RNA seq on two primary pancreatic cancer cell lines (cancer-collagen1 knockout cell line and control pancreatic cancer cell line)
Ontology highlight
ABSTRACT: RNA sequencing analysis on two primary pancreatic cancer cell lines from transgenic mice: (1) cancer-collagen1 knockout cell line from KPPC;Col1pdxKO cancer-collagen1 knockout tumor and (2) control pancreatic cancer cell line from KPPC tumor
Project description:Here, we sought to evaluate the impact of KrasG12D and KrasG12C inhibitors on pancreatic cancer cells. A murine pancreatic cancer cell line with KrasG12D mutation was treated with MRTX1133 (KrasG12D inhibitor) and MRTX849 (KrasG12C inhibitor) and scRNA-seq performed to evaluate transcriptional changes. We further evaluated transcriptional changes in cancer cells, as well as in the tumor microenvironment of immunodeficient (NSG) and immunocompetent (C57BL6/J) mice orthotopically implanted with KPC689 cells and spontaneous KPPC tumors in response to MRTX1133 and MRTX849.
Project description:RNA-sequencing analyses were performed on cancer cell lines from KPPC and PPSSC pancreatic tumors, so as to identify the changes of tumor immune microenvironment upon Trp53 and Smad4 deletion without KRAS mutation.
Project description:RNA seq on primary pancreatic cancer (KPPC;Col1pdxKO cancer-collagen1 knockout) cells growing on collagen 1 homotrimers and heterotrimers. In this study, we identify that pancreatic cancer cells produce a unique Collagen1 homotrimer variant, in contrast to the Collagen1 heterotrimer produced by normal cells (such as fibroblasts). The variant forms of Collagen1 (homotrimer and heterotrimer) have distinct effects on cancer cell behaviors. We culture the pancreatic cancer cells on purified Collagen1 homotrimer and heterotrimer (as well as vehicle control) and examine the global changes of gene expression profile in cancer cells by variant Collagen1 subtypes.
Project description:The goal of the study was to examine the transcriptional profile of pancreatic cancer cell lines and assess if the molecular subtypes observed in tumor samples were represented in existing cell line models. Cell line models allow us to investigate if the molecular subtype observed in tumor have unique sensitivity profiles to anticancer drugs. 29 pancreatic cancer cell lines were compared to a mixed reference pool of 30 pancreatic cancer cell lines to identify cell line specific gene expression.
Project description:tumor-stroma crosstalk drives pancreatic carcinogenesis we used time-resolved genome-wide transcriptional profiling to analyse changes caused by co-exposure of pancreatic tumor and stellate cells pancreatic tumor cell line MiaPaca2 was treated with a supernatant of pancreatic stelalte cells, primed with cumulative TC-supernatant (of 8 tumor cell lines, TC) and harvested hourly at 1-7, and 24 hours post exposure for RNA extraction and hybridization on Affymetrix microarrays.
Project description:RNA sequencing analysis on tumor samples from two groups of mice (1) KPPC;Col1pdxKO cancer-collagen1 knockout group and (2) KPPC control group
Project description:tumor-stroma crosstalk drives pancreatic carcinogenesis we used time-resolved genome-wide transcriptional profiling to analyse changes caused by co-exposure of pancreatic tumor and stellate cells pancreatic tumor cell line MiaPaca2 was treated with a supernatant of pancreatic stellate cells and harvested hourly at 1-7, and 24 hours post exposure for RNA extraction and hybridization on Affymetrix microarrays.
Project description:Project describes the proteomics analysis using pSILAC approach to identify and quantify the hypoxia induced protein under serum and serum free conditions in pancreatic cancer cell line (MiaPaCa-2)