ORIGINAL PAPER
Altered expression of selenium-binding protein 1 in gastric
carcinoma and precursor lesions
Jin Zhang
•
Na Zhan
•
Wei-guo Dong
Received: 30 March 2010 / Accepted: 4 May 2010 / Published online: 18 May 2010
Ó Springer Science+Business Media, LLC 2010
Abstract Selenium-binding protein 1 (SBP1) has been
shown to be greatly reduced in various human cancers.
The purpose of this study was to evaluate the expression of
SBP1 in precursor lesions and gastric carcinoma (GC) and
to discuss the specific role of SBP1 in gastric carcinogen-
esis. Using tissue microarray (TMA) technology and
immunohistochemical (IHC) survey, SBP1 expressions
were evaluated based on a semi-quantitative scoring sys-
tem developed for this study in 25 paired of GC and cor-
responding nonneoplastic epithelia tissues, 21 gastric ulcer,
13 gastric polyp, 19 chronic atrophic gastritis, 20 intestinal
metaplasia, and 16 dysplasia tissues. We found abundant
expression of SBP1 in most precursor lesions in addition to
the nonneoplastic epithelia tissues. However, the expres-
sion of SBP1 was severely suppressed in most of the GC
tissues (P = 0.000). Although no statistical differences
were found between the expressions of SBP1 in gastric
tissues with different levels of intestinal metaplasia or
dysplasia (P [ 0.05), the reduction in SBP1 seems to be
correlated with clinical stage of GC (P = 0.044). Thus,
SBP1 can be supposed as a diagnosis marker of GC.
The suppression of SBP1 may be a late event in gastric
carcinogenesis.
Keywords Selenium-binding protein 1 Á Gastric
carcinoma Á Precursor lesion Á Tissue microarray Á
Immunohistochemistry
Introduction
Gastric carcinoma (GC) is the second leading cause of
cancer-related deaths worldwide owing to the difficulty in
early detection and high postsurgical recurrence rate [1].
Patients afflicted with GC are often asymptomatic, and the
lack of sensitive and reliable biomarkers for the early
detection of GC means that diagnosis normally occurs late,
when surgical intervention is not an option. Today, there
are no effective drugs for curing GC. For patients with
increased risk of GC, such as those with dietary, racial, or
familial risks of GC, the ability to detect asymptomatic
precursor lesions may have therapeutic benefit.
Epidemiologic studies have discovered that lung cancer,
liver cancer, colon carcinoma, prostate carcinoma, and
pancreatic cancer were related to dietary selenium (
75
Se)
deficiency [2–5]. Many investigations have demonstrated
that selenium can inhibit tumor cell growth and tumori-
genesis [6–8].
In mammals, selenium is an essential nutrient. It is
incorporated in the selenoaminoacid, Se-Cys, which is
required for the translation of several proteins involved in
cell defense or hormone regulation [9, 10] and can as well
be bound by binding proteins such as selenium-binding
protein 1 (SBP1) [11] in a mode that is distinct from con-
ventional selenocysteine-containing selenoproteins [12].
Although a physiological function has not yet been
assigned to SBP1, the abnormal suppression of SBP1 has
been reported in several tumor types. Specifically, SBP1
is known to play a key role in the development and
J. Zhang Á W. Dong (&)
Department of Gastroenterology, Renmin Hospital of Wuhan
University, 9 # Ziyang Road, 430060 Wuhan,
Hubei Province, China
e-mail: dongwg1009@yahoo.com.cn
N. Zhan
Department of Pathology, Renmin Hospital of Wuhan
University, 9 # Ziyang Road, 430060 Wuhan,
Hubei Province, China
123
Med Oncol (2011) 28:951–957
DOI 10.1007/s12032-010-9564-6