More than a Tumor Suppressor: E-Cadherin Loss Drives Lung Cancer Metastasis

• Published in: American journal of respiratory cell and molecular biology Vol. 59; no. 2; pp. 141 - 142
• Main Authors: Devlin, Jennifer R, Verschuren, Emmy W
• Format: Journal Article
• Language: English
• Published: United States American Thoracic Society 01.08.2018
• Subjects: Adenocarcinoma; Angiogenesis; Biology; Cadherins - metabolism; Cell adhesion & migration; Extracellular matrix; Humans; Lung cancer; Lung Neoplasms - metabolism; Lung Neoplasms - pathology; Metastases; Metastasis; Microenvironments; miRNA; Neoplasm Metastasis - pathology; Pathology; Proto-Oncogene Proteins p21(ras) - metabolism; Regulation; Tumor cells; Tumor suppressor genes
• ISSN: 1044-1549; 1535-4989
• DOI: 10.1165/rcmb.2018-0063ED

Tumor metastasis is the multistage process by which primary tumor cells disseminate to distant locations in the body. It is dynamically regulated by biologically complex tumor-microenvironment interactions, both at the primary tumor site and at the metastatic niche. In 1889, the surgeon Stephen Paget proposed that the homing of tumor cells to specific organs is regulated by interactions between selected tumor cells, or seeds, and distant tumor microenvironments, or soil. It is only during the past three decades that much of the molecular and cellular basis of this seminal seed and soil model has been dissected. Numerous recent studies have identified putative novel regulators of lung adenocarcinoma metastasis, ranging from noncoding RNAs and microRNAs to tumor-stromal interactions, including those involving immune cells.