, the transcriptome analysis of Japanese monkey can provide several unique genes specific to vermillion keratinocytes, which is required to develop a human lip/vermillion in vitro model.
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Project description:BCG therapy is the most effective immunotherapy for bladder cancer, but it sometimes causes serious adverse events because of infection with live BCG bacteria. To develop more effective and less toxic immunotherapeutic agents, we have developed formulations using BCG cell wall components. Trehalose dimycolate (TDM) is a predominant glycolipid that constitutes the cell wall of BCG, and reported to show activation of innate immunity and have adjuvant effect. We already established hydrophilic cationic liposomes incorporating TDM, and reported that local administration of the cationic liposome TDM (Lip-TDM) exerted antitumor effect to subcutaneously inoculated tumors by inducing activation of CD8+ T cells via dendritic cell maturation. In present study, we demonstrated that intraperitoneal administration of Lip-TDM exerted antitumor effects in orthotopic bladder carcinogenesis mouse model induced by N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN). In this model, intraperitoneal administration of Lip-TDM enhanced the systemic activation of dendric cells and macrophages, and increased infiltration of adaptive immune cells such as CD8+ T cells. Furthermore, Lip-TDM treatment induced Natural Killer (NK) cells to be cytotoxic NK cells in tumors and regulatory NK cells in lymphoid tissues. Lip-TDM treatment induced activation of DCs and cytotoxic CD8+ T cells and exerted antitumor effect in WT mice, but not in NK cell-depleted mice. These results indicate NK cells are essential for Lip-TDM to induce sufficient acquired immune response. Our findings elucidate the mechanism of the antitumor effect by Lip-TDM and suggest that Lip-TDM is a non-infectious agent which can be administered intraperitoneally and has potential to be an alternative to BCG.
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