Identifying the regulators of adhesion-independent Golgi organization in lung cancer cells

Abstract

The orchestration of resident proteins in Golgi is critical for the monolithic morphology and maintenance of glycosylation of the cells. Golgi organization is known to be altered in many cancers ranging from condensation to dispersion of Golgi. Alteration of the Golgi phenotype opens the door to a cascade of fatal pathways that can aid cancer progression and metastasis. Normal cells rely on adhesion signals for membrane trafficking of target proteins and Glycosylation, which is known to affect cancers. In the recent decade, multiple studies have elucidated multiple regulators role in the regulation of Golgi phenotype in cells. But how the phenotype of Golgi is regulated upon loss of adhesion is still enigmatic. NSCLC, anchorage-independent cancer, remained as the global primary lung cancer burden contributing to the majority of lungs cancer cases across the globe. This study identified 14 putative regulators of Golgi organization, which are differentially expressed between anchorage-independent lungs cancer cell lines (A549 and CaLu1) by multi-omics approach.