Differential Kras^V12 protein levels control a switch regulating lung cancer cell morphology and motility.

ABSTRACT:

Introduction

Oncogenic Kras mutations are important drivers of lung cancer development and metastasis. They are known to activate numerous cellular signaling pathways implicated in enhanced proliferation, survival, tumorigenicity and motility during malignant progression.

Objectives

Most previous studies of Kras in cancer have focused on the comparison of cell states in the absence or presence of oncogenic Kras mutations. Here we show that differential expression of the constitutively active mutation Kras^V12 has profound effects on cell morphology and motility that drive metastatic processes.

Methods

The study relies on lung cancer cell transformation models, patient-derived lung cancer cell lines, and human lung tumor sections combined with molecular biolo

SUBMITTER: Schafer C 

PROVIDER: S-EPMC5648346 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature