Growing evidence demonstrated the presence of an association between IL1A rs3783553 polymorphism and the risk of various cancers. We aimed to evaluate whether the 4-bp insertion/deletion polymorphism (rs3783553) within the 3' untranslated region (3'UTRs) of IL1A was associated to the risk of prostate cancer (PCa) in a sample of Iranian population. A case-control study, including 150 prostate cancer patients and 155 healthy men, was done to examine the possible association between IL1A 4-bp ins/del polymorphism and PCa risk in a sample of southeast Iranian population. Mismatched polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was designed for genotyping the studied variant. Our findings showed that 4-bp ins/del polymorphism significantly increased the risk of PCa in codominant, recessive and allelic inheritance model. We also evaluated the association between the IL1A 4-bp ins/del polymorphism and clinicopathological characteristics of the patients, and found a significant association between 4-bp ins/del variant and stage, perineural invasion and surgical margin of tumor samples. Bioinformatics analysis revealed that the ins/del variant affected the IL1A mRNA stability leading to a structural shift in IL1A mRNA and has-miR-125a-3p hybrid. In conclusion, our findings proposed an association between IL1A 4-bp ins/del polymorphism and PCa risk. Additional studies with enlarged sample size and diverse ethnicities are required to validate our finding.

4-bp insertion/deletion (rs3783553) polymorphism within the 3'UTR of IL1A contributes to the risk of prostate cancer in a sample of Iranian population.

The Cyclin-Dependent Kinase Inhibitor p16 (p16) acts as a tumor suppressor in most cells, but for HPV transformed cervical cancer, in which oncoprotein E7 expressed by human papillomavirus (HPV) mediates the degradation of retinoblastoma protein (Rb), p16 exhibits oncogenic activity. Our study was conducted to study the mechanism underling p16 mediated promoting effect of cell proliferation in cervical cancer cell lines. CCK8 assay and EdU incorporation were conducted to evaluate cell proliferation. Loss-of-function assay was used to silence p16 in Ca Ski and SiHa cells. Next, western blot, qPCR, RNA silencing, luciferase activity assay, run-on assay, mRNA stability assay, RNA immunoprecipitation, co-immunoprecipitation Immunofluorescence were performed to examine the interaction between CDK6, HuR, and IL1A mRNA in p16 mediated proliferation promoting effect. Our results showed that: (1) Silencing p16 inhibited the proliferation of cervical cancer cells by decreasing the half-life of IL1A mRNA in CDK6 dependent manner; (2) The stabilization of IL1A mRNA was regulated by HuR which could be inactivated by p16/CDK6 mediated phosphorylation at Ser202; (3) IL1A mediated the oncogenic activity of p16 in cervical carcinoma cell lines. In conclusion, p16 promotes proliferation in cervical carcinoma cells through CDK6-HuR-IL1A axis.

/pdf/p16-promotes-proliferation-in-cervical-carcinoma-cells-2anilfi2i0.pdf

p16 promotes proliferation in cervical carcinoma cells through CDK6-HuR-IL1A axis.

PURPOSE Previous studies have reported the association of an insertion/deletion (Ins/Del) polymorphism (rs3783553) in the 3' untranslated region of interleukin-1A (IL-1A) with the risk of cancer, such as oral squamous cell carcinoma, nasopharyngeal carcinoma, and cervical carcinoma. However, the results are still inconsistent. The present meta-analysis aimed to clarify the association of IL-1A rs3783553 polymorphism with cancer risk. METHODS All eligible studies were selected from PubMed, Web of Science, and Chinese National Knowledge Infrastructure up to September 2, 2015. Summary odds ratios (ORs) and 95% confidence intervals (CIs) were used to evaluate cancer risk. RESULTS A total of ten case-control studies with 4,514 cases and 6,689 controls were included this meta-analysis. We found that IL-1A rs3783553 polymorphism was significantly associated with cancer risk (Ins/Ins + Ins/Del vs Del/Del: OR =0.79, 95% CI =0.67-0.92; Ins/Ins vs Del/Del: OR =0.61, 95% CI =0.47-0.79; Ins/Ins vs Ins/Del + Del/Del: OR =0.67, 95% CI =0.55-0.83; Ins vs Del: OR =0.81, 95% CI =0.72-0.92). In the stratified analyses, significant effects were found among Asian populations (Ins/Ins + Ins/Del vs Del/Del: OR =0.81, 95% CI =0.69-0.95) and cervical carcinoma (Ins/Ins vs Del/Del: OR =0.51, 95% CI =0.34-0.76; Ins/Ins vs Ins/Del + Del/Del: OR =0.52, 95% CI =0.35-0.78). CONCLUSION Our meta-analysis suggests that the IL-1A rs3783553 polymorphism contributes to susceptibility to cancer. However, well-designed studies with larger sample sizes are required to verify the results.

/pdf/association-between-an-insertion-deletion-polymorphism-in-il-3wystbg02v.pdf

Association between an insertion/deletion polymorphism in IL-1A gene and cancer risk: a meta-analysis.

Introduction: The prostate is a gland that surrounds men's urethra and helps to produce semen. In developed countries, prostate cancer (PCa.) is the second most common and lethal disease in men. Hereditary history of PCa. is a major contributor to this cancer? While a number of genetic and molecular changes have been reported in PCa, the general picture of the genetic aberrations is needed in Iranian population.Methods: In this study, a literature search from Jan. 2000 to June 2018 was performed through the PubMed, Google Scholar, Scopus, Web of Science, IranMedex, MEDLIB, IranDoc and Scientific Information databases using the keywords “genetic polymorphisms”, “prostate cancer”, “Iranian, and compare with regional and international population”.Results: The results revealed that several genome-wide association studies (such as rs2070744 and rs1799983 in the eNOS, rs243865 in the MMP2, rs1902023 in the UGT2B15, rs266882 in the PSA, rs10625775443 in the GNB3, rs 1800682 in the FAS, rs12052398 and rs13393577 in the ERBB4, rs181133 in the MTHFR, rs 1805087 in the MTR, rs1805355 in the MSH3, (rs60271534 in the CYP19, rs2234693 and rs9340799 in the ER-a, rs4986938 and rs1256049 in the ER-b) and single-nucleotide polymorphisms in important pathways (such as angiogenesis, androgen receptor binding site, cell signaling, folate metabolism, DNA repair, hormone synthesis and metabolism polymorphisms ) involved in prostate cancer occurrence and mechanism could serve as candidate biomarkers for the detection of PCa. The most important results of the all studied articles is summarized in Table 1 and 2.Conclusion: Several studies have been conducted on the family history of PCa. The main reason for this gathering is to inherit the involved genes. Additional studies are required to decipher precisely the gene combinations and personalize the management of prostate cancer. This article is the first comprehensive overview of genetic investigations of gene polymorphisms on PCa. in Iran.

/pdf/gene-polymormisms-and-prostate-cancer-a-systematic-review-32ry4t90ts.pdf

Gene Polymormisms and Prostate Cancer: A Systematic Review

An updated meta-analysis on the association between 4-bp insertion/deletion (rs3783553) polymorphism within the 3`UTR of IL1A and the risk of cancer

OBJECTIVE To identify the association between the insertion/deletion polymorphism of interleukin- 1A gene (IL1A) and the susceptibility of prostate cancer (PCA). METHODS We performed a case-control study enrolling 131 PCA patients and 229 healthy control subjects in a Chinese Han population. The TTCA insertion/ deletion polymorphism (rs3783553) in 3'-UTR of IL1A gene was genotyped by PCR-RFLP method. RESULTS The genotype distribution of rs3783553 in both groups met the requirements of Hardy-Weinberg equilibrium. Significantly reduced PCA risk was associated with D/I and I/I genotype compared to D/D genotype (P<0. 001, OR=O. 48, 95%CI: 0.31-0.74), and allele I is associated with the reduced PCA risk (P=0. 001,OR=0. 56,95% CI: 0. 40-0. 79). CONCLUSION TTCA insertion allele of rs3783553 contributes to the reduction of the susceptibility to prostate cancer.

[Insertion/deletion polymorphism of IL1A 3'-UTR associated with the susceptibility of prostate cancer ].

Abnormalities of the ERCC1 gene can affect DNA repair pathways, thereby having a vital effect on genomic stability. A growing amount of case-control studies have focused on making an investigation of the association between ERCC1 rs11615 polymorphism and cervical cancer susceptibility. However, the controversial results have raised concerns. To draw a more accurate conclusion, six studies were elaborately selected from the electronic databases for this meta-analysis, with 753 cervical cancer cases and 851 healthy controls. We applied pooled ORs combined with 95% CIs to test the potential associations. Significant associations were revealed in Chinese populations (T vs C: OR = 1.557 and 95%CI = 1.234–1.966; TT vs CC: OR = 3.175 and 95%CI = 1.754–5.748; TT/CT vs CC: OR = 1.512 and 95%CI = 1.126–2,031; and TT vs CT/CC: OR = 2.836 and 95%CI = 1.592–5.051). Even when the studies deviating from HWE were excluded, an increased cervical cancer susceptibility was observed in Chinese. These results disclose that there is an obvious correlation between the risk of cervical cancer and ERCC1 rs11615 polymorphism, especially in Chinese populations, and the T variant is the risky one. Also, our findings need further studies to validate.

/pdf/association-of-ercc1-rs11615-polymorphism-with-the-risk-of-2xx5ob28.pdf

Association of ERCC1 rs11615 Polymorphism with the Risk of Cervical Cancer Especially in Chinese Populations: A Meta-Analysis

Chromosomal Aberrations in Pediatric Patients with Moderate/Severe Developmental Delay/Intellectual Disability with Abundant Phenotypic Heterogeneities: A Single-center Study

Deletion in the Xp22.31 region is increasingly suggested to be involved in the etiology of epilepsy. Little is known regarding the genomic and clinical delineations of X-linked epilepsy in the Chinese population or the sex-stratified difference in epilepsy characteristics associated with deletions in the Xp22.31 region. In this study, we reported two siblings with a 1.69 Mb maternally inherited microdeletion at Xp22.31 involving the genes VCX3A, HDHD1, STS, VCX, VCX2, and PNPLA4 presenting with easily controlled focal epilepsy and language delay with mild ichthyosis in a Chinese family with a traceable 4-generation history of skin ichthyosis. Both brain magnetic resonance imaging results were normal, while EEG revealed epileptic abnormalities. We further performed an exhaustive literature search, documenting 25 patients with epilepsy with gene defects in Xp22.31, and summarized the epilepsy heterogeneities between sexes. Males harboring the Xp22.31 deletion mainly manifested with child-onset, easily controlled focal epilepsy accompanied by X-linked ichthyosis; the deletions were mostly X-linked recessive, with copy number variants (CNVs) in the classic region of deletion (863.38 kb–2 Mb). In contrast, epilepsy in females tended to be earlier-onset, and relatively refractory, with pathogenic CNV sizes varying over a larger range (859 kb–56.36 Mb); the alterations were infrequently inherited and almost combined with additional CNVs. A candidate region encompassing STS, HDHD1, and MIR4767 was the likely pathogenic epilepsy-associated region. This study filled in the knowledge gap regarding the genomic and clinical delineations of X-linked recessive epilepsy in the Chinese population and extends the understanding of the sex-specific characteristics of Xp22.31 deletion in regard to epilepsy.

/pdf/case-report-sex-specific-characteristics-of-epilepsy-2w8iahn0.pdf

Case report: Sex-specific characteristics of epilepsy phenotypes associated with Xp22.31 deletion: a case report and review

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[Insertion/deletion polymorphism of IL1A 3'-UTR associated with the susceptibility of prostate cancer ].

Association of ERCC1 rs11615 Polymorphism with the Risk of Cervical Cancer Especially in Chinese Populations: A Meta-Analysis

Chromosomal Aberrations in Pediatric Patients with Moderate/Severe Developmental Delay/Intellectual Disability with Abundant Phenotypic Heterogeneities: A Single-center Study

Case report: Sex-specific characteristics of epilepsy phenotypes associated with Xp22.31 deletion: a case report and review