Impact of HOTAIR Gene Polymorphism and Environmental Risk on Oral Cancer

2018 ◽  
Vol 97 (6) ◽  
pp. 717-724 ◽  
Author(s):  
S.C. Su ◽  
M.J. Hsieh ◽  
C.W. Lin ◽  
C.Y. Chuang ◽  
Y.F. Liu ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Odds Ratio ◽  
Gene Polymorphisms ◽  
Clinical Stage ◽  
Interactive Effect ◽  
Clinical Status ◽  
Betel Quid ◽  
Nucleotide Polymorphisms ◽  
Advanced Clinical Stage ◽  
Betel Quid Chewing

Genetic and acquired factors are thought to be interrelated and imperative to estimate the risk and prognosis of oral squamous cell carcinoma (OSCC). HOX transcript antisense intergenic RNA ( HOTAIR) plays crucial roles in gene regulation and is regulated in a variety of cancers. Polymorphisms in HOTAIR have been recently linked to the predisposition to diverse malignancies. In the present study, we aimed to evaluate the influences of HOTAIR gene polymorphisms, combined with environmental triggers, on the susceptibility to oral tumorigenesis. Four single-nucleotide polymorphisms of the HOTAIR gene— rs920778, rs1899663, rs4759314, and rs12427129—were tested in 1,200 control participants and 907 patients with OSCC. We detected a significant association of rs1899663 with the risk of OSCC (adjusted odds ratio, 2.227; 95% confidence interval [95% CI], 1.197 to 4.146; P = 0.012) after adjustment for 3 potential confounders: smoking, betel quid chewing, and alcohol consumption. In further analyses where habitual exposure to each of 3 environmental factors was excluded, we found that, in addition to rs1899663, non–betel quid users who carried the polymorphic allele of rs920778 were more prone to develop OSCC than were those homozygous for wild-type allele (TC: odds ratio [OR], 1.472; 95% CI, 1.069 to 2.029; P = 0.018; TC+CC: OR, 1.448; 95% CI, 1.060 to 1.977; P = 0.020). Moreover, in exploring the relationship between HOTAIR gene polymorphisms and the clinical status of only patients with OSCC who were non–betel quid chewers (excluding the advanced clinical stage), we found that rs920778 and rs4759314 were correlated with the development of large-size tumors (OR, 1.891; 95% CI, 1.027 to 3.484; P = 0.04) and increased lymph node metastasis (OR, 4.140; 95% CI, 1.785 to 9.602; P = 0.001), respectively. Further functional assessments link rs920778 to the regulation of HOTAIR expression and epigenetic status. Our results reveal an interactive effect of HOTAIR gene polymorphisms and betel quid chewing on the development and progression of oral cancer.

scholarly journals IGF2BP2 Polymorphisms Are Associated with Clinical Characteristics and Development of Oral Cancer

2020 ◽  
Vol 21 (16) ◽  
pp. 5662
Author(s):  
Chia-Hsuan Chou ◽  
Chien-Yuan Chang ◽  
Hsueh-Ju Lu ◽  
Min-Chien Hsin ◽  
Mu-Kuan Chen ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Clinical Characteristics ◽  
Clinical Stage ◽  
The Cancer Genome Atlas ◽  
Nucleotide Polymorphisms ◽  
Advanced Clinical Stage ◽  
Increased Risk ◽  
Cancer Genome Atlas ◽  
Male Patients ◽  
Mrna Binding

Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is associated with insulin resistance, lipid metabolism, and tumorigenesis. However, the association between the IGF2BP2 polymorphism and oral cancer risk remains unclear. We recruited 1349 male patients with oral cancer and 1198 cancer-free controls. Three single nucleotide polymorphisms IGF2BP2 rs11705701, rs4402960, and rs1470579 were assessed using real-time polymerase chain reaction. The results indicate that the male patients with oral cancer and with the rs11705701 GA+AA, rs4402960 GT+TT, and rs1470579 AC+CC genotypes had increased risk of advanced clinical stage, larger tumor, and progression of lymph node metastasis compared with those with wild-type IGF2BP2. Moreover, according to The Cancer Genome Atlas dataset, high expression of the IGF2BP2 gene is associated with poor survival in patients with head and neck squamous cell carcinoma. In conclusion, our results suggest that IGF2BP2 polymorphisms are associated with less favorable oral cancer clinical characteristics.

scholarly journals Effect of MACC1 Genetic Polymorphisms and Environmental Risk Factors in the Occurrence of Oral Squamous Cell Carcinoma

2021 ◽  
Vol 11 (6) ◽  
pp. 490
Author(s):  
Rei-Hsing Hu ◽  
Chun-Yi Chuang ◽  
Chiao-Wen Lin ◽  
Shih-Chi Su ◽  
Lun-Ching Chang ◽  
...  
Keyword(s):  
Risk Factors ◽  
Oral Cancer ◽  
Cancer Patients ◽  
Environmental Risk ◽  
Clinicopathological Characteristics ◽  
Environmental Risk Factors ◽  
Betel Quid ◽  
Nucleotide Polymorphisms ◽  
Betel Quid Chewing ◽  
Oral Cancer Patients

MACC1 (Metastasis Associated in Colon Cancer 1) is found to regulate the hepatocyte growth factor (HGF)/Met signal pathway, and plays an important role in tumor proliferation, angiogenesis, and metastasis. However, the relationships between MACC1 SNPs (single nucleotide polymorphisms) and oral cancer are still blurred. In this study, five SNPs (rs3095007, rs1990172, rs4721888, rs975263, and rs3735615) were genotyped in 911 oral cancer patients and 1200 healthy individuals by real-time polymerase chain reaction (PCR), and the associations of oral cancer with the SNP genotypes, environmental risk factors, and clinicopathological characteristics were further analyzed. Our results showed that individuals who had GC genotype or C-allele (GC + CC) in rs4721888 would have a higher risk for oral cancer incidence than GG genotype after adjustment for betel quid chewing, cigarette smoking, and alcohol drinking. Moreover, the 715 oral cancer patients with a betel quid chewing habit, who had C-allele (TC + CC) in rs975263, would have a higher risk for lymph node metastasis. Further analyses of the sequences of rs4721888 revealed that the C-allele of rs4721888 would be a putative exonic splicing enhancer. In conclusion, MACC1 SNP rs4721888 would elevate the susceptibility for oral cancer, and SNP rs975263 would increase the metastasis risk for oral cancer patients with a betel quid chewing habit. Our data suggest that SNP rs4721888 could be a putative genetic marker for oral cancer, and SNP rs975362 may have the potential to be a prognostic marker of metastasis in an oral cancer patient.

scholarly journals Combined Genetic Biomarkers and Betel Quid Chewing for Identifying High-Risk Group for Oral Cancer Occurrence

2017 ◽  
Vol 10 (6) ◽  
pp. 355-362 ◽  
Author(s):  
Chia-Min Chung ◽  
Chien-Hung Lee ◽  
Mu-Kuan Chen ◽  
Ka-Wo Lee ◽  
Cheng-Che E. Lan ◽  
...  
Keyword(s):  
High Risk ◽  
Oral Cancer ◽  
Risk Group ◽  
High Risk Group ◽  
Betel Quid ◽  
Genetic Biomarkers ◽  
Cancer Occurrence ◽  
Betel Quid Chewing

scholarly journals Acrolein is involved in the synergistic potential of cigarette smoking- and betel quid chewing-related human oral cancer.

2019 ◽  
pp. cebp.1033.2018 ◽  
Author(s):  
Hsiang-Tsui Wang ◽  
Han-Hsing Tsou ◽  
Chih-Hung Hu ◽  
Jin-Hui Liu ◽  
Chung-Ji Liu ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cigarette Smoking ◽  
Betel Quid ◽  
Betel Quid Chewing

Accumulation of mitochondrial DNA deletions in human oral tissues — effects of betel quid chewing and oral cancer

2001 ◽  
Vol 493 (1-2) ◽  
pp. 67-74 ◽  
Author(s):  
Hsin-Chen Lee ◽  
Pen-Hui Yin ◽  
Tzu-Ning Yu ◽  
Yeong-Dar Chang ◽  
Wen-Chen Hsu ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Oral Cancer ◽  
Betel Quid ◽  
Betel Quid Chewing ◽  
Dna Deletions

Betel quid chewing, cigarette smoking and alcohol consumption related to oral cancer in Taiwan

1995 ◽  
Vol 24 (10) ◽  
pp. 450-453 ◽  
Author(s):  
Ying-Chin Ko ◽  
Yung-Li Huang ◽  
Chien-Hung Lee ◽  
Mei-Ju Chen ◽  
Li-Min Lin ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Oral Cancer ◽  
Cigarette Smoking ◽  
Betel Quid ◽  
Betel Quid Chewing

P3.18. Oral cancer susceptibility is associated with XRCC4 polymorphisms, smoking and betel quid chewing

2009 ◽  
Vol 3 (1) ◽  
pp. 207
Author(s):  
K.Y. Shun ◽  
T.H. Chang ◽  
T.Y. An ◽  
C.H. Shiang ◽  
L.S. Yun ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Susceptibility ◽  
Betel Quid ◽  
Betel Quid Chewing

scholarly journals Association of Sex Determining Region Y-Box 17 Gene Polymorphisms and Intracranial Aneurysm: A Case-Control Study and Meta-analysis

Neurosurgery ◽  
2019 ◽  
Vol 66 (Supplement_1) ◽  
Author(s):  
Museung Park ◽  
Yong-Jun Cho ◽  
Jin Sue Jeon
Keyword(s):  
Single Nucleotide Polymorphisms ◽  
Confidence Interval ◽  
Odds Ratio ◽  
Gene Polymorphisms ◽  
Meta Analysis ◽  
East Asian ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Unruptured Aneurysms ◽  
Asian Populations

Abstract INTRODUCTION Genome-wide association studies have revealed an association between SRY (Sex Determining Region Y)-box 17 (SOX17) gene and intracranial aneurysm (IA) formation. However, results were mainly derived from European and Japanese populations. We investigated the association between SOX17 gene polymorphisms and IA in a homogeneous Korean population. We performed a meta-analysis to assess these results in East-Asian populations. METHODS This cross-sectional study included 187 age- and sex-matched patients with IA and 372 control subjects. Genetic association analysis was performed in the generalized linear model to identify associations between 4 single nucleotide polymorphisms and IA, including 95 patients with ruptured aneurysms and 92 with unruptured aneurysms. The East-Asian meta-analysis of 5100 IA cases and 7930 control cases was conducted under an inverse variance model. RESULTS Among 4 single nucleotide polymorphisms that passed quality control tests, the minor C allele of rs1072737 was significantly associated with IA (odds ratio 0.69, 95% confidence interval 0.49-0.96, P = .03). None of the 4 single nucleotide polymorphisms showed a significant association between patients with ruptured and unruptured aneurysms. Meta-analysis revealed that G alleles of rs10958409 and rs9298506 were significantly associated with IA in the East-Asian population after removing study heterogeneity (odds ratio 1.11, 95% confidence interval 1.04-1.19, P = .0023 and odds ratio 1.19, 95% confidence interval 1.07-1.32, P = .0016). CONCLUSION Identification of genetic variants located near SOX17 is likely to be clinically significant for IA formation. rs10958409 and rs9298506 may increase risk of IA in East-Asian populations. Our findings may help in the identification of IA pathogenesis.

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