J Cancer 2024; 15(8):2354-2360. doi:10.7150/jca.94187 This issue Cite
Research Paper
1. Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
2. School of Medicine, China Medical University, Taichung, Taiwan.
3. Department of Pathology, China Medical University Hospital, Taichung, Taiwan.
4. School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
5. Department of Otolaryngology, Chung Shan Medical University Hospital, Taichung, Taiwan.
6. Department of Otolaryngology, St. Martin De Porres Hospital, Chiayi, Taiwan.
7. Institute of Oral Sciences, Chung Shan Medical University, Taichung, Taiwan.
8. Department of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan.
9. Department of Neurosurgery, Show Chwan Memorial Hospital, Changhua, Taiwan.
10. Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
11. Whole-Genome Research Core Laboratory of Human Diseases, Chang Gung Memorial Hospital, Keelung, Taiwan.
12. Department of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Oral squamous cell carcinoma (OSCC) is a prevalent and lethal malignancy with a diverse etiology. LINC00312 is a long intergenic non-coding RNA that functions as a signal hub to regulate the progression and treatment of head and neck cancer. The aim of this study was to evaluate the effect of LINC00312 single nucleotide polymorphisms (SNPs) on the development of oral cancer. Two LINC00312 SNPs, namely rs12497104 and rs164966, were investigated among 469 male patients with cancer of buccal mucosa and 1194 gender- and age-matched controls. No significant correlation was observed between these two SNPs and the occurrence of OSCC in the case and control groups. While assessing the clinicopathological features, carriers of at least one minor allele of rs164966 (GA and GG) were less prone to develop lymph node metastasis (adjusted odds ratio [AOR], 0.666; 95% confidence interval [CI], 0.447-0.991; p=0.045) in comparison with homozygous carriers of the major allele (AA). Subsequent stratifying surveys revealed that this genetic association with nodal spread was seen only in cases who habitually chewed betel quid (AOR, 0.616; 95% CI, 0.386-0.985; p=0.042) or smoked cigarettes (AOR, 0.612; 95% CI, 0.393-0.953; p=0.029), but undetected in cases free of these main behavioral risks. Our results indicate an interactivity of LINC00312 rs164966 with lifestyle-related risks on modulating OSCC progression.
Keywords: LINC00312, genetic variants, OSCC, chewed betel quid