Dataset: Transcription profiling of mouse 344SQ lung adenocarcinoma cells with high metastatic potential (syngeneic mouse model)

The biologic basis for NSCLC metastasis is not well understood. Here we addressed this deficiency by transcriptionally profiling tumors from a genetic mouse model of human lung adenocarcinoma that develops metastatic disease owing to the expression of K-rasG12D and p53R172H. As a tool to investigate the biologic basis for metastasis in this model and to query the roles of specific genes in this signature, we isolated adenocarcinoma cell lines from these mice and used them to develop a syngeneic tumor model in wild-type littermates. Transcriptional profiling of the highly metastatic subcutaneous tumors revealed genes that regulate, among other processes, epithelial-to-mesenchymal transition and intra-tumoral inflammation and angiogenesis, whereas the non-metastatic tumors did not. Experiment Overall Design: Cell lines from p53R172H∆g/+ K-rasLA1/+ mice were derived from tumor tissues removed at autopsy from two different mice (#344 and #393). The tissues were minced, placed in culture, and passed serially in RPMI 1640 supplemented with 10% fetal bovine serum (FBS), which yielded mass populations of tumor cells derived from primary lung tumors (344P and 393P), mediastinal lymph nodes (344LN and 393LN), and a subcutaneous site (344SQ). Syngeneic tumors were isolated, carefully dissected to remove the adjacent tissue, snap-frozen in liquid nitrogen and stored at -80° until use. Part of each dissected tumor was histologically evaluated by a board-certified pathologist. Snap-frozen samples were processed and analyzed on Affymetrix Mouse Expression Array 430A 2.0 chips. Experiment Overall Design: Expression profiling performed on 344SQ, 393P, and 393LN

Species:

mouse

Samples:

12

Source:

E-GEOD-14458

PubMed:

19759262

Updated:

Dec.12, 2014

Registered:

Nov.10, 2014