&lt;p&gt;lncRNA SNHG1 Promotes Progression of Cervical Cancer Through miR-195/NEK2 Axis&lt;/p&gt;

Ji, Yuan; Meng, Man; Miao, Yi

doi:10.2147/cmar.s277064

Cited by 15 publications

(6 citation statements)

References 27 publications

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“…The lncRNA SNHG17 has been reported to enhance glioma cell proliferation, migration, and invasion by inducing zinc fingers and homeoboxes 1 (ZHX1) expression via inhibiting miR-23b-3p [ 31 ]. The lncRNA SNHG1 promotes cervical cancer progression by regulating NIMA-related kinase 2 (NEK2) expression via inhibiting miR-195 [ 32 ]. In addition, SNHG1 enhances cell proliferation, migration and invasion in esophageal cancer by regulating cell division cycle 42 (Cdc42) expression via inhibiting miR-195 [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Identification and Characterization of mRNA and lncRNA Expression Profiles in Age-Related Hearing Loss

Kim¹,

Lee²,

Lee³

et al. 2023

Clin Exp Otorhinolaryngol

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Objectives. Age-related hearing loss (ARHL), or presbycusis, is caused by disorders of sensory hair cells and auditory neurons. Many studies have suggested that the accumulation of mitochondrial DNA damage, the production of reactive oxygen species, noise, inflammation, and decreased antioxidant function are associated with subsequent cochlear senescence in response to aging stress. Long non-coding RNA (lncRNA) has been reported to play important roles in various diseases. However, the function of lncRNA in ARHL remains unclear. In this study, we analyzed the common expression profiles of messenger RNA (mRNA) and lncRNA through ARHL-related RNA-sequencing datasets.Methods. We selected and downloaded three different sets of RNA-sequencing data for ARHL. We performed differential expression analysis to find common mRNA and lncRNA profiles in the cochleae of aged mice compared to young mice. Gene Ontology (GO) analysis was used for functional exploration. Real-time quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was performed to validate mRNAs and lncRNAs. In addition, we performed trans target prediction analysis with differentially expressed mRNAs and lncRNAs to understand the function of these mRNAs and lncRNAs in ARHL.Results. We identified 112 common mRNAs and 10 common lncRNAs in the cochleae of aged mice compared to young mice. GO analysis showed that the 112 upregulated mRNAs were enriched in the defense response pathway. When we performed qRT-PCR with 1 mM H2O2-treated House Ear Institute-Organ of Corti 1 (HEI-OC1) cells, the qRT-PCR results were consistent with the RNA-sequencing analysis data. lncRNA-mRNA networks were constructed using the 10 common lncRNAs and 112 common mRNAs in ARHL.Conclusion. Our study provides a comprehensive understanding of the common mRNA and lncRNA expression profiles in ARHL. Knowledge of ARHL-associated mRNAs and lncRNAs could be useful for better understanding ARHL and these mRNAs and lncRNAs might be a potential therapeutic target for preventing ARHL.

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Section: Discussionmentioning

confidence: 99%

Identification and Characterization of mRNA and lncRNA Expression Profiles in Age-Related Hearing Loss

Kim¹,

Lee²,

Lee³

et al. 2023

Clin Exp Otorhinolaryngol

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“…However, the resistance of cervical cancer cells to therapeutic drugs and the side effects of chemotherapy are the main obstacles to the treatment of cervical cancer [ 18 ]. Therefore, the discovery of new biomarkers for cervical cancer is necessary for the early diagnosis, prevention, and treatment [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA FAM13A-AS1 Regulates Proliferation and Apoptosis of Cervical Cancer Cells by Targeting miRNA-205-3p/DDI2 Axis

Qiu

et al. 2022

Journal of Oncology

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The aim of this study was to explore the function of long noncoding RNA (lncRNA) FAM13A-AS1 and its associated mechanism in cervical cancer. A total of 30 cervical cancer tissues and adjacent tissues were collected. Cervical cancer cell lines, including SiHa and HeLa, were transfected with constructs expressing LV-FAM13A-AS1, silencing RNA LV-siFAM13A-AS1, miRNA mimics, and miRNA inhibitors. RT-qPCR was used to detect the expression of FAM13A-AS1 in cervical cancer tissues, including SiHa, HeLa, and HUCEC cells. MTT, flow cytometry, and transwell assays were performed to explore the influence of FAM13A-AS1 on cervical cancer cell proliferation, apoptosis, invasion, and migration. A bioinformatics analysis and a dual-luciferase assay were carried to confirm the target relationship between FAM13A-AS1 or DDI2 and miRNA-205-3p. Finally, in vivo tumorigenesis experiments were performed in nude mice to explore the effect of FAM13A-AS1 expression on cervical cancer. Low FAM13A-AS1 expression and high miRNA-205-3p expression were observed in cervical cancer tissues and cell lines (SiHa and HeLa). Upregulating the expression of FAM13A-AS1 inhibited proliferation, migration, and invasion of SiHa and HeLa cells, while the apoptosis of SiHa and HeLa cells was increased. More importantly, LV-FAM13A-AS1 could improve tumor development in vivo. In addition, FAM13A-AS1 negatively regulated the expression of miRNA-205-3p, while miRNA-205-3p reduced DDI2 expression, and miRNA-205-3p mimic reversed the effects of FAM13A-AS1 overexpression in vitro. In conclusion, FAM13A-AS1 inhibits the progression of cervical cancer by targeting the miRNA-205-3p/DDI2 axis, suggesting that FAM13A-AS1 might be a potential target for cancer cell treatment.

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“…lncRNAs are transcribed RNA molecules with a length of more than 200 nucleotides that do not bind to proteins [7]. Recent studies have shown that lncRNAs regulate important biological processes, including cell proliferation, survival, apoptosis, and differentiation [8][9][10]. They have also been found to be associated with cerebral I/R injury [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA LOC366613 alleviates the cerebral ischemic injury via regulating the miR-532-5p/phosphatase and tensin homolog axis

Wei

et al. 2021

Bioengineered

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Cerebral infarction (CI) has become a leading cause of death in China. Long non-coding RNAs (lncRNAs) are intensively involved in the progression of CI. Here, we aimed to investigate the effects of lncRNA LOC366613 (LOC366613) on cerebral I/R injury, as well as its possible mechanism. Transient middle cerebral artery occlusion (MCAO) was used to establish a mouse model of cerebral I/R, and the PC12 cell line was used to establish an in vitro oxygen-glucose deprivation (OGD) injury model. The MTT assay was used to determine cell viability, and qRT-PCR was used to determine RNA levels. Western blotting was conducted to detect protein expression levels. The TUNEL assay and flow cytometry were used to measure cell apoptosis, and 2,3,5-triphenyltetrazolium chloride (TTC) was used to determine cerebral infarct volume. Finally, RNA pull-down and luciferase activity assays were used to examine interactions between miR-532-5p and LOC366613, as well as between miR-532-5p and phosphatase and tensin homolog (PTEN). LOC366613 was overexpressed in patients with cerebral I/R injury. In PC12 cells, knockdown of LOC366613 reduced the apoptosis rate and lactic acid dehydrogenase (LDH) expression, while increasing cell viability. Moreover, miR-532-5p was shown to be a target of LOC366613, as predicted. Downregulation of miR-532-5p reversed the effects of LOC366613 knockdown on PC12 cell apoptosis, LDH release, and cell viability. Finally, PTEN was verified as a target of miR-532-5p. LOC366613 participates in cerebral I/R injury by regulating the miR-532-5p/PTEN axis, potentially providing a new CI treatment target.

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<p>lncRNA SNHG1 Promotes Progression of Cervical Cancer Through miR-195/NEK2 Axis</p>

Cited by 15 publications

References 27 publications

Identification and Characterization of mRNA and lncRNA Expression Profiles in Age-Related Hearing Loss

Identification and Characterization of mRNA and lncRNA Expression Profiles in Age-Related Hearing Loss

LncRNA FAM13A-AS1 Regulates Proliferation and Apoptosis of Cervical Cancer Cells by Targeting miRNA-205-3p/DDI2 Axis

Long non-coding RNA LOC366613 alleviates the cerebral ischemic injury via regulating the miR-532-5p/phosphatase and tensin homolog axis

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