Impact of Maspin Polymorphism rs2289520 G/C and Its Interaction with Gene to Gene, Alcohol Consumption Increase Susceptibility to Oral Cancer Occurrence

Yang, Po Yu; Miao, Nae‐Fang; Lin, Chiao‐Wen; Chou, Ying-Hsiang; Yang, Shun Fa; Huang, Hui; Chang, Hsiu Ju; Tsai, Hsiu Ting

doi:10.1371/journal.pone.0160841

Cited by 10 publications

(7 citation statements)

References 25 publications

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“…Single-nucleotide polymorphisms (SNPs), the most common type of DNA sequence variation influenced gene expression, protein function and disease susceptibility in particular individuals. SNP had potential predictive significance risk of oral cancer in previous studies [ 7 – 9 ]. Although the relationship between genetic polymorphisms and the environmental carcinogens was also reported [ 10 , 11 ], identifying principal genes related to the susceptibility for OSCC is important for disease early detection.…”

Section: Introductionmentioning

confidence: 99%

Impact of CCL4 gene polymorphisms and environmental factors on oral cancer development and clinical characteristics

et al. 2017

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In Taiwan, oral cancer has causally been associated with environmental carcinogens. CCL4 (C-C chemokine ligand 4), a macrophage inflammatory protein with a key role in inflammation and immune-regulation, was implicated in carcinogenesis by facilitating instability in the tumor environment. The purpose of this study was to identify gene polymorphisms of CCL4 specific to patients with oral squamous cell carcinoma (OSCC) susceptibility and clinicopathological characteristics. A total of 2,053 participants, including 1192 healthy people and 861 patients with oral cancer, were recruited for this study. Three single-nucleotide polymorphisms (SNPs) of the CCL4 gene were analyzed by a real-time PCR. We found that the T/T homozygotes of CCL4 rs1634507 G/T polymorphism and the GG haplotype of 2 CCL4 SNPs (rs1634507 and rs10491121) combined were associated with oral-cancer susceptibility. In addition, TA haplotype significantly decreased the risks for oral cancer by 0.118 fold. Among 1420 smokers, CCL4 polymorphisms carriers with the betel-nut chewing habit had a 15.476–20.247-fold greater risk of having oral cancer compared to CCL4 wild-type (WT) carriers without the betel-nut chewing habit. Finally, patients with oral cancer who had A/G heterozygotes of CCL4 rs10491121 A/G polymorphism showed a lower risk for an advanced tumor size (> T2) (p=0.046), compared to those patients with AA homozygotes. Our results suggest that the CCL4 rs1634507 SNP have potential predictive significance in oral carcinogenesis. Gene-environment interactions of CCL4 polymorphisms might influence oral-cancer susceptibility. CCL4 rs10491121 may be a factor to predict the tumor size in OSCC patients.

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Section: Introductionmentioning

confidence: 99%

Impact of CCL4 gene polymorphisms and environmental factors on oral cancer development and clinical characteristics

et al. 2017

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“…The abnormality of cell proliferation is generally due to the abnormal expression of related genes, which gives rise to the occurrence and development of tumors [ 11 , 12 ]. In this study, we first identified the DEGs in HRNM_T versus HRNM_N, LRYM_T versus LRYM_N, and HRNM_T versus LRYM_T.…”

Section: Discussionmentioning

confidence: 99%

RNA-Sequence Analysis Reveals Differentially Expressed Genes (DEGs) in Patients Exhibiting Different Risks of Tumor Metastasis

Dong

Long

et al. 2017

Med Sci Monit

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BackgroundBreast cancer is one of the most common malignancies in women. In a previous study, we found that for two patients who had a high risk of lymphatic metastasis, lymphatic metastasis did not occur; whereas, for two patients who had a low risk of lymphatic metastasis, lymphatic metastasis did occur.Material/MethodsWe analyzed the differential gene expressions of these four patients by RNA-sequence. The data (HRNM_T versus HRNM_N, LRYM_T versus LRYM_N, and HRNM_T versus LRYM_T) was then processed using differentially expressed genes (DEGs) analysis, functional analysis for DEGs, and PPI network construct.ResultsFor HRNM_T versus HRNM_N, there were 224 DEGs. There were 504 DEGs for LRYM_T versus LRYM_N, and 88 DEGs for LRYM_T versus LRYM_N. For HRNM_T versus HRNM_N, DEGs were up-regulated mainly in the cell cycle, the IL-17 signaling pathway, and the progesterone-mediated oocyte maturation; DEGs were down-regulated mainly in the IL-17 signaling pathway. For LRYM_T versus LRYM_N, DEGs were up-regulated mainly in protein digestion and absorption, and cytokine-cytokine receptor interaction; DEGs were down-regulated mainly in ECM-receptor interaction. For HRNM_T versus LRYM_T, DEGs were up-regulated mainly in the PPAR signaling pathway; DEGs were downregulated mainly in the adipocytokine signaling pathway. The DEGs were screened to construct PPI networks.ConclusionsThe GO and KEGG functional enrichments of HRNM_T versus HRNM_N, and LRYM_T versus LRYM_N were consistent with earlier studies. For HRNM_T versus LRYM_T, DEGs were up-regulated mainly in PPAR signaling; DEGs were down-regulated mainly in the adipocytokine pathway.

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“…To predict the risk and prognosis of a cancer, genotyping SNPs in a relative community and comparing the differences of distribution frequency in positive and negative group (eg, patients and control) is an often used strategy. By this, certain SNPs on predictive risk of oral cancer and raised sensitivity on carcinogen‐induced cancer have been reported. To explore the occasion of oral cancerization, the independent and interactive effects of environmental carcinogens and gene polymorphisms should be considered.…”

Section: Introductionmentioning

confidence: 90%

Leptin −2548 G/A polymorphisms are associated to clinical progression of oral cancer and sensitive to oral tumorization in nonsmoking population

Hung

Tsai

Lin

et al. 2019

J of Cellular Biochemistry

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Oral cancer is causally associated with environmental carcinogens, and the susceptibility to carcinogen‐mediated tumorigenesis is proposed to be genotype‐dependent. Leptin (LEP) and leptin receptor (LEPR) both play a crucial role in the mediation of physiological reactions and carcinogenesis and may serve as a candidate biomarker of oral cancer. The current case‐control study aimed to examine the effects of LEP −2548 G/A (rs7799039), LEPR K109R (rs1137100), and LEPR Q223R (rs1137101) single‐nucleotide polymorphisms (SNPs) with or without interacting to environmental carcinogens on the risk for oral squamous cell carcinoma. The SNPs of three genetic allele, from 567 patients with oral cancer and 560 healthy controls in Taiwan were analyzed. The results shown that the patients with polymorphic allele of LEP −2548 have a significant low risk for the development of clinical stage (A/G: adjusted odds ratio [AOR] = 0.670, 95% confidence interval [CI] = 0.454‐0.988, P < 0.05; A/G + G/G: AOR = 0.676, 95% CI = 0.467‐0.978, P < 0.05) compared to patients with ancestral homozygous A/A genotype. In addition, an interesting result was found that the impact of LEP −2548 G/A SNP on oral carcinogenesis in subjects without tobacco consumption is higher than subjects with tobacco consumption. These results suggest that the genetic polymorphism of LEP −2548 G/A (rs7799039), LEPR K109R (rs1137100), and LEPR Q223R (rs1137101) were not associated to the susceptibility of oral cancer; SNP in LEP −2548 G/A showed a poor clinicopathological development of oral cancer; population without tobacco consumption and with polymorphic LEP −2548 G/A gene may significantly increase the risk to have oral cancer.

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Impact of Maspin Polymorphism rs2289520 G/C and Its Interaction with Gene to Gene, Alcohol Consumption Increase Susceptibility to Oral Cancer Occurrence

Cited by 10 publications

References 25 publications

Impact of CCL4 gene polymorphisms and environmental factors on oral cancer development and clinical characteristics

Impact of CCL4 gene polymorphisms and environmental factors on oral cancer development and clinical characteristics

RNA-Sequence Analysis Reveals Differentially Expressed Genes (DEGs) in Patients Exhibiting Different Risks of Tumor Metastasis

Leptin −2548 G/A polymorphisms are associated to clinical progression of oral cancer and sensitive to oral tumorization in nonsmoking population

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