Evaluation of the plasma level of long non‐coding RNA PCAT1 in prostatic hyperplasia and newly diagnosed prostate cancer patients

2020 ◽  
Vol 22 (10) ◽  
Author(s):  
Setareh Rezatabar ◽  
Emadoddin Moudi ◽  
Farzin Sadeghi ◽  
Soraya Khafri ◽  
Tayebeh Azramezani Kopi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Plasma Level ◽  
Cancer Patients ◽  
Prostatic Hyperplasia ◽  
Newly Diagnosed ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Analysis of the Link between rs4977574 Single Nucleotide Polymorphism of the Long Non-Coding RNA ANRIL Gene and Prostate Cancer Development

2021 ◽  
Vol 6 (6) ◽  
pp. 93-99
Author(s):  
A. D. Volkogon ◽  
◽  
V. Yu. Harbuzova ◽  
O. V. Ataman
Keyword(s):  
Prostate Cancer ◽  
Gene Polymorphism ◽  
Real Time ◽  
Cancer Patients ◽  
Malignant Tumors ◽  
Chromosome 9 ◽  
Polycomb Repressive Complex ◽  
Non Coding Rna ◽  
Significant Difference ◽  
Long Non Coding Rna

The purpose of the study was to investigate the possible association between ANRIL gene rs4977574-polymorphism and prostate cancer occurrence among men of the Ukrainian population. Materials and methods. A total of 250 males were enrolled in the study. Of these, the experimental group included 184 prostate cancer patients, and the control group included 66 men without a history of malignant tumors. Genotyping of the ANRIL rs4977574 locus was performed by real-time polymerase chain reaction. The reaction was performed on a Quant Studio 5 DX Real-Time instrument (Applied Biosystems, USA) in the presence of TaqMan assays (TaqMan®SNP Assay C_31720978_30). The genotyping results were statistically processed using the SPSS software package (version 17.0). Values of p less than 0.05 were considered as statistically significant. Results and discussion. ANRIL (Antisense Non-coding RNA in the INK4 Locus), also known as CDKN2B-AS1, is a long non-coding RNA (3.8-kb) transcribed from the short arm of the human chromosome 9 (p21.3). ANRIL transcripts promote their main molecular effects through interaction with proteins of Polycomb repressive complex 1 and Polycomb repressive complex 2. Ultimately, this leads to epigenetic cis-inactivation of the tumor growth suppressor genes located in the Chr9p21 region: CDKN2A/p16INK4A, CDKN2A/p14ARF, CDKN2B/p15INK4B. Recent experimental studies have demonstrated the involvement of ANRIL in the development of malignant tumors of different localization. At the same time, there is almost no information about the role of the gene polymorphisms of this RNA in the occurrence of prostate cancer. The possible link between ANRIL gene polymorphism and prostate cancer risk in the Ukrainian population is not fully understood. It was found that the control men and prostate cancer patients did not differ significantly in the frequency of rs4977574-genotypes (p = 0.886). No significant difference was found during the corresponding comparison separately among persons with normal weight, overweight, without, and with the habit of smoking (p >0.05). Analysis of the association of different rs4977574 genotypes of the ANRIL gene with the risk of prostate cancer using logistic regression also did not show a reliable relationship under different models of inheritance, both before and after adjustment for age, body mass index and smoking (p >0.05). Conclusion. Thus, for the first time, we performed an analysis of the relation between ANRIL gene polymorphism and the development of malignant tumors of the genitourinary system in the Ukrainian population. The results showed that the polymorphic locus rs4977574 is not associated with the risk of prostate cancer

scholarly journals Unraveling the dark matter, long non-coding RNAs, in male reproductive diseases: A narrative review

2020 ◽  
Author(s):  
Masoud Dehghan Tezerjani ◽  
Seyed Mehdi Kalantar
Keyword(s):  
Prostate Cancer ◽  
Noncoding Rna ◽  
Expression Profiles ◽  
Prostatic Hyperplasia ◽  
Functional Roles ◽  
Sperm Abnormalities ◽  
Non Coding Rna ◽  
Wide Range ◽  
Posttranslation Modification ◽  
Long Non Coding Rna

Recent advances in human transcriptome have revealed the fundamental and functional roles of long non-coding RNA in the susceptibility to diverse diseases and pathological conditions. They participate in wide range of biological processes such as the modulating of chromatin structure, transcription, translation, and posttranslation modification. In addition, based on their unique expression profiles and their association with clinical abnormalities such as those of related to male reproductive diseases, they can be used to develop therapeutic methods and biomarkers for screening of the diseases. In this study, we will review the identified lncRNAs and their molecular functions in the pathogenesis of male reproductive diseases such as prostate cancer, benign prostatic hyperplasia, prostatitis, testicular cancer, varicocele, and sperm abnormalities. Key words: Long noncoding RNA, Prostate cancer, Prostatic hyperplasia, Prostatitis, Varicocele, Sperm abnormalities.

598: Increased Risk of Newly Diagnosed Comorbidities in Prostate Cancer Patients Treated with Androgen Deprivation Therapy

2007 ◽  
Vol 177 (4S) ◽  
pp. 200-200 ◽  
Author(s):  
Andrea Gallina ◽  
Pierre I. Karakiewicz ◽  
Jochen Walz ◽  
Claudio Jeldres ◽  
Quoc-Dien Trinh ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Patients ◽  
Androgen Deprivation Therapy ◽  
Androgen Deprivation ◽  
Newly Diagnosed ◽  
Increased Risk

289: Assessment of Indirect Costs of Newly Diagnosed Prostate Cancer Patients

2007 ◽  
Vol 177 (4S) ◽  
pp. 97-97
Author(s):  
Ravishankar Jayavedappa ◽  
Sumedha Chhatre ◽  
Richard Whittington ◽  
Alan J. Wein ◽  
S. Bruce Malkowicz
Keyword(s):  
Prostate Cancer ◽  
Cancer Patients ◽  
Indirect Costs ◽  
Newly Diagnosed

scholarly journals Long non‐coding RNA NORAD promotes the prostate cancer cell extracellular vesicle release via microRNA-541-3p-regulated PKM2 to induce bone metastasis of prostate cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Chuan-yi Hu ◽  
Juan Chen ◽  
Xin-hua Qin ◽  
Pan You ◽  
Jie Ma ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Marrow ◽  
Bone Metastasis ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Marrow Stromal Cells ◽  
Downstream Target ◽  
Non Coding Rna ◽  
Target Molecules ◽  
Long Non Coding Rna

Abstract Background Bone metastasis is the leading cause of mortality and reduced quality of life in patients with metastatic prostate cancer (PCa). Long non-coding RNA activated by DNA damage (NORAD) has been observed to have an abnormal expression in various cancers. This article aimed to explore the molecular mechanism underlying the regulatory role of NORAD in bone metastasis of PCa. Methods NORAD expression in clinical PCa tissues and cell lines was detected with the application of qRT-PCR. Cancer cells were then transfected with plasmids expressing NORAD, after which Transwell assay and CCK-8 assay were carried out to detect proliferation, migration, and bone metastasis of PCa. NORAD downstream target molecules were screened through bioinformatics analysis, followed by further verification using dual luciferase assay. Extracellular vesicles (EVs) were labeled with PKH67 and interacted with bone marrow stromal cells. The gain- and loss-function method was applied to determine the internalization and secretion of PCa cells-derived EVs under the intervention of downstream target molecules or NORAD. Results PCa tissues and cell lines were observed to have a high expression of NORAD, particularly in tissues with bone metastasis. NORAD knockdown resulted in reduced secretion and internalization of EVs, and suppressed proliferation, migration, and bone metastasis of PCa cells. It was indicated that NORAD interacted with miR-541-3p, leading to the upregulation of PKM2. Forced expression of PKM2 promoted the transfer of PKH67-labeled EVs to bone marrow stromal cells. Conclusions NORAD might serve as a ceRNA of miR-541-3p to promote PKM2 expression, thereby enhancing the development of bone metastasis in PCa by promoting internalization and transfer of EVs of cancer cells, providing an insight into a novel treatment for the disorder.

scholarly journals Recent trend of ADT in newly‐diagnosed prostate cancer patients: comparing between high‐ and middle income Asian countries

2021 ◽  
Author(s):  
Jasmine Lim ◽  
Mizuki Onozawa ◽  
Marniza Saad ◽  
Teng Aik Ong ◽  
Rohan Malek ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Patients ◽  
Recent Trend ◽  
Newly Diagnosed ◽  
Asian Countries ◽  
Middle Income

scholarly journals Long non-coding RNA AFAP1-AS1 accelerates lung cancer cells migration and invasion by interacting with SNIP1 to upregulate c-Myc

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Yu Zhong ◽  
Liting Yang ◽  
Fang Xiong ◽  
Yi He ◽  
Yanyan Tang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Cancer Metastasis ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Lung Cancer Patients ◽  
Lung Cancer Metastasis ◽  
Non Coding Rna ◽  
Long Non Coding Rna

AbstractActin filament associated protein 1 antisense RNA 1 (named AFAP1-AS1) is a long non-coding RNA and overexpressed in many cancers. This study aimed to identify the role and mechanism of AFAP1-AS1 in lung cancer. The AFAP1-AS1 expression was firstly assessed in 187 paraffin-embedded lung cancer and 36 normal lung epithelial tissues by in situ hybridization. The migration and invasion abilities of AFAP1-AS1 were investigated in lung cancer cells. To uncover the molecular mechanism about AFAP1-AS1 function in lung cancer, we screened proteins that interact with AFAP1-AS1 by RNA pull down and the mass spectrometry analyses. AFAP1-AS1 was highly expressed in lung cancer clinical tissues and its expression was positively correlated with lung cancer patients’ poor prognosis. In vivo experiments confirmed that AFAP1-AS1 could promote lung cancer metastasis. AFAP1-AS1 promoted lung cancer cells migration and invasion through interacting with Smad nuclear interacting protein 1 (named SNIP1), which inhibited ubiquitination and degradation of c-Myc protein. Upregulation of c-Myc molecule in turn promoted the expression of ZEB1, ZEB2, and SNAIL gene, which ultimately enhanced epithelial to mesenchymal transition (EMT) and lung cancer metastasis. Understanding the molecular mechanism by which AFAP1-AS1 promotes lung cancer’s migration and invasion may provide novel therapeutic targets for lung cancer patients’ early diagnosis and therapy.

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