A new identified lncBCAS1-4_1 associated with Vitamin D signaling and EMT in ovarian cancer cells
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PROVIDER: PRJNA726436 | ENA |
REPOSITORIES: ENA
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Project description:Long non-coding RNAs (lncRNAs) has been identified rapidly due to the important role of lncRNAs in many biological processes and human diseases including cancer. Vitamin D compounds are supported to be applied as preventative and therapeutic anticancer agents. However, the expression profile of lncRNAs regulated by 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3] in ovarian cancer remains to be clarified. In the present study, we identified 244 differentially expression (DE) lncRNAs and 102 DE mRNAs by our microarray data. GO and KEGG pathway analysis indicated that the DE genes were mainly enriched in TGF-β, MAPK, Ras, PI3K-Akt and Hippo signaling pathways, as well as vitamin D-related pathway. We further assessed the potential lncRNAs linking vitamin D signaling with EMT, and lncBCAS1-4_1 was identified. Moreover, we found the most upregulation lncBCAS1-4_1 has 75% transcripts same to CYP24A1, metabolic enzyme of 1α,25(OH)2D3. Finally, we established lncBCAS1-4_1 gain-of-function cell models and demonstrated that knockdown of lncBCAS1-4_1 inhibited proliferation and migration of ovarian cancer cells by regulating EMT-related mRNAs. Furthermore, our results also indicated that high lncBCAS1-4_1 obviously resisted the anti-tumor effect of 1α,25(OH)2D3 by upregulating ZEB1. These data will provide new evidence that lncRNAs are served as a target for the anti-tumor of 1α,25(OH)2D3.
2021-05-01 | GSE173633 | GEO
Project description:Elucidation of new roles for vitamin B12 in regulation of folate, ubiquinone, and methionine metabolism
2018-10-22 | PXD005723 | Pride
Project description:Recent findings show that EMT in cancer is dynamic and display a number of intermediate stages along the transition to obtain a high phenotypic and functional cellular plasticity. To comprehend transcriptional regulation among major EMT-transcription factors (EMT-TFs) along the EMT spectrum, we performed gene expression profiles of EMT-TFs (SNAI1/2, ZEB1/2, TWIST1) overexpressing epithelial (PEO1, OVCA420) and intermediate epithelial (OVCA429) ovarian cancer cell clones. Our results show that these factors generate an unidirectional repressive regulation in cells with epithelial phenotype (PEO1, OVCA420), whereas a bidirectional activation regulation in cells with intermediate epithelial phenotype (OVCA429). Microarray data analysis of these EMT-TFs overexpression clones revealed a distinct signature of gene expression for each phenotype and the overlapping gene set show a strong negative correlation with EMT scores, indicating that loss of this gene set is essential to trigger EMT.
2022-05-25 | GSE145553 | GEO
Project description:Long noncoding RNAs (lncRNAs) were identified rapidly due to their important role in many biological processes and human diseases including cancer. 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3] and its analogues are widely applied as preventative and therapeutic anticancer agents. However, the expression profile of lncRNAs regulated by 1α,25(OH)2D3 in ovarian cancer remains to be clarified. In the present study, we found 606 lncRNAs and 102 mRNAs that showed differential expression (DE) based on microarray data. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that the DE genes were mainly enriched in TGF-β, MAPK, Ras, PI3K-Akt, and Hippo signaling pathways, as well as the vitamin D-related pathway. We further assessed the potential lncRNAs that linked vitamin D signaling with EMT, and lncBCAS1-4_1 was identified in the first time. Moreover, we found that the most upregulated lncBCAS1-4_1 showed 75% same transcripts with CYP24A1 (metabolic enzyme of 1α,25(OH)2D3). Finally, the lncBCAS1-4_1 gain-of-function cell model was established, which demonstrated that the knockdown of lncBCAS1-4_1 inhibited the proliferation and migration of ovarian cancer cells. Furthermore, lncBCAS1-4_1 could resist the antitumor effect of 1α,25(OH)2D3, which was associated with upregulated ZEB1. These data provide new evidences that lncRNAs served as a target for the antitumor effect of 1α,25(OH)2D3.
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Project description:Gene expression data of EMT-TFs overexpressing ovarian cancer cell lines
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Project description:The resistance of cancer cell to therapy is responsible of the death of most cancer patients. Epithelial to mesenchymal transitions (EMT) has been associated with resistance to therapy in different cancer cells. However, the mechanisms by which EMT mediates resistance to therapy remain poorly understood. Here, using a mouse model of skin squamous cell carcinoma (SCC) undergoing spontaneous EMT during tumorigenesis, we identified EMT tumor subpopulations displaying different intrinsic resistance mechanisms to a wide range of anti-cancer therapy both in-vivo and in-vitro. We found that RhoJ, a small GTPase, preferentially expressed in EMT cancer cells controls resistance to therapy. Using genome-wide transcriptomic and proteomic profiling combined with functional assays following loss of RhoJ functions, we found that RhoJ regulated EMT associated resistance to chemotherapy by promoting DNA damage response and the formation of new replication forks allowing EMT tumor cells to repair DNA lesions more rapidly and survive under the replicative stress induced by chemotherapy. Altogether, our study uncovers RhoJ as a key regulator of EMT associated resistance to chemotherapy with important implications for the development of new strategies to overcome resistance to therapy in cancer.
2023-01-13 | PXD025737 | Pride
Project description:Vitamin D is the strongest known natural anti-proliferative. A large number of studies in a wide spectrum of cancers, including epidemiological, in vitro and animal models, demonstrate that the active form of Vitamin D has anti-cancer benefits, affecting both progression and metastasis. Alike the role in calcium Vitamin D regulation, its anti-proliferative effect is thought to function through the Vitamin D receptor (VDR), although convincing evidence is lacking. Notwithstanding, separation of the calcemic and the anti-proliferative activity of Vitamin D analogues has been a major obstacle in developing new drugs for the treatment of cancer. The work presented attempts to unveil the molecular mechanism behind the anti-proliferative action of Vitamin D using genomic tools. For that purpose four independently developed Vitamin D sensitive/resistant MCF7 cell line pairs were collected. These unique biological replicates enabled us, both to increase the power of our study and to omit the use of Vitamin D. We deem this omission crucial since in the presence of Vitamin D only downstream genes involved in proliferation and cell cycle would be identified rather than causal resistance genes. The use of a variety of genomic techniques including expression, NMD and oligo CGH arrays reveal in the resistant cell lines the 11q13-14 as a region of DNA copy number loss and an altered expression of EGFR signaling pathway genes. Surprisingly, no genes known from calcium Vitamin D regulation were identified, nor did the VDR silencing by RNAi induce resistance to the sensitive cell lines. Keywords: Expression microarray, cell type comparision Several MCF7 breast tumor cell lines independently derived from the human breast cancer cell line, both resistant and sensitive to Vitamin D, were used. The pairs of cell lines (parental-resistant) were developed in different laboratories and using different methodologies; while some cell lines acquired resistance by long exposure to the physiological concentration of Vitamin D (100nM), others were induced to resistant by being exposed to increasing amounts of Vitamin D. A total of 14 microarray expression experiments were carried out, including four biological replicates and 10 technical replicates including dye swaps. In all microarray experiments RNA from the Vitamin D resistant cell line was hybrizided agains RNA from the respsective sensitive/parental cell line.
2008-05-31 | E-GEOD-9867 | biostudies-arrayexpress
Project description:Analysis of mouse ovarian cancer cell line HM-1 transfected with shRNA targeting Snail, an EMT inducer. Anti-tumor immuty in state of EMT remains unclear. We focused on Snail, a major EMT inducer, and explored the influence of Snail on immune ivasion into ovarian tumors by generating Snail knockdown cell line. Elucidating the mechanisms of Snail-induced immune evasion will lead to the development of novel treatment strategies for tumor undergoing EMT.
2018-01-27 | GSE109688 | GEO
Project description:Vitamin D is the strongest known natural anti-proliferative. A large number of studies in a wide spectrum of cancers, including epidemiological, in vitro and animal models, demonstrate that the active form of Vitamin D has anti-cancer benefits, affecting both progression and metastasis. Alike the role in calcium Vitamin D regulation, its anti-proliferative effect is thought to function through the Vitamin D receptor (VDR), although convincing evidence is lacking. Notwithstanding, separation of the calcemic and the anti-proliferative activity of Vitamin D analogues has been a major obstacle in developing new drugs for the treatment of cancer. The work presented attempts to unveil the molecular mechanism behind the anti-proliferative action of Vitamin D using genomic tools. For that purpose four independently developed Vitamin D sensitive/resistant MCF7 cell line pairs were collected. These unique biological replicates enabled us, both to increase the power of our study and to omit the use of Vitamin D. We deem this omission crucial since in the presence of Vitamin D only downstream genes involved in proliferation and cell cycle would be identified rather than causal resistance genes. The use of a variety of genomic techniques including expression, NMD and oligo CGH arrays reveal in the resistant cell lines the 11q13-14 as a region of DNA copy number loss and an altered expression of EGFR signaling pathway genes. Surprisingly, no genes known from calcium Vitamin D regulation were identified, nor did the VDR silencing by RNAi induce resistance to the sensitive cell lines. Keywords: Expression microarray, cell type comparision
2008-06-01 | GSE9867 | GEO
Project description:Chemo-resistance to platinum such as cisplatin is critical in the treatment of ovarian cancer. Recent evidences have linked epithelial-mesenchymal transition (EMT) with the drug resistance as a contributing mechanism. The current study explored the connection between cellular responses to cisplatin with EMT in ovarian cancer. 46 ovarian carcinoma cell lines expression data with and without Cisplatin treatment.
2014-07-29 | E-GEOD-47856 | biostudies-arrayexpress