Project description:ELMOD2 cDNA from the IMAGE clone 3897166 was cloned into the pDsRed-Monomer-N1 expression vector. ELMOD2 was overexpressed in the A549(adenomcarcinoma)cell line and cells transfected with empty vector were considered controls. Transcript profiles were compared with the Affymetrix Hgu133plus2 arrays. Three biological replicates of each condition were included.
Project description:Aberrant mucin-type O-glycosylation affects many cellular properties and is associated with many cancers. N-acetylgalactosaminyltransferase 10 (GALNT10) is a GalNAc-transferase that initiates protein O-glycosylation. The aim of this study was to explore the role of GALNT10 in lung adenocarcinoma. Immunohistochemistry was performed to study the expression of GALNT10 in an lung adenocarcinoma tissue microarray. We found that GALNT10 is frequently down-regulated in lung adenocarcinoma tissues and is associated with pathological classification and TNM stage. Additionally, we demonstrated that knockdown of GALNT10 with small interference (si) RNA promoted cell proliferation, cell colony formation and cell invasion capacity in A549 cells by using CCK8 assay, flow cytometry, cell colony formation, and transwell invasion assay.Moreover, whole genome microarray analysis showed that 287 genes were up-regulated and 137 were down-regulated in A549 cells upon GALNT10 knockdown. Functional enrichment analysis reveal that GALNT10 knockdown in A549 cells leads to differential gene expression in pathways, including TNF signaling pathway. These findings suggest that down-regulation of GALNT10 plays an important role in the cell proliferation and invasive behavior of lung adenocarcinoma via modifying O-glycosylation and activity of TNF pathway. In addition, we suggest that GALNT10 may be a tumor suppressor gene in lung adenocarcinoma and that targeting GALNT10 could be a promising approach for lung adenocarcinoma therapy.
Project description:IGFBP2 is one of the putative biomarker of Afatinib response we identified. To dissect the biological processes sustained by IGFBP2 expression, we performed bulk 3’ RNA-seq of MDA-MB-468 cell line over-expressing it
Project description:Genomic changes in low and highly metastatic A549 cells were analyzed by 500K SNP arrays. A large number of genomic alterations were present in A549 cells but no significant differences were observed between the low or highly metastatic A549 cell lines. We generated a NSCLC line with highly increased propensity to form tumor nodules in murine lungs after intravenous injections. Extravasation and growth at a distant site are important parts of the metastatic process and we regarded these as a surrogate marker for in vivo aggressiveness and potential metastatic capability. A549 lung asdenocarcimona cell line with initially low metastatic potential was used for this purpose; these cells formed multiple small nodules in NOD/SCID mice after first i.v.-injection, round 1 (R1). Removal of tumor nodules from the lungs and subsequent re-injection led to a rapid increase in metastatic capacity. A highly aggressive phenotype which was stable over time was evident after three rounds (R3) of in vivo selection for the A549 cell line.