Downregulation of the long noncoding <scp>RNA <i>SNHG1</i></scp> inhibits tumor cell migration and invasion by sponging <scp>miR</scp>‐195 through targeting <i>Cdc42</i> in oesophageal cancer

Chen, Yu; Deng, Fang; Cai, Lily

doi:10.1002/kjm2.12318

Cited by 13 publications

(6 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…20 This study found that CDC42 was highly expressed in CC tissues and was negatively correlated with miR-101-5p expression. Studies have shown that CDC42 is targeted and regulated by miR-195 in esophageal cancer, 35 and in this study, we found that CDC42 was a target gene of miR-101-5p. Further, our results showed that MYLK-AS1 regulated CC progression through the miR-101-5p/CDC42 axis, and knockdown of CDC42 or upregulation of miR-101-5p partially reversed the effects caused by upregulation of MYLK-AS1 is required for WASP/N-wasp activation.…”

Section: Discussionsupporting

confidence: 70%

LncRNA MYLK antisense RNA 1 activates cell division cycle 42/Neutal Wiskott‐Aldrich syndrome protein pathway via microRNA‐101‐5p to accelerate epithelial‐to‐mesenchymal transition of colon cancer cells

Quan,

Xu,

Huang

et al. 2023

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

Long noncoding RNA MYLK antisense RNA 1 (MYLK‐AS1) is the crux in multiple diseases. Therefore, the purpose of this study was to investigate the possible mechanism of MYLK‐AS1. A total of 62 colon cancer (CC) specimens and paired adjacent normal tissues were collected, and the expression of MYLK‐AS1, microRNA (miR)‐101‐5p/cell division cycle 42 (CDC42) was detected. CC cell lines were transfected with MYLK‐AS1, miR‐101‐5p, CDC42‐related plasmids, and the biological functions and markers of epithelial‐mesenchymal transition (EMT) were analyzed. The binding relationship between MYLK‐AS1, miR‐101‐5p, and CDC42 was evaluated. In CC tissues and cell lines, MYLK‐AS1 and CDC42 were highly expressed, and miR‐101‐5p was lowly expressed. Inhibition of MYLK‐AS1 or upregulation of miR‐101‐5p can inhibit CC cell growth and EMT. miR‐101‐5p inhibited CDC42/N‐wasp axis activation in CC cells by targeting CDC42. Knockdown of CDC42 or upregulation of miR‐101‐5p partially reversed the effects caused by upregulation of MYLK‐AS1. MYLK‐AS1, which is significantly upregulated in CC, may be a molecular sponge for miR‐101‐5p, and MYLK‐AS1 promotes the activation of the CDC42/N‐wasp axis in CC cells by targeting CDC42 through miR‐101‐5p, which in turn promotes tumor development. MYLK‐AS1 may be a potential biomarker and target for CC therapy.

show abstract

Section: Discussionsupporting

confidence: 70%

LncRNA MYLK antisense RNA 1 activates cell division cycle 42/Neutal Wiskott‐Aldrich syndrome protein pathway via microRNA‐101‐5p to accelerate epithelial‐to‐mesenchymal transition of colon cancer cells

Quan,

Xu,

Huang

et al. 2023

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

show abstract

“…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 ]. lncRNA SNHG15 was increased in human cancers and can contribute to cell proliferation by acting as a sponge for miRNAs [ 34 ].…”

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

View full text Add to dashboard Cite

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.

show abstract

“…The binding of lncRNAs (as ceRNAs) to miRNAs prevents the latter from recognizing their targets, which consequently results in mRNA upregulation. Therefore, during malignant transformation, oncogenic lncRNAs intensify cancer promotion via the downregulation of miRNAs targeting different driver oncogenes (24,25).…”

Section: Introductionmentioning

confidence: 99%

Construction and analysis of the CDKN2B-AS1 ceRNA network associated with KRAS-dependent tumorigenesis in colorectal and pancreatic cancer

Saliani,

Javadmanesh,

Gonbadi

et al. 2024

Preprint

View full text Add to dashboard Cite

Kirsten rat sarcoma viral oncogene homolog (KRAS) exhibits the highest mutation rate in colorectal cancer (CRC) and pancreatic cancer (PC), highlighting the need for a comprehensive understanding of KRAS-dependent pathogenesis. Given the regulatory role of long noncoding RNAs (lncRNAs) in gene expression, this study focused on constructing a competing endogenous RNA (ceRNA) network of selected KRAS-related lncRNAs. By analyzing the transcriptional profiles of CRC and PC cell lines with and without KRAS mutations, differentially expressed genes (DEGs) were identified using sequencing data from the Sequencing Read Archive database. Notably, the analysis revealed 42 common upregulated DEGs (uDEGs), including differentially expressed lncRNAs and protein-coding genes, between KRAS-mutant and KRAS-wild-type cells. Among them, CDKN2B-AS1 emerged as a key KRAS-related lncRNA for the construction of the ceRNA network. Using LncTarD, miRWalk, and ToppCluster servers, a robust ceRNA network of CDKN2B-AS1 was constructed to elucidate the interactions between corresponding miRNAs and target genes. This network included 21 miRNAs and 34 genes selected from common uDEGs. Enrichment analysis of ceRNA target genes validated their involvement in critical cancer-related pathways and biological processes. Crucially, expression and survival analysis underscored the prognostic significance of selected target genes within the CDKN2B-AS1 ceRNA network. By delineating the regulatory mechanisms of the CDKN2B-AS1 ceRNA network, this study sheds light on the molecular and cellular pathways involved in KRAS-associated tumorigenesis.

show abstract

Downregulation of the long noncoding RNA SNHG1 inhibits tumor cell migration and invasion by sponging miR‐195 through targeting Cdc42 in oesophageal cancer

Cited by 13 publications

References 25 publications

LncRNA MYLK antisense RNA 1 activates cell division cycle 42/Neutal Wiskott‐Aldrich syndrome protein pathway via microRNA‐101‐5p to accelerate epithelial‐to‐mesenchymal transition of colon cancer cells

LncRNA MYLK antisense RNA 1 activates cell division cycle 42/Neutal Wiskott‐Aldrich syndrome protein pathway via microRNA‐101‐5p to accelerate epithelial‐to‐mesenchymal transition of colon cancer cells

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

Construction and analysis of the CDKN2B-AS1 ceRNA network associated with KRAS-dependent tumorigenesis in colorectal and pancreatic cancer

Contact Info

Product

Resources

About