Association of insertion-deletions polymorphisms with colorectal cancer risk and clinical features

Marques, Denílson Bezerra; Ferreira-Costa, Layse Raynara; Corrêa, Romualdo da Silva; Borges, Aline Maciel Pinheiro; Ito, Fernanda Ribeiro; Ramos, Carlos César de Oliveira; Bortolin, Raul Hernandes; Luchessi, André Ducati; Ribeiro-dos-Santos, Ândrea; Santos, Sidney Emanuel Batista dos; Silbiger, Vivian Nogueira

doi:10.3748/wjg.v23.i37.6854

Cited by 24 publications

(17 citation statements)

References 116 publications

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“…Using the above mentioned database, we firstly identified 59 potentially relevant published records. After literature screening and abstracts reading, we kept 7 publications in the analysis 16 - 22 . We also extracted 1 article from the references of the retrieval articles 23 .…”

Section: Resultsmentioning

confidence: 99%

CASP8 rs3834129 (-652 6N insertion/deletion) Polymorphism and Colorectal Cancer Susceptibility: An Updated Meta-Analysis

Yin

et al. 2018

J. Cancer

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CASP8 rs3834129 polymorphism (-652 6N insertion/deletion) is a genetic alteration which might affect the apoptosis pathway caspase enzyme. The impaired caspase enzyme would lead to the change of cancer risk. By now, the role of CASP8 rs3834129 polymorphism has been widely investigated. However, the relationship of this genetic variant on colorectal cancer (CRC) susceptibility still remains inconsistent. Therefore, we further investigated the role of rs3834129 polymorphism on CRC risk. Eligible published studies were retrieved from EMBASE, PubMed, CNKI and WANFANG database updates to March 2018. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the relationship strengths. In general, we successfully retrieved 13 studies (8 publications) involving 13058 cases and 14418 controls. The meta-analysis results demonstrated that rs3834129 polymorphism was associated with a decreased CRC risk in heterozygous model (ID vs. II: OR = 0.94, 95% CI = 0.88-0.99), but not the homozygous and allele models. Furthermore, significantly decreased risk was also found among Asian (ID vs. II: OR = 0.86, 95% CI = 0.76-0.98), and high quality score group (ID vs. II: OR = 0.90, 95% CI = 0.81-1.00) in the stratified analyses. Taken together, we showed that CASP8 rs3834129 polymorphism influences CRC susceptibility in a weak impact manner. More case-control studies are warranted to validate such relationship.

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Section: Resultsmentioning

confidence: 99%

CASP8 rs3834129 (-652 6N insertion/deletion) Polymorphism and Colorectal Cancer Susceptibility: An Updated Meta-Analysis

Yin

et al. 2018

J. Cancer

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“…Finally, eight studies with complete text were enrolled in this meta-analysis in accordance with the inclusion and exclusion criteria. 13–20 These enrolled studies were published between 2007 and 2017. The diagram of the selection process is shown in Figure 1.…”

Section: Resultsmentioning

confidence: 99%

Renin–angiotensin system gene polymorphisms and colorectal cancer risk: a meta-analysis

Cheng

Liu

2019

J Renin Angiotensin Aldosterone Syst

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Objective:The renin–angiotensin system gene has been implicated in the progression of colorectal cancer. Nevertheless, the details of that role remain controversial. We performed a meta-analysis to investigate the correlation between renin–angiotensin system gene polymorphisms and colorectal cancer.Methods:We retrieved relevant studies from PubMed and Embase. Subsequently, fixed or random-effects models were used to calculate pooled odds ratios (ORs) with 95% confidence intervals (CIs).Results:We identified six studies of the angiotensin-converting enzyme insertion/deletion (I/D) polymorphism, and two studies of the angiotensinogen M235T polymorphism. The angiotensin-converting enzyme I/D polymorphism did not significantly correlate with colorectal cancer risk in the total population (DD vs. II: OR 0.77, 95% CI 0.39–1.50; DI vs. II: OR 1.05, 95% CI 0.85–1.30; dominant model: OR 0.94, 95% CI 0.68–1.31; recessive model: OR 1.01, 95% CI 0.80–1.27). Similarly, the angiotensinogen M235T polymorphism was not associated with colorectal cancer risk (TT vs. MM: OR 1.38, 95% CI 0.52–3.67; TM vs. MM: OR 1.19, 95% CI 0.96–1.47; dominant model: OR 1.28, 95% CI 0.77–2.14; recessive model: OR 1.17, 95% CI 0.53–2.59).Conclusion:Our findings suggest that the angiotensin-converting enzyme I/D and angiotensinogen M235T polymorphisms are unlikely to correlate with colorectal cancer.

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“…SGSM3 increases Cx43 turnover by accelerating the internalization of Cx43 from the plasma membrane [37]. On the other hand, several studies have shown that SGSM3 is associated with the risk of some cancers, including liver, breast, colorectal and bladder cancers [38][39][40][41].…”

Section: Plos Onementioning

confidence: 99%

Small G protein signaling modulator 3 (SGSM3) knockdown attenuates apoptosis and cardiogenic differentiation in rat mesenchymal stem cells exposed to hypoxia

et al. 2020

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Connexin 43 (Cx43) may be important in cell death and survival due to cell-to-cell communication-independent mechanisms. In our previous study, we found that small G protein signaling modulator 3 (SGSM3), a partner of Cx43, contributes to myocardial infarction (MI) in rat hearts. Based on these previous results, we hypothesized that SGSM3 could also play a role in bone marrow-derived rat mesenchymal stem cells (MSCs), which differentiate into cardiomyocytes and/or cells with comparable phenotypes under low oxygen conditions. Cx43 and Cx43-related factor expression profiles were compared between normoxic and hypoxic conditions according to exposure time, and Sgsm3 gene knockdown (KD) using siRNA transfection was performed to validate the interaction between SGSM3 and Cx43 and to determine the roles of SGSM3 in rat MSCs. We identified that SGSM3 interacts with Cx43 in MSCs under different oxygen conditions and that Sgsm3 knockdown inhibits apoptosis and cardiomyocyte differentiation under hypoxic stress. SGSM3/Sgsm3 probably has an effect on MSC survival and thus therapeutic potential in diseased hearts, but SGSM3 may worsen the development of MSC-based therapeutic approaches in regenerative medicine. This study was performed to help us better understand the mechanisms involved in the therapeutic efficacy of MSCs, as well as provide data that could be used pharmacologically.

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Association of insertion-deletions polymorphisms with colorectal cancer risk and clinical features

Cited by 24 publications

References 116 publications

CASP8 rs3834129 (-652 6N insertion/deletion) Polymorphism and Colorectal Cancer Susceptibility: An Updated Meta-Analysis

CASP8 rs3834129 (-652 6N insertion/deletion) Polymorphism and Colorectal Cancer Susceptibility: An Updated Meta-Analysis

Renin–angiotensin system gene polymorphisms and colorectal cancer risk: a meta-analysis

Small G protein signaling modulator 3 (SGSM3) knockdown attenuates apoptosis and cardiogenic differentiation in rat mesenchymal stem cells exposed to hypoxia

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