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Pancreatic cancer cell CFPAC-1: shBACH1 vs. shControl

ABSTRACT: Pancreatic cancer cell CFPAC-1: shBACH1 vs. shControl

PROVIDER: PRJNA437243 | ENA |

REPOSITORIES: ENA

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Pancreatic cancer cell CFPAC-1: shBACH1 vs. shControl

Project description:Gene expression profiling of pancreatic cancer cell CFPAC-1 when BACH1 knockdown. BACH1 is a transcription repressor and its regulation networks is poorly understood in pancreatic ductal adenocarcinoma. We used the total RNA from shControl and shBACH1 CFPAC-1 cells to analyze the differentially expressed genes which were regulated by BACH1, and further explored the biological processes that BACH1 may involved.

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Pancreatic Cancer HPAF/CD18 cells: Ecd knockdown vs Scrambled

Project description:Purpose: To study the expression and function of a novel cell cycle regulatory protein, human ecdysoneless (Ecd), during pancreatic cancer (PC) pathogenesis. Experimental Design: Immunohistochemical expression profiling of Ecd was done in non-neoplastic normal pancreatic tissues and pancreatic ductal adenocarcinoma lesions (from tissue microarray and Rapid Autopsy program) as well as precancerous PanIN lesions and metastatic organs. To analyze the biological significance of Ecd in PC progression, Ecd was stably knocked down in PC cell line followed by in vitro and in vivo functional assays. Results: Normal pancreatic ducts show very weak to no Ecd expression compared to significant positive expression in PC tissues (mean±SE composite score: 0.3±0.2 and 3.8±0.2 respectively, p<0.0001) as well as in PanIN precursor lesions with a progressive increase in Ecd expression with increasing dysplasia (PanIN-1 to PanIN-3). Analysis of matched primary tumors and metastases from PC patients revealed that Ecd is highly expressed in both primary pancreatic tumor and in distant metastatic sites. Further, knockdown of Ecd suppressed cell proliferation in vitro and tumorigenicity of PC cells in mice orthotopic tumors. Microarray study revealed that Ecd regulates expression of glucose transporter GLUT4 in PC cells and was subsequently shown to modulate glucose uptake, lactate production and ATP generation by PC cells. Finally, knockdown of Ecd also reduced level of pAkt, key signaling molecule known to regulate aerobic glycolysis in cancer cells. Conclusion: Ecd is a novel tumor promoting factor that is differentially expressed in pancreatic cancer and potentially regulates glucose metabolism within cancer cells. Two-condition experiment, Ecd knockdown vs Scrambled cells. Biological replicates: 3 Ecd knockdownl, 3 Scrambled, independently grown and harvested. One replicate per array

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pancreatic cancer

Project description:pancreatic cancer

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Pancreatic cancer

Project description:Pancreatic cancer

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Transcriptome analysis of human pancreatic cancer cell lines and gemcitabine-resistant pancreatic cancer cell lines

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