There is an increasing body of evidence which highlights the critical functions of long non-coding RNAs in the carcinogenicity mechanism of a variety of cancers. It has been reported that HOX transcript antisense intergenic RNA, a member of long non-coding RNA family, increases breast cancer risk. To date, no data regarding the association between HOX transcript antisense intergenic RNA polymorphisms and the risk of breast cancer development has been reported in Iran. Here, we examine the possible association between HOX transcript antisense intergenic RNA gene polymorphisms and breast cancer in a sample of southeast Iranian female population. The HOX transcript antisense intergenic RNA rs920778, rs12826786, rs4759314, and 1899663 gene polymorphisms were genotyped in 220 cases and 231 controls by polymerase chain reaction-restriction fragment length polymorphism. Our findings indicated that rs920778 polymorphism has significant positive association with breast cancer; rs12826786 and rs1899663 polymorphisms demonstrated significant negative association with breast cancer; and the rs4759314 variant was not associated with breast cancer risk. Haplotype analysis revealed that TGAC, CTAT, and TTAT haplotypes significantly decreased the risk of breast cancer compared with rs920778T/rs1899663G/rs4759314A/rs12826786T haplotype. In conclusion, we investigated only four variants of HOX transcript antisense intergenic RNA gene, and the findings suggest that HOX transcript antisense intergenic RNA rs920778, rs12826786, and rs1899663 polymorphisms may be associated with breast cancer risk in a sample of southeast Iranian population. Further replication studies with other polymorphisms of HOX transcript antisense intergenic RNA gene involving a greater sample size and different ethnicities are necessary to verify our findings.
Abstract. The aim of the present study was to determine whether there is an association between the long non-coding RNA (lncRNA) prostate cancer-associated non-coding RNA 1 (PRNCR1) polymorphisms and prostate cancer (PCa) risk in a sample of the Iranian population. This case-control study was performed on 178 patients with PCa and 180 subjects with benign prostatic hyperplasia (BPH). Genotyping assay was performed by polymerase chain reaction-restriction fragment length polymorphism. The findings indicated that the GG genotype of the rs13252298 A>G variant significantly increased the risk of PCa (odds ratio=3.49, 95% confidence interval: 1.79-6.81, P=0.0001) compared with AA+AG. As regards the rs1456315 G>A polymorphism, the AG genotype and G allele significantly increased the risk of PCa. As regards the rs7841060 T>G variant, the findings demonstrated that this TG genotype and the G allele significantly increased the risk of PCa. The rs7007694 T>C variant was not found to be associated with the risk of PCa. Haplotype analysis indicated that GTGA and GTGG significantly increased the risk of PCa compared with rs1456315A/rs7007694T/rs7841060T/rs13252298G (ATTG). The PRNCR1 variants were not found to be significantly associated with the clinicopathological characteristics of PCa patients. In conclusion, our findings support an association between PRNCR1 variants and the risk of PCa in a sample of the Iranian population.
Introduction: Programmed cell death-1 (PD-1) and its ligands (PD-L1 and PD-L2) play a critical role as a regulator of immune-system cells, including T cell, natural killer T (NKT), monocytes, dendritic cells (DC), and B cells. Objective: This study aimed to find a possible association between PD-1 (rs11568821, rs2227981, rs2227982), and PD-L1 (rs4143815, rs2890658) variants and Breast Cancer (BC) risk in a sample of southeast Iranian women. Method: The case-control study consisted of 520 individuals, including 260 histologically confirmed BC patients and 260 non-cancer age-matching healthy women as the control group. The Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) and Tetra-Primer Amplification Refractory Mutation System-Polymerase Chain Reaction (T-ARMS-PCR) methods were used for genotyping of PD-1 (rs11568821, rs2227981, rs2227982), and PD-L1 (rs4143815, rs2890658) polymorphisms. Results and Conclusion: Our findings indicated that the PD-L1 rs4143815 (G/C) variant meaningfully reduced the risk of BC. However, the PD-L1 rs2890658 variant increased the BC risk in the AC genotype as well as the A allele. Furthermore, we could not find a meaningful association between PD-1 rs11568821, PD-1 rs2227981, PD-1 rs2227982, and BC. Our team examined the possible association between variants and clinicopathological characteristics, including age, size of tumour, lymph node, histology, grade of tumour, estrogen and progesterone receptors status as well as human growth factor receptor 2 (HER2). Our findings demonstrated that PD-L1 rs4143815, PD-L1 rs2890658, PD-1 rs2227982 had a significant association with age. Additionally, we found a significant relation between PD-1 rs2227982 variant and tumour size. Statistical analyzes of PD-1 rs2227981 and PD-1 rs11568821 variants showed a meaningful relation between tumour grade and tumour stage (p=0.006), respectively.
Introduction: MicroRNAs (miRNAs) play an essential role in the susceptibility and development of cancer cells. Objective: Examining the dependency of breast cancer risk with genetic polymorphisms of miR-1307, miR-1269, and miR-3117 in a sample of Iranian women (southeast region). Methods: The case-control study consisted of 520 individuals (260 diagnosed BC patients, 260 healthy individuals). The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was used for genotyping of miR-1307 rs7911488, miR-1269 rs73239138, and miR-3117 (rs4655646 and rs7512692) polymorphisms. Results and Conclusion: This study provided evidence that miR-1307 rs7911488 polymorphism significantly reduced the risk of BC in heterozygous AG genotype, as well as dominant (AG+GG) genotype and G allele. A significant correlation was found between dominant (AA+AG) genotype, the A allele and protection against BC due to miR-1269 rs73239138 in the sample of study. In contrast, our findings suggested that AG genotype and G allele of miR-3117 rs4655646 polymorphism could increase BC's susceptibility among the southeastern Iranian females. The miR-3117 rs7512692 variant also increased the risk of BC in codominant, dominant and recessive models, as well as the T allele. The possible dependency of miR-1307, miR-1269, and miR-3117 variants with patients' clinicopathological characteristics and BC was also studied. It was concluded that there is a correlation between miR-3117 rs7512692 variant and tumor grade (p=0.031); also, a correlation between miR-1269 rs73239138 variant and progesterone receptor status (p=0.006). The current investigation revealed that miR-1307, miR-1269, and miR-3117 polymorphisms might play a crucial role in the Iranian population's vulnerability to BC.
Abstract. The present study aimed to examine the impact of a 3-bp indel (rs57408770) polymorphism within the pre-microRNA (miR)-3131 polymorphism on prostate cancer (PCa) risk in a sample of an Iranian population. In total, 340 subjects, including 177 patients with PCa and 170 patients with benign prostatic hyperplasia, were enrolled in the present case-control study. A mismatch polymerase chain reaction-restriction fragment length polymorphism method was designed for genotyping the 3-bp indel (rs57408770) polymorphism. The present findings demonstrated that the indel variant significantly increased the risk of PCa in codominant [odds ratio (OR)=2.23, 95% confidence interval (CI)=1.13-4.37; P=0.021, insertion (ins)/ins vs. deletion (del)/del] and recessive (OR=2.33, 95% CI=1.25-4.36; P=0.009, ins/ins vs. del/del + del/ins). In conclusion, to the best of our knowledge, the present findings for the first time proposed that a 3-bp indel variant of miR-3131 may be a risk factor for susceptibility to PCa in a sample of an Iranian population. Further studies with different ethnicities and larger sample sizes are required to validate the present findings. IntroductionProstate cancer (PCa), the second most common malignancy in men, is the fifth leading cause of cancer-related mortality among men globally (1). The incidence rate of PCa in Iran is lower than that in the rest of the world (2-4). Despite the high prevalence of PCa, little is known about the mechanisms underlying the development and progression of PCa. It has been proposed that genomic and environmental factors contribute to the development and progression of PCa (5-8). Twin studies have indicated that 42% of the variation in PCa risk may be attributed to genetics (9). Single nucleotide polymorphisms (SNPs), the most common type of genetic variation in the human genome, have been demonstrated to be associated with the risk of developing PCa (10-12).MicroRNA (miR) are small, non-coding, endogenous, single-stranded RNA molecules that are ~22 nucleotides in length (13,14). They regulate gene expression by directing sequence-specific degradation or inhibiting translation of target mRNA (13,14). Mounting evidence has suggested that mutation or SNPs in miR genes may affect target-binding activity, expression, or processes of mature miR, thus affecting the expression of their target genes (15,16). Polymorphisms in mature and/or pre-miR sequences may affect miR biogenesis and be associated with the development of various types of cancer (17-21). Small insertions and deletion (indels) polymorphisms are one of the most common genetic alterations in the human genome that influence human traits and diseases (22,23). There is limited information regarding the association between pre-miR-3131 polymorphisms and cancer risk. Recently, Wang et al (20) investigated the impact of a 3-bp indel polymorphism (rs57408770) in pre-miR-3131 on hepatocellular carcinoma (HCC) and observed that the insertion (ins) allele significantly increased the risk of HCC in a Chinese population. ...
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