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Atypical expression and distribution of embryonic stem cell marker, OCT4, in human lung adenocarcinoma
Author(s) -
Karoubi Golnaz,
CortesDericks Lourdes,
Gugger Mathias,
Galetta Domenico,
Spaggiari Lorenzo,
Schmid Ralph A.
Publication year - 2010
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.21665
Subject(s) - adenocarcinoma , carcinogenesis , embryonic stem cell , lung cancer , stem cell , cancer stem cell , cancer research , pathology , biology , adenocarcinoma of the lung , medicine , cancer , microbiology and biotechnology , genetics , gene
Background and Objectives Lung cancer is one of the leading causes of cancer‐related deaths in the world. Although the origin still remains to be resolved, a prevailing hypothesis implies the involvement of cancer stem cells (CSCs) responsible for tumor initiation, maintenance, and progression. Embryonic stem cell marker, OCT4, encoding the spliced variants OCT4A and OCT4B, has recently been shown to have a dual role; as a potential adult stem cell marker and as a CSC marker in germline and somatic tumors. Methods We investigated the expression and intracellular distribution of OCT4A and OCT4B using flow cytometry, Western blot and quantitative RT‐PCR analyses in normal and lung adenocarcinoma cell lines, primary cultures and tissue biopsies. Results We demonstrate for the presence of rare OCT4A + and OCT4B + cells in normal lung. Notably, we observed higher levels of expression and atypical cytoplasmic distribution of OCT4A and not OCT4B, in the malignant setting, strongly indicating an oncogenic role in lung adenocarcinoma. Conclusions We postulate that OCT4A + cells are involved in the oncogenesis of lung adenocarcinoma. Identification of these cells and the biological processes vital for their subsistence, will guide the development of diagnostic and therapeutic clinical approaches with the goal of eliminating lung adenocarcinoma. J. Surg. Oncol. 2010;102:689–698. © 2010 Wiley‐Liss, Inc.