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

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

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Long Non-Coding RNA (lncRNA) Sequences: FAM3D-AS1, LINC01230, LINC01315 and LINC01468 – Are They Associated with Endometrial Cancer?

10.21203/rs.3.rs-832389/v1 ◽

2021 ◽

Author(s):

Jan Bieńkiewicz ◽

Hanna Romanowicz ◽

Bożena Szymańska ◽

Daria Domańska-Senderowska ◽

Miłosz Wilczyński ◽

...

Keyword(s):

Body Mass Index ◽

Endometrial Cancer ◽

Real Time ◽

Cancer Patients ◽

Body Mass ◽

Real Time Pcr ◽

Protective Factor ◽

Non Coding Rna ◽

Long Non Coding Rna ◽

Lower Expression

Abstract Background: The analysis of long non-coding RNA (lncRNA) in endometrial cancer is quite a novel field of science. Although numerous lncRNA sequences have been identified up until today, their correlation with endometrial cancer is still undetermined. The aim of this study was to analyse the expression of four lncRNA sequences: FAM3D-AS1, LINC01230, LINC01315 and LINC01468 and to investigate their significance in the risk of developing endometrial cancer.Methods: LncRNA sequences have been investigated in paraffin embedded tissue blocks (archival postoperative specimens) in endometrial cancer patients (Cases, n=120) and in cancer-free controls (n=80) using real-time PCR assay.Results: This study revealed a lower expression of LINC01468 in endometrial cancer patients than in controls. Both LINC01468 and FAM3D-AS1 were positively correlated with Body Mass Index (BMI) in cancer-free controls.Conclusions: LncRNA LINC01468 may be a protective factor in development of endometrial cancer.

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Role of long non-coding RNA NEAT1 in the prognosis of prostate cancer patients

Medicine ◽

10.1097/md.0000000000020204 ◽

2020 ◽

Vol 99 (22) ◽

pp. e20204 ◽

Cited By ~ 1

Author(s):

Junchao Bai ◽

Guangyi Huang

Keyword(s):

Prostate Cancer ◽

Cancer Patients ◽

Non Coding Rna ◽

Long Non Coding Rna

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

The Journal of Gene Medicine ◽

10.1002/jgm.3239 ◽

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

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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

Journal of Experimental & Clinical Cancer Research ◽

10.1186/s13046-021-01891-0 ◽

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.

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

Signal Transduction and Targeted Therapy ◽

10.1038/s41392-021-00562-y ◽

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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