Association of Interleukin-10 -592C/A Polymorphism and Cervical Cancer Risk: a Meta- Analysis

doi:10.21203/rs.3.rs-1438222/v1

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Association of Interleukin-10 -592C/A Polymorphism and Cervical Cancer Risk: a Meta- Analysis

https://doi.org/10.21203/rs.3.rs-1438222/v1

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Background

The literature review showed some discrepancies regarding the association of -592C/A with the risk of cervical cancer. To allow more precise analysis of the data by increasing the number of cases studied and more acceptable generalization by considering results from different sources, the present meta-analysis was performed on available published studies that explored the relationship between SNP − 592C/A of the IL-10 gene and the risk of cervical cancer.

Methods

Eleven available studies, including 4187 cases and 3311 controls were included in this study investigating the relationship between the − 592C/A polymorphism of IL-10 and cervical cancer risk. Fixed-effects or random-effects models were performed by pooled odds ratios (ORs). Heterogeneity and bias tests were performed by the inconsistency test and funnel plot, respectively.

Results

The overall analysis showed an increased susceptibility to cervical cancer with the − 592C/A polymorphism of the IL-10 gene for the recessive model (OR = 1.30, 95% CI = 1.14–1.49), dominant (OR = 1.36, 95% CI = 1.09–1.70) and additive (OR = 1.25, 95% CI = 1.09–1.44). Regarding ethnicity, a significant association of the − 592C/A polymorphism of the IL-10 gene was linked to an elevated risk of cervical cancer for all genetic models (recessive model, dominant and additive) in the Caucasian and Asian population with P < 0.05.

Conclusions

-592C/A polymorphism of IL-10 gene may be considered a risk factor for cervical cancer.

IL-10

-592C/A polymorphism

Gene

Cervical cancer

Meta-analysis

Cervical cancer is the fourth most common cancer in the world, accounting for 6.5% of all cancers, after breast, colorectal and lung cancer. It is also the fourth highest cause of cancer death in women, in both high-income and low-middle income countries, with an estimated mortality rate of 7.7% worldwide (GLOBOCAN 2020) (Sung et al. 2021). Exposure to high-risk Human papillomavirus (HPV) is required, but is not sufficient cause of cervical cancer (Moore et al. 2012; Xiao et al. 2019). Oncogenic HPV DNA is present in nearly 100% of invasive cervical cancer. A limited immune response to HPV linked to the host’s genetic make-up, may increase the risk of cervical cancer (Howell 2013). Many authors have been interested in the research of risk factors related with cervical cancer throughout the last few decades (Machalek et al. 2017). It appears from their investigations that genetic factors seem to exert a significant influence on the carcinogenesis of the cervix. It should be noted that the reported results are conflicting. However, mutations in genes involved in cytokines synthesis like interleukin 10 (IL-10) appear to be strong predictors of cervical cancer risk (Zidi et al. 2015; Du et al. 2019; Datta et al. 2020). Physiologically, IL-10 is an essential cytokine for inflammatory modulation. Several cell types are involved in the production of this cytokine including Th1, Th2, Th17 lymphocytes, B lymphocytes, mast cells, eosinophils, monocytes, macrophages, and dendritic cells (Stumhofer et al. 2007; Saraiva et al. 2009). The IL-10 gene, which contains five exons, has been found on the long arm of chromosome 1q31-32 in humans (Eskdale et al. 1997; Trifunović et al. 2015). The significance of the IL-10 gene in the control of immune-mediated illness responses has resulted in the discovery of numerous polymorphisms in different portions of the gene, including the promoter region (Eskdale et al. 1997; Howell 2013). The majority of identified genetic polymorphisms are single nucleotide polymorphisms (SNPs). SNP − 592C/A of the IL-10 gene promoter is located near a number of transcription factor binding sites. This SNP has been reported to be implicated in the pathogenesis of cutaneous malignant melanoma, and prostate, breast, gastric and cervical cancer (Nagano et al. 2008; Torres-Poveda et al. 2016; Guo et al. 2018; Wang et al. 2018; Li et al. 2020; Abbas et al. 2020; Datta et al. 2020). Association studies, carried out in different populations, have shown that this SNP increases the risk of developing cervical cancer (Singhal et al. 2015; Torres-Poveda et al. 2016; Datta et al. 2020). However, other studies have reported conflicting results (Bai et al. 2016; Du et al. 2019; Pereira et al. 2020). Furthermore, the expression of the IL-10 gene and/or the production of IL-10 has been demonstrated in various types of tumors, suggesting that IL-10 could, by promoting the escape from the immune system, constitute a step in the tumorigenesis (Hiroki et al. 2015; Niu et al. 2015; de Oliveira et al. 2015). Given the contradictory results of numerous studies on the role of SNP − 592C/A of the IL-10 gene in the pathogenesis of cervical cancer, we conducted a meta-analysis to assess the association between SNP − 592C/A in the IL-10 gene and the risk of cervical cancer.

Literature search strategy

The identification of initial manuscripts or published articles, available in English, was performed using the online databases Pubmed, the Havard University Library, Web of Science, and Genetics Medical Literature Database. Additional articles were identified from references cited in relevant reports and journals. The key search words “Interleukin-10"or “IL-10", "-592C/A" or “-592C > A” or "rs1800872", "polymorphism" or "variant" or " mutation" or "gene" and "cervical tumor" or "cervical cancer" were used to locate and select the articles.

Inclusion Criteria

Eligibility criteria were: (1) case-control study design evaluating the association of the − 592C/A polymorphisms of the IL-10 gene with the risk of cervical cancer, (2) availability of the full scientific manuscript, (3) distribution of polymorphisms in the controls in agreement with Hardy-Weinberg equilibrium (HWE), (4) availability of proportions of the different genotypes (CC, CA, AA for − 592C/A of IL-10 gene) in both cases and controls and (5) no significant change in the value of the odds ratio (OR).

Data Extraction

Three authors independently carried out the literature search in order to optimize convergence of retrieved data, including principal author, year of publication, study design, study population, racial and ethnic groups, sample size, genotypic and allelic proportions in cases and controls, HWE calculation, and genetic models tested.

Statistical analysis

The statistical analyses were conducted using Review Manager v5.3 and MedCalc v14.8.1. The distribution of -592C/A polymorphism of the IL-10 gene in agreement with HWE in the controls was evaluated by a Chi2 test, with p < 0.05. A Pooled OR test with a 95 percent confidence interval (CI) was used to assess the strength of association between − 592C/A polymorphism in IL-10 gene and the risk of cervical cancer, including the recessive model: AA vs. CC + CA, dominant model: AA + CA vs. CC, and the additive model: A vs. C. An inconsistency (I²) statistical test was used to determine heterogeneity (DerSimonian and Laird 2015; Cumpston et al. 2019). If there was no heterogeneity (I² < 50%), a fixed effect model (FEM) was retained for interpretation of a global OR. In case of heterogeneity, the OR was interpreted using a random-effect model (REM). A funnel plot was used to determine bias (Egger et al. 1997).

Characteristic of eligible studies

Four Caucasian studies with 2221 cases and 1240 controls (Zoodsma et al. 2005; Ivansson et al. 2007; Torres-Poveda et al. 2016; Pereira et al. 2020) and seven Asian studies with 1966 cases and 2071 controls (Roh et al. 2002; Xiong et al. 2010; Yu et al. 2011; Shekari et al. 2012; Bai et al. 2016; Du et al. 2019; Datta et al. 2020) were eligible to conduct the current meta-analysis out of thirteen studies (Fig. 1) (Table 1). Only one study on Africans was found, and it was discarded due to Hardy Weinberg's imbalance (Zidi et al. 2015). Another study that had a major impact on overall OR was also excluded (Singhal et al. 2015).

Figure 1. Flow diagram of eligible studies included

Table 1

Genotypic distribution of the *IL-10 -592C/A* polymorphism in eligible studies.
		Cases				Controls
Author/Year	Race/Ethnicity	N	CC	CA	AA	N	CC	CA	AA	HWE
Bai et al. 2016	Asian	165	20	82	63	165	15	80	70	0.24
Datta et al. 2020	Asian	240	49	133	58	204	65	111	28	0.07
Du et al. 2019	Asian	1044	380	522	142	1100	458	520	122	0.15
Ivansson et al. 2007	Caucasian	1282	736	464	82	288	162	112	14	0.33
Pereira et al. 2020	Caucasian	85	24	50	11	146	68	62	16	0.74
Roh et al. 2002	Asian	144	11	56	77	179	15	77	87	0.72
Shekari et al. 2012	Asian	200	16	96	88	200	17	102	81	0.05
Torres-Poveda et al. 2016	Caucasian	200	44	98	58	200	85	85	30	0.25
Xiong et al. 2010	Asian	70	12	23	35	108	13	44	51	0.46
Yu et al. 2011	Asian	103	7	37	59	115	19	44	52	0.07
Zoodsma et al. 2005	Caucasian	654	393	231	30	606	405	175	26	0.20
N: Number

Quantitative analysis

Table 2 denotes the association between cervical cancer and SNP − 592 C/A of the IL-10 for the genetic models. Overall, a significant association was found between the risk of cervical cancer and the three genetic models, including the recessive (OR [FEM] = 1.30, 95% CI = 1.14–1.49, P = 0.0001), dominant (OR [REM] = 1.36, 95% CI = 1.09–1.70, P = 0.006) and additive models (OR [REM] = 1.25, 95% CI = 1.09–1.44, P = 0.001) (Fig. 2).

Table 2

Genetic models and *SNP − 592C/A in the IL-10 gene* in cervical cancer.
				Effect estimate/Statistical method		Heterogeneity
Study	N	Cases/Controls	Models	OR (95% CI)	P-value	I²	P’
All studies	11	4187/3311
			Recessive	1.30 (1.14–1.49) FEM	0.0001	28%	0.18
			Dominant	1.36 (1.09–1.70) REM	0.006	66%	< 0.05
			Additive	1.25 (1.09–1.44) REM	0.001	66%	< 0.05
Caucasian	4	2221/1240
			Recessive	1.50 (1.12-2.00) FEM	0.006	39%	0.18
			Dominant	1.57 (1.03–2.40) REM	0.04	84%	< 0.05
			Additive	1.15 (1.15–1.46) REM	< 0.0001	81%	< 0.05
Asian	7	1966/2071
			Recessive	1.25 (1.07–1.46) FEM	0.004	24%	0.25
			Dominant	1.26 (1.09–1.46) FEM	0.002	42%	0.11
			Additive	1.19 (1.08–1.30) REM	0.0002	50%	0.06
N: Number; P: p value OR; P’: p value of Heterogeneity; I²: Inconsistency; recessive model: AA vs. CC + CA; dominant model: AA + CA vs. CC; additive model: A vs. C; FEM = Fixed effect model, REM = Random effect model; N = Number

Figure 2. Forest plots of the association between − 592C/A polymorphism of the IL-10 gene and cervical cancer for the (a) recessive model, (b) dominant model and (c) additive model. The pooled OR is represented by a black diamond; the OR in each study is represented by blue squares with square sizes inversely proportionate to the standard error of the OR, and the horizontal lines represent 95% CI.

Based on analysis by race/ethnic (Table 2), the − 592C/A polymorphism of the IL-10 gene was significantly associated with an increased risk of cervical cancer in Caucasians for the recessive model (OR [FEM] = 1.50, 95% CI = (1.12-2.00, P = 0.006), dominant model (OR [REM] = 1.57, 95% CI = 1.03–2.40, P = 0.04) and additive model (OR [FEM] = 1.15, 95% CI = 1.15–1.46, P < 0.0001) (Fig. 3). Furthermore, an association of this polymorphism with cervical cancer was observed in the Asian populations for the recessive (OR [FEM] = 1.25, 95% CI = 1.07–1.46, P = 0.004), dominant (OR [FEM] = 1.26, 95% CI = 1.09–1.46, P = 0.002) and additive (OR [FEM] = 1.19, 95% CI = 1.08–1.30, P = 0.0002) models (Fig. 4).

Figure 3. Forest plots of the association between SNP − 592C/A in the IL-10 gene and cervical cancer for the (a) recessive model, (b) dominant model, and (c) additive model in the Caucasian population. The pooled OR is represented by a black diamond; the OR in each study is represented by blue squares with square sizes inversely proportionate to the standard error of the OR, and horizontal lines represent 95% CI.

Figure 4. Forest plots of the association between − 592C/A polymorphism of the IL-10 gene and cervical cancer for the (a) recessive model, (b) dominant model and (c) additive model in the Asian population. The black diamond represents the pooled OR; blue squares show the OR in each study with square sizes inversely proportional to the standard error of the OR; and horizontal lines denote the 95% CI.

Sensitivity analysis

The stability of the meta-analysis was maintained by removing studies that significantly changed the overall OR and p-value, after excluding those that deviated from HWE (Zidi et al. 2015). In this regard, only the article by Singhal et al has been omitted (Singhal et al. 2015)

Heterogeneity source

We found heterogeneity for the dominant and additive models with I² > 50 and I² = 66 percent, respectively, when we excluded studies that deviated from HWE and the one that significantly affected the cumulative OR value (Fig. 2b and 2c). The genetic models showed no heterogeneity in the race/ethnicity study, except for the dominating pattern in Caucasians (I² = 84 percent, P = 0.0003). (Fig. 3b).

Publication Bias

The evaluation of publication bias was conducted by performing funnel plots. An absence of publication bias was observed for the recessive, dominant and additive models after removing studies not in agreement with the HWE and the study modifying the value of the pooled OR (Fig. 5).

Figure 5. Funnel plots of the (a) recessive model, (b) dominant model and (c) additive model precision by OR

HPV infection is one of the leading causes of cervical cancer, yet it is not sufficient to trigger cervix carcinogenesis. Smoking, HIV, fetal exposure to diethylstilbestrol, and oral contraceptives have all been identified as additional risk factors. Although genetic variables have been linked to carcinogenesis, the mechanism by which the IL-10 gene polymorphism causes cervical cancer is unknown. In vitro, IL-10 has been shown to have powerful immunosuppressive and anti-inflammatory activities (de Vries 1995; Katayama et al. 2003; Hervás-Salcedo et al. 2021).

This cytokine is produced by a variety of cell types, such as CD4 T cells and monocytes/macrophages (Gabryšová et al. 2014; Rutz and Ouyang 2016). Macrophages' ability to present antigens to T cells, as well as their ability to provide a costimulatory signal to T cells, is reduced by Il-10. It performs this function by inhibiting the activation of class II MHC-11 molecules and specific accessory molecules on their surfaces, including the B7.1 molecule (Berti et al. 2018). By blocking cell-mediated immune responses and inflammatory reactions, IL-10 can promote carcinogenesis by limiting the development of an adequate antitumor response against tumor cells (Lin and Karin 2007; Berti et al. 2018).

It's worth noting that, in addition to its inhibitory characteristics, IL-10 stimulates antibody production, as well as the differentiation and proliferation of B lymphocytes, which in turn produce IL-10 (Rousset et al. 1992; Couper et al. 2008; Sabat et al. 2010). Furthermore, the expression of the IL10 gene has been confirmed in various tumors, suggesting that IL-10 could play a non-negligible role in carcinogenesis by allowing the immune system to escape (Howell 2013).

In the present study, including 4187 cases and 3311 controls we noted that the − 592C/A polymorphism of the IL-10 gene was found to be correlated with the overall risk of cervical cancer for the recessive, dominant, and additive models. This finding is in line with a previous meta-analysis that identified a significant association between the − 592C/A polymorphism and an increased risk of cervical cancer in 2396 cases and 1388 controls (Ni et al. 2013). Contrary to our results, Guo et al. reported, in a meta-analysis of 3,149 cases and 2,237 controls, that the − 592C/A polymorphism was not globally correlated with cervical cancer for the three genetic models (Guo et al. 2018). A recent meta-analysis with 1,393 cases and 1,307 controls also found conflicting results (Wang et al. 2021). In Caucasians and Asians, our meta-analysis adjusted for race and ethnicity found an association between the − 592C/A polymorphism and cervical cancer in all models. Some meta-analyses supported our conclusions in some respects. This was the case in the meta-analysis by Guo et al on the Caucasian population, which found that only the recessive model was associated with an increased risk of cervical cancer (Guo et al. 2018), and another meta-analysis from the Asian population, who found that the additive model was associated with the risk of cervical cancer (Ni et al. 2013). However, Wang et al found that the − 592C/A polymorphism had no effect on the risk of cervical cancer in Caucasian and Asian populations across all genetic models tested (Wang et al. 2021).

Furthermore, Torres-Poveda et al. and Pereira et al. found a correlation between the − 592C/A polymorphism and cervical cancer in the Mexican and Brazilian populations for all three models, respectively (Torres-Poveda et al. 2016; Pereira et al. 2020). Zoodsma et al., Du et al. and Datta et al. reported that the risk of cervical cancer was correlated with the − 592C/A SNP in IL-10 gene for the dominant and additive models in Netherlander, Chinese, and Bangladeshi populations, respectively (Zoodsma et al. 2005; Du et al. 2019; Datta et al. 2020). These discrepancies between studies can be explained by a few factors, including: (1) sample size differences between studies, (2) inclusion of studies with allele frequencies that deviate from the HWE, (3) inclusion of studies that change the pooled OR value, (4) population genetic background and (5) inclusion of studies based on non-cancerous cervical lesions (Singhal et al. 2015; Zidi et al. 2015; Duvlis et al. 2020).

Based on an analysis of a large sample with precise inclusion criteria, this study reveals that women with the − 529C/A polymorphism of the IL-10 gene promoter have a high risk of cervical cancer for genetic models and provides evidence of an association of the IL-10 gene promoter in the pathogenesis of cervical cancer.

AA vs. CC+CA:Recessive model; AA+CA vs. CC: Dominant model; A vs. C: Additive model; CI: Confidence interval; FE: Fixed effect; Fig.: Figure; HWE: Hady-Weinberg Equilibrium; I²: Inconsistency; IL-10: Interleukin-10; N: Number; OR: Odd ratio; RE: Random effect; vs.: Versus.

Acknowledgments

The authors thank the National Institutes of Health/NCI (D43CA260658) for their support and HBNU Consortium, Global Health, FIC (D43 TW010543) for their training support. We also thank the Faculty of Medicine and Odontostomatology of the Université des Sciences, Techniques et Technologies de Bamako, University hospital of Point G and the team of the “Laboratoire de Recherche et de Formation sur les Pathologies Moléculaires” (LARFPAM: Laboratory of Research and Training in Molecular Pathology) for logistical support.

Funding

The National Institutes of Health/National Cancer Institute funded the research mentioned in this article under Award Number 1D43CA260658. The authors are entirely responsible for the material, which does not necessarily reflect the views of the National Institutes of Health.

Competing interests

There are no competing interests declared by the authors.

Authors’ contributions

The final manuscript has been read and approved by all authors.

Study concept and design: BD, YK, MM, LH. View, collection, analysis, and interpretation of the meta-analysis data: BD, YK, MM, GD, OK, JLH, LH. Drafting of the manuscript: BD with assistance from by YK, MM, GD, OK, JM, IMB, BT, CBT, BK, AC, SN, RLM, JLH, LH. Critical review of the manuscript for significant intellectual content: YK, MM, GD, OK, JM, IMB, BT, CBT, BK, AC, SN, RLM, JLH, LH. Work supervision: JLH, LH, RLM.

Ethics Approval and Consent to participate

Not applicable

Availability of data and materials

The Additional file 1 represents all the data analyzed in this meta-analysis study.

Consent for publication

Not applicable.

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Association of Interleukin-10 -592C/A Polymorphism and Cervical Cancer Risk: a Meta- Analysis

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Abstract

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Background

Methods

Inclusion Criteria

Data Extraction

Statistical analysis

Results

Characteristic of eligible studies

Quantitative analysis

Sensitivity analysis

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