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4.4.2 Polymorphisms in Mucin Genes
As previously mentioned, Peek and Blaser have proposed the mechanisms by which
gastritis is induced by Helicobacter pylori inside the gastric mucosa and increasing
the risk for intestinal-type of GC (Peek and Blaser 2002). The chronic gastric
infection with Helicobacter pylori relates to several mutations in genes of epithelial
cells, which may prevent apoptosis but stimulate cell proliferation. Epithelial cells of
gastric epithelium indicate the presence of mucosal pathogens and activate inflam-
matory pathways (Candido and Hagemann 2013). Mucins are recognized as a group
of glycosylated glycoprotein that covers the epit helial surface of the gastrointestinal
tract working in the first-line of defense for the host against physical and environ-
mental threats and participating in epithelial protection and renewal (McGuckin et al.
2011). In 2010, an analysis of common genetic variation had indicated that the
MUC1 gene has a direct association and risk of gastric cancer (Jia et al. 2010). Mucin
1 (MUC1) is encoded by the MUC1 gene and produced by the stomach to secrete
mucus that lubricates the epithelial surface and captures undesired agents (Boltin and
Niv 2013).
During Helicobacter pylori infection, the surface of gastric epithelial cells
expresses MUC1 to interact with Helicobacter pylori and prevents its binding to
the epithelial cells. Several studies have examined the role of MUC1 as an important
gene associated with the risk of gastric carcinogenesis, which reported that it plays
an important role in the development of gastric cancer (Jing et al. 2019). In cancer
cells, MUC1 believes to have an anti-apoptotic role, but in normal mucosa, MUC1
believed to have had a role in protecting gastric epithelial cells from attacks that
cause inflammation and carcinogenesis (Liu et al. 2014). Also, it functions by
eliminating Helicobacter pylori colonization by preventing the adhesion of its
surface outer membrane protein blood group antigen-binding adhesin (BabA) to
sialic acid-binding adhesin (SabA) at the gastric epithelial (Kable et al. 2017; Skoog
et al. 2012). Also, it was reported that overexpression of MUC1 stimulates cell
signaling cascades of events leading to escalating the activity of transcription factors
and increasing cellular growth, proliferation, and decreasing cellular apoptosis (Liu
and Zeng 2020). Also, in 2012, Guang et al. have reported that overexpression of
MUC1 reduces CagA/β-catenin co-IP and decreases bacteria-driven β-catenin
nuclear localization. Therefore, their findings suggest that MUC1 might serve as
an excellent target in which regulating of MUC1 level in gastric epithelia may be a
therapeutic option to reduce Helicobacter pylori virulence and inhibit IL-8 produc-
tion and gastric inflammation (Guang et al. 2012). Examining insights into the
pathogenesis of gastric cancer searching for novel susceptibility loci for gastric
cancer drives us to MUC1 G > A (rs4072037) and MUC1 G > A (rs2070803)
that are associated with MUC1 (Saeki et al. 2014).
MUC1 G > A (rs4072037), an SNP within the MUC1 gene, which is located at
chromosome 1q22, found to reduce the intracellular levels of reactive oxygen
species (ROS); thus, it was reported that altered MUC1 expression is associated
with multiple types of cancer among Chinese populations (Abnet et al. 2010). Jia
et al. have reported there are two major transcripts in gastric epithelium. MUC1
104 I. A. Malli
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G > A (rs4072037), which is located in the second exon, determines the splicing
site, which determines the type of alleles that increase the expression of some
variants. Thus, functional deletion of rs4072037 loci at MUC1 was associated with
the reduced transcriptional activity; therefore, a reduction in its protein expression in
gastric cancer tissue (Jia et al. 2010). Thus this results in reducing MUC1 expression,
enabling Helicobacter pylori to interact and penetrate through the gastric epithelium
(Sheng et al. 2013). In Asia, the incidence rate of Helicobacter pylori infection and
gastric adenocarcinoma is similar; however, there are subjects with positive pylori
infection reported to have low incidence rates of gastric adenocarcinoma (Fock and
Ang 2010).
Using meta-analysis, Saeki et al. demonstrated that MUC1 G > A (rs4072037)
affects promoter activity and determines the major splicing sites of MUC1 in the
gastric epithelium. Therefore, individuals who carry it have a high risk of developing
diffuse-type gastric cancer (Saeki et al. 2011). Also, in 2013, Saeki et al. study the
susceptibility to diffuse-type gastric cancer; he reported increased susceptibility of
gastric cancer-associated Japanese population who carry MUC1 G > A (rs4072037)
(Saeki et al. 2013). Even though Saeki et al. have documented a strong association
and increased risk to gastric cancer, Zhang et al. reported a lack of association
between common polymorphisms of MUC1 G > A (rs4072037) and Helicobacter
pylori infection and non-cardia gastric cancer risk in a Chinese population (Ma et al.
2013; Zhang et al. 2013). Also, in 2014, Liu et al. conducted a comprehensive
database search to reveal inconsistent results with different pathology. Evaluating
the relationship between MUC1 G > A (rs4072037) and gastric cancer susceptibil-
ity, they concluded this MUC1 G > A (rs4072037) might protect the subject against
gastric, and this protection is associated with a significant decreased gastr ic cancer
risk in Asians but not Cau casians (Liu et al. 2014). Similar results were replicated
concerning the association of MUC1 G > A (rs4072037) with gastric cancer in the
Caucasian population (Palmer et al. 2012). Furthermore, MUC1 G > A (rs2070803)
is another less studied functional SNP that showed the association with diffuse
gastric cancer, which was replicated in additional Japanese and Korean. Besides
mentioned SNPs in the Chinese population, the association of SNPs in MUC1 with
non-cardia intestinal GC was successfully replicated and demonstrated in other
ethnicities, such as the Korean population (Li et al. 2012; Song et al. 2014).
4.4.3 Polymorphisms in E-Cadherin Gene
Helicobacter pylori expresses CagA that modifies intercellular adherence, disrupts
the cytoskeleton, alters cell polarity, and increases the expression level of
proinflammatory and inflammatory cytokines (Fazeli et al. 2016). CagA furthermore
alters the β-catenin pathway; MUC1 interacts with β-catenin and CagA to form
another co-IP complex, which consequently transactivates the promoter of the IL-8
gene (Guang et al. 2010). E-cadherin is encoded by the CDH1 gene located in a
cluster along with other adhesion molecules such as cadherins (Xu et al. 2020). It is
considered as a Ca2
+
-dependent adhesion protein essential for initiating and
4 From Inflammation to Cancer: Role of Genetic Polymorphisms of Inflammatory.. . 105
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maintaining the attachment of molecules to the epithelial surfaces (Baum and
Georgiou 2011). E-cadherin is mainly involved in epithelial cell adhesion and the
formation of zipper-like structures. The refore, genetic alterations in E-cadherin lead
to epithelial cellular adhesion impairment and dysfunction, which disturb cell
migration (Paredes et al. 2012).
Dysfunction or reduced expression of E-cadherin due to decreased expression at
messenger RNA (mRNA) and protein levels has been reported in most of the diffuse
gastric cancer. Thus, downregulation or deletions of the E-cadherin gene are
associated with gastric cancer poor survival (Geng et al. 2012). Also, CDH1 may
be involved in the invasion and metastasis of cancer genes by altering the transcrip-
tional activity of epithelial cells (Menbari et al. 2013). Three SNPs have been
associated with the risk of diffuse gastric cancer risk: CDH1 C-160A (rs16260),
CDH1 C2076T, and CDH1 C 2253 T. CDH1 C160A located in the promoter region
of CDH1 plays significant roles in cancer risk for sporadic diffuse gastric cancer
(Van Roy 2014). Even though a significant association was observ ed between the
CDH1 C-160A (rs16260) and the risk of gastric cancer, other studies showed
contradictory findings (Zhan et al. 2012). In 2015, Jiang et al. had reported a lack
of association between the CDH1 C-160A (rs16260) and the risk of gastric cancer
(Jiang et al. 2015). A small sample size can explain the discrepancies that were
reported by Zhan et al.’s study. In conclusion, the association between CDH1
C-160A (rs16260) and the risk of gastric cancer should be validated and confirmed
by a large-scale study.
4.5 Conclusion
In conclusion, gastric carcinoma is one of the most widespread malignancies around
the world. It has been recognized as one of the highly aggressive types of cancer. As
it is usually manifested at a very late diagnosis stage, gastric cancer cases have very
low survival rates. Prevention is the most effective way to decrease the risk of
developing gastric cancer and reduce susceptibility rates. SNPs are considered
genetic markers that predispose individuals and increase their genetic risk for gastric
cancer development. Genetic alterations of genes that are responsible for inflamma-
tion are considered ultimate targets for their role in regulating gastric cancer. This
chapter investigated the genetic association of SNPs and gastric cancer risk progres-
sion. In order to understand the impact of each genetic polymorphi sm on gastric
cancer progression, this chapter reviewed polymorphisms at IL-1B, IL-8, IL-10,
IL17A, IL-17F, TNF-α, MUC1, and E-cadherin genes and risk of gastric carcinoma.
Therefore, molecular mechanisms of gastric cancer and its management are consid-
ered a significant factor for progressing gastric can cer develo pment. Thus, a better
understanding of the role of these SNPs creates more promises to enhance the
development of personalized medicine toward treating patients infected with
Helicobacter pylori and develop a higher risk of developing gastric cancer.
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