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 ].

Abstract Background The traditional prostate cancer (PCa) model is established by injecting cell suspension and is associated with a low tumor formation rate. Cell sheet technology is one of the advancements in tissue engineering for 3D cell-based therapy. In this study, we established ectopic and orthotopic PCa models by cell sheet technology, and then compared the efficiency of tumor formation with cell suspension injection. Methods DU145 cells were seeded on 35 mm temperature-sensitive dishes to form PCa cell sheets, while the cell suspension with the same cell density was prepared. After transplanting into the nude mice, the tumor volumes were measured every 3 days and the tumor growth curves were conducted. At the time points of 2 weeks and 4 weeks after the transplantation, magnetic resonance imaging (MRI) was used to evaluate the transplanting site and distant metastasis. Finally, the mice were sacrificed, and the related tissues were harvested for the further histological evaluation. Results The orthotopic tumor formation rate of the cell sheet injection group was obviously better than that in cell suspension injection group (100% vs 67%). Compared with cell suspension injection, the tumors of DU145 cell sheet fragments injection had the higher density of micro-vessels, more collagen deposition, and lower apoptosis rate. There was no evidence of metastasis in forelimb, lung and liver was found by MRI and histological tests. Conclusion We successfully cultured the DU145 cell sheet and can be used to establish ectopic and orthotopic PCa tumor-bearing models, which provide an application potential for preclinical drug development, drug-resistance mechanisms and patient individualized therapy. 

/pdf/establishment-and-evaluation-of-ectopic-and-orthotopic-1teejsxq.pdf

Establishment and evaluation of ectopic and orthotopic prostate cancer models using cell sheet technology

Prostate cancer (PCa), the most prevalent malignancy among male genitourinary cancers, is distinguished by its immunologically ”cold” phenotype with persistently high incidence and mortality. Radical prostatectomy and radiotherapy represent the current standard of care for localized prostate cancer. However, recurrence or progression occurs frequently, and advanced or metastatic disease is common at initial presentation. Recent progress in cancer immunotherapy reveals that modulation of immune responses represents an effective strategy for enhancing antitumor activity. Programmed Cell Death Protein 1 and Programmed Cell Death Ligand 1 (PD-1/PD-L1) inhibitors, which restore T-cell function and remodel the tumor immune microenvironment, have achieved clinical success in melanoma, lymphoma and non-small-cell lung cancer. Although their efficacy as monotherapy in PCa remains limited and optimal patient selection criteria are lacking, emerging evidence suggests that combination immunotherapy regimens may offer clinically significant benefits. This review critically evaluates current clinical trial outcomes involving PD-1/PD-L1 inhibitors for prostate cancer and outlines priority directions for future investigation.

Advances in the application of PD-1/PD-L1 immunotherapy for prostate cancer: a review

/pdf/establishment-and-evaluation-of-ectopic-and-orthotopic-ud1jnvnn.pdf

PSMA PET/CT for prostate cancer diagnosis: current applications and future directions

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

Establishment and evaluation of ectopic and orthotopic prostate cancer models using cell sheet technology

Advances in the application of PD-1/PD-L1 immunotherapy for prostate cancer: a review

Establishment and evaluation of ectopic and orthotopic prostate cancer models using cell sheet technology

PSMA PET/CT for prostate cancer diagnosis: current applications and future directions