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MiRNA signatures underly chemoresistance in the gemcitabine-resistant pancreatic ductal adenocarcinoma cell line MIA PaCa-2 GR

ABSTRACT: miRNA signatures underly chemoresistance in the gemcitabine-resistant pancreatic ductal adenocarcinoma cell line MIA PaCa-2 GR

PROVIDER: PRJNA1120481 | ENA |

REPOSITORIES: ENA

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miRNA signatures underly chemoresistance in the gemcitabine-resistant pancreatic ductal adenocarcinoma cell line MIA PaCa-2 GR

Project description:Chemotherapy resistance is a major clinical issue for pancreatic adenocarcinoma (PDAC). MicroRNAs (miRNAs) play an important role in cancer progression and chemoresistance. In this study, we addressed the association between miRNA expression profiles and gemcitabine (Gem) resistance. A Gem sensitive (GS) PDAC cancer cell line, MIA PaCa-2, and its Gem resistant (GR) progeny MIA PaCa-2 GR, was used to determine miRNA expression changes by resistance to Gemcitabine. miRNA-seq was used to determine the miRNA expression profiles in these cell lines. Ingenuity Pathway Analysis (IPA) was performed to determine the biological functions of differentially expressed miRNAs. In total, 1867 miRNAs were detected in the two cell lines. We found that the miRNA expression profiles were different between the GR and its sensitive isogenic parental GS cell line, and certain differentially expressed miRNAs were only detected in one or the other of these PDAC cell lines. A total of 97 (5.2%) miRNAs were significantly differentially expressed between GR and the GS cell lines, of which 65 (3.5%) miRNAs were upregulated and 32 (1.7%) miRNAs were downregulated. The miRNAs with the most significant differential expression in the GR cell line as compared with GS were primarily involved in the following biological processes: cell proliferation, cell migration & invasion, chemo-sensitization, alternative splicing, apoptosis, and angiogenesis. These miRNAs from cell lines were further refined to a subset and were analyzed in patient samples where expression was used to identify patients with recurrent tumors. Taken together, the results suggest that these miRNAs may play important roles in Gem resistance in PDAC. This study’s findings provides a basis for further research in the diagnosis and treatment selection for PDACs with gemcitabine resistance.

2024-07-01 | GSE269190 | GEO

MIA PaCa-2 cells treated with Gemcitabine

Project description:Pancreatic cancer cells (MIA PaCa-2) were treated with Gemcitabine and overall protein changes were studied

2022-09-15 | PXD030861 | Pride

siRNA knockdown of C1GALT1 in MIA PaCa-2 cells

Project description:To determine the C1GALT1 regulated gene expression profile in MIA PaCa-2 cells.

2017-12-04 | GSE90668 | GEO

mRNA expression data from RalGAPβ-deficient human pancreatic ductal adenocarcinoma cells (MIA PaCa-2), MIA PaCa-2 parental cells, and MIA PaCa-2 control cells

Project description:mRNA expression data from RalGAPβ-deficient human pancreatic ductal adenocarcinoma cells (MIA PaCa-2), MIA PaCa-2 parental cells, and MIA PaCa-2 control cells

| PRJNA925906 | ENA

RNA Sequencing Facilitates Quantitative Analysis of LINC00901 overexpression and Control MIA PaCa-2 Cell Transcriptomes

Project description:RNA Sequencing Facilitates Quantitative Analysis of LINC00901 overexpression and Control MIA PaCa-2 Cell Transcriptomes

2022-05-01 | GSE169660 | GEO

mRNA expression data from RalGAPβ-deficient human pancreatic ductal adenocarcinoma cells (MIA PaCa-2), MIA PaCa-2 parental cells, and MIA PaCa-2 control cells

Project description:Pancreatic ductal adenocarcinoma, caused by activating mutation in K-Ras, is an aggressive malignancy due to its early invasion and matastasis. Ral GTPases, negatively regulated by RalGAP, are activated downstream of Ras and play a crucial role in development and progression of pancreatic ductal adenocarcinoma. However, the underlying mechanisms remain unclear. We used microarrays to detail the global programme of gene expression underlying the human pancreatic ductal adenocarcinoma cell line, MIA PaCa-2 with RalGAPβ deficiency or not, and identified distinct classes of Ral activation-related mRNA.

2023-04-24 | GSE223382 | GEO

LYSET/TMEM251 KO secretome from MIA PaCa-2 cells

Project description:Analysis of proteins secreted over 24 h in OptiMEM by LYSET/TMEM251 knockout and control MIA PaCa-2 cells.

2022-09-29 | PXD029658 | Pride

RNA expression analysis after Mia PaCa 2 cell treatment with demethylating agent 5-Aza-2’-deoxycitidine (5-Aza)

Project description:Transcriptional profiling of Mia PaCa 2 cells treated with 5-Aza for 96 h. Relative abundance to untreated control cells was used to estimate the effect of DNA demethylation on the expression of the RNAs. Two-condition experiment, 5-Aza-treated vs. untretated Mia PaCa 2 cells. Biological replicates: 2. Technical replicates: 2.

2015-06-30 | E-GEOD-62959 | biostudies-arrayexpress

LYSET/TMEM251 SILAC Co-IP from MIA PaCA-2

Project description:Endogenous LYSET/TMEM251 was isolated via Co-IP from MIA PaCa-2 cells. LYSET KO cells were used as controls. Cells were grown in SILAC medium for 3 passages

2022-09-29 | PXD035821 | Pride

CRISPR deletion of ELAVL1 (HuR) in MIA PaCa-2 in vitro cells and in vivo tumors

Project description:To investigate the impact of the mRNA stabilty factor HuR on the pancreatic cancer transcriptome in MIA PaCa-2 in vitro cell line and in vivo tumors at multiple time points of tumor growth

2023-01-01 | GSE221250 | GEO

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