Dataset: Identification of Metastasis-prone Lung Adenocarcinoma Cell Population That Is Sensitive to Notch Inhibition

Tumor cells that give rise to metastatic disease are a primary cause of cancer-related death and have not been fully elucidated in patients with lung cancer. Here, we addressed this question by using tissues from a mouse that develops metastatic lung adenocarcinoma owing to expression of mutant K-ras and p53. We identified a metastasis-prone population of tumor cells that differed from those with low metastatic capacity on the basis of having sphere-forming capacity in Matrigel cultures, increased expression of CD133 and Notch ligands, and relatively low tumorigenicity in syngeneic mice. Knockdown of jagged1 or pharmacologic inhibition of its downstream mediator phosphatidylinositol 3-kinase abrogated the metastatic but not the tumorigenic activity of these cells. We conclude from these studies on a mouse model of lung adenocarcinoma that CD133 and Notch ligands mark a population of metastasis-prone tumor cells and that the efficacy of Notch inhibitors in metastasis prevention should be explored. Keywords: two group comparison 344SQ subcutaneous tumors (from a lung adenocarcinoma cell line derived from a KrasLA1/+; p53R172HdelG/+ mouse that metastasizes widely following subcutaneous injection into syngeneic mice) were sorted by flow cytometry into CD133high and CD133low fractions. RNA samples from these fractions were processed and analyzed on Affymetrix Mouse Expression Array 430A 2.0 chips.

Species:

mouse

Samples:

6

Source:

E-GEOD-15587

Updated:

Dec.12, 2014

Registered:

Nov.11, 2014