ZNRD1-AS1 knockdown alleviates malignant phenotype of retinoblastoma through miR-128-3p/BMI1 axis

Background: ZNRD1-AS1 plays an important role in liver cancer, endometrial cancer and other diseases. However, the relationship between ZNRD1-AS1 and retinoblastoma has not been studied in detail. This study aimed to determine the role of ZNRD1-AS1 in retinoblastoma.
Methods: Differentially expressed genes in retinoblastoma downloaded from GEO database were identified by Limma package, and the expression and cell location of ZNRD1-AS1 were detected by real-time quantitative PCR (RT-qPCR). The relationships between miR-128-3p and two genes (ZNRD1-AS1 and BMI1) were analyzed by bioinformatics and dual-luciferase assay.
After manipulating the expressions of ZNRD1-AS1, miR-128-3p and BMI1, cell viability, tube length, migration, invasion and the protein expressions (PCNA, E-Cadherin, N-Cadherin) of retinoblastoma cells were determined by cell counting kit-8 (CCK-8), tube formation, transwell and Western blot assays, respectively.
Subcutaneous transplantation tumor assay, immunohistochemistry, and RT-qPCR were applied to verify the functions of the target gene in vivo.
Results: ZNRD1-AS1 was up-regulated in the cytoplasm of retinoblastoma and regulated BMI1 via sponging miR-128-3p.
ZNRD1-AS1 knockdown alleviated the malignant phenotype (viability, tube length, migration and invasion) of retinoblastoma cells, reduced tumor volume, and weight, and inhibited BMI1 and CD34 expressions.
Different from miR-128-3p mimic, miR-128-3p inhibitor promoted malignant phenotype of retinoblastoma cells, and partially reversed the inhibitory effect of siZNRD1-AS1. MiR-128-3p mimic down-regulated BMI1, PNCA, N-Cadherin expressions, and up-regulated p16 and E-Cadherin expressions. The regulatory effect of miR-128-3p was partially reversed by BMI1.
Conclusion: ZNRD1-AS1, acting as a “sponge” of miR-128-3p, up-regulates BMI1, thereby promoting the progression of retinoblastoma.
Keywords: BMI1; Retinoblastoma; ZNRD1-AS1; biological characteristics; miR-128-3p.

Knockdown of lncRNA ZNRD1-AS1 suppresses gastric cancer cell proliferation and metastasis by targeting the miR-9-5p/HSP90AA1 axis

LncRNAs play an important role in a variety of biological processes, such as cancer pathogenesis. The lncRNA zinc ribbon domain containing 1 antisense RNA 1 (ZNRD1-AS1) is a natural antisense transcript of ZNRD1. In this study, we found that ZNRD1-AS1 levels were significantly upregulated in gastric cancer tissues compared to those in adjacent healthy gastric tissues.
ZNRD1-AS1 levels were correlated with lymph node metastasis, distal metastasis, and TNM stage, but were not correlated with age and sex. ZNRD1-AS1 knockdown suppressed cell proliferation, migration, and invasion, and promoted apoptosis.
ZNRD1-AS1 overexpression had the opposite effect. ZNRD1-AS1 knockdown suppressed tumor growth and pulmonary metastasis in a nude mouse model ZNRD1-AS1 can bind to miR-9-5p and ZNRD1-AS1 knockdown can decrease the protein level of heat shock protein 90 alpha family class A member 1 (HSP90AA1), which is the target of miR-9-5p.
The miR-9-5p inhibitor rescued the effect of ZNRD1-AS1 knockdown, and the mutant of miR-9-5p binding site on ZNRD1-AS1 sequence blocked the effect of ZNRD1-AS1 overexpression.
In conclusion, ZNRD1-AS1 levels were upregulated in gastric cancer tissues, and knockdown of ZNRD1-AS1 suppressed gastric cancer cell proliferation and metastasis by targeting the miR-9-5p/HSP90AA1 axis.
Our findings provide novel insights into the mechanism underlying the role of ZNRD1-AS1 in gastric cancer.

Association of single nucleotide polymorphisms in HLA-C and ZNRD1 genes with HIV-1 mother to child transmission in Zambia population

Background: Human leukocyte antigen C (HLA-C) and Zinc ribbon domain containing 1 (ZNRD1) are considered HIV-1 restriction factors and are expressed in the placenta. Variations in HLA-C and ZNRD1 genes are known to influence HIV-1 infection, including viral replication and progression to AIDS. Little is known about the role of variants in these genes in HIV-1 mother-to-child transmission (MTCT).
Methods: We evaluated the distribution of HLA-C (rs10484554, rs9264942) and ZNRD1 (rs8321, rs3869068) variants in a Zambian population composed of 333 children born to HIV-1+ mothers (248 HIV-1 non-infected/ 85 HIV-1 infected) and 97 HIV-1+ mothers.
Results: Genotypic distribution of HLA-C and ZNRD1 were in Hardy-Weinberg equilibrium, except for HLA-C rs10484554 in both groups. In mothers, no significant differences were observed in their allele and genotypic distributions for both genes. The T and TT variants (rs10484554 – HLA-C) were significantly more frequent among HIV-1+ children, specifically, those who acquired the infection in utero (IU) and intrapartum (IP). For ZNRD1, the T allele (rs3869068) was more frequent in HIV-1 children, showing significant differences in relation to those infected via IP and postpartum (PP). The CT and TT genotypes were significantly more frequent in HIV-1 children.
Conclusions: Variations in HLA-C (T and TT – rs10484554) and ZNRD1 (T and CT/TT – rs3869068) can increase and decrease the susceptibility to HIV-1 infection via MTCT, respectively.
Further studies are encouraged focusing on a greater number of variants and sample size, with functional validation and in other populations.

Knockdown of lncRNA ZNRD1-AS1 inhibits progression of bladder cancer by regulating miR-194 and ZEB1

Background: Bladder cancer (BC) is a common urinary neoplasm with high incidence worldwide. Long noncoding RNA zinc ribbon domain containing 1 antisense RNA 1 (ZNRD1-AS1) has been reported to be upregulated in BC. However, the exact role of ZNRD1-AS1 as well as its mechanism remains poorly understood.
Methods: Zinc ribbon domain containing 1 antisense RNA 1, and its potential downstream genes microRNA-194 (miR-194) and zinc finger E-box binding homeobox 1 (ZEB1) levels were detected via quantitative real-time polymerase chain reaction or western blot. Cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) were detected to assess the influences of ZNRD1-AS1, miR-194 and ZEB1 on BC cells by colony formation, cell counting kit-8 (CCK-8), transwell analysis or western blot. The relationship between miR-194 and ZNRD1-AS1 or ZEB1 was analyzed by luciferase activity analysis. The xenograft experiment was performed to assess the function of ZNRD1-AS1 in vivo.
Results: Zinc ribbon domain containing 1 antisense RNA 1level was upregulated in BC. ZNRD1-AS1 silence repressed proliferation, migration, invasion and EMT in BC cells. MiR-194 was identified as a target of ZNRD1-AS1, and miR-194 upregulation repressed proliferation, migration, invasion, and EMT by ZNRD1-AS1 sponging. ZEB1 was targeted via miR-194 and its interference impeded proliferation, migration, invasion, and EMT. Moreover, ZNRD1-AS1 regulated ZEB1 expression via miR-194. Besides, inhibition of ZNRD1-AS1 attenuated tumor growth by miR-194/ZEB1 axis in vivo.
Conclusion: Knockdown of ZNRD1-AS1 suppressed BC cell development in vitro and in vivo via targeting miR-194 to regulate ZEB1, indicating a novel avenue for treatment of BC.
Keywords: EMT; ZEB1; ZNRD1-AS1; bladder cancer; miR-194; proliferation.

ZNRD1-AS1 Promotes Nasopharyngeal Carcinoma Cell Invasion and Metastasis by Regulating the miR-335-ROCK1 Axis

Background: Long noncoding RNAs (lncRNAs) are known as key regulators in many cancer types, but their biological functions in nasopharyngeal carcinoma (NPC) remain largely unknown. In the present study, we aim to explore the role of the lncRNA ZNRD1-AS1 in NPC tumor development.
Methods: The role of ZNRD1-AS1 in NPC tissues and cells was explored by using a quantitative real-time PCR assay. Cellular behavioral experiments were used in testing NPC cell proliferation, invasion, and migration. Luciferase reporter assay, RNA-binding protein immunoprecipitation, and Western blot analysis were used in estimating the associations among ZNRD1-AS1, miR-335, and ROCK1.
Results: ZNRD1-AS1 expression was elevated in the NPC tissues and cells, and ZNRD1-AS1 overexpression was positively correlated with advanced TNM stage and the presence of lymph node metastasis. Our biological experiments indicated that ZNRD1-AS1 knockdown reduces NPC cell invasion and metastasis. Further analyses revealed that ZNRD1-AS1 as a ceRNA promotes the migration and invasion of NPC cells by sponging miR-335. We provided evidence that ZNRD1-AS1 facilitates the invasion and metastasis of NPC cells via the miR-335-ROCK1 axis.
Conclusion: Our data shed light on the oncogenic role of ZNRD1-AS1 in NPC tumor development, and a promising therapeutic target for NPC was identified.
Keywords: ZNRD1-AS1; miR-335; nasopharyngeal carcinoma.

ZNRD1 and Its Antisense Long Noncoding RNA ZNRD1-AS1 Are Oppositely Regulated by Cold Atmospheric Plasma in Breast Cancer Cells

Cold atmospheric plasma (CAP) has been recognized as a potential alternative or supplementary cancer treatment tool, which is attributed by its selective antiproliferation effect on cancer cells over normal cells. Standardization of the CAP treatment in terms of biological outputs such as cell growth inhibition and gene expression change is essential for its clinical application.
This study aims at identifying genes that show consistent expression profiles at a specific CAP condition, which could be used to monitor whether CAP is an appropriate treatment to biological targets. To do this, genes showing differential expression by two different CAP treatment conditions were screened in the MCF-7 breast cancer cells.
As a result, ZNRD1 was identified as a potential marker with being consistently upregulated by 600 s but downregulated by the 10 × 30 s CAP treatment scheme.
Expression of ZNRD1 was increased in breast cancer tissues compared to normal tissues, judged by cancer tissue database analysis, and supported by the antiproliferation after siRNA-induced downregulation in MCF-7.

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Interestingly, the antisense long noncoding RNA (lncRNA) of ZNRD1, ZNRD1-AS1, was regulated to the opposite direction of ZNRD1 by CAP. The siRNA-based qPCR analysis indicates that ZNRD1 downregulates ZNRD1-AS1, but not vice versa. ZNRD1-AS1 was shown to increase a few cis-genes such as HLA-A, HCG9, and PPP1R11 that were also regulated by CAP. Altogether, this study identified a pair of gene and its antisense lncRNA of which expression is precisely controlled by CAP in a dose-dependent manner.
These genes could help elucidate the molecular mechanism how CAP regulates lncRNAs in cancer cells.

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