&lt;p&gt;Long Noncoding RNA X-Inactive Specific Transcript Facilitates Cellular Functions in Melanoma via miR-139-5p/ROCK1 Pathway&lt;/p&gt;

Tian, Kui; Sun, Da; Chen, Min; Yang, Yifei; Wang, Fang; Guo, Taotao; Shi, Zhimin

doi:10.2147/ott.s225661

Cited by 14 publications

(7 citation statements)

References 29 publications

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“…Notably, XIST upregulation has been observed in some malignant tumors and was found to be associated with tumor cell growth, infiltration, and migration, higher TNM staging, and positive lymph node metastasis. 18 XIST has been shown to function as a “molecular sponge” of miR-139-5p in melanoma, 19 regulate the miR-133a/SOX4 axis in glioma 20 and miR-497 in gastric cancer, 11 and promote cell proliferation, invasion, and metastasis. In addition, XIST methylation status has been reported to modulate prostate cancer progression.…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA XIST Promotes Wilms Tumor Progression Through the miR-194-5p/YAP Axis

He¹,

Luo²,

Dong³

et al. 2021

CMAR

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Purpose Although the long non-coding RNA (lncRNA) X inactive-specific transcript (XIST) has been reported to have an anti-tumor effect in multiple malignant tumors, its role in Wilms tumor (WT) progression has not been characterized. Thus, we investigated the underlying mechanism by which XIST regulates WT progression. Patients and Methods We performed microarray analysis and real-time quantitative PCR (RT-qPCR) to detect the expression levels of XIST lncRNA, microRNA-194-5p (miR-194-5p), and YAP (yes-associated protein in Hippo pathway) in tumor and matched adjacent normal tissues and blood collected from 49 WT patients. We also conducted bioinformatics analyses to identify differentially expressed genes. We measured the effects of XIST overexpression and knockdown on cell proliferation, apoptosis, migration, and invasion, and its association with the miR-194-5p/YAP pathway in the rhabdoid G401cell line using flow cytometry, transwell assays, immunohistochemistry, Western blot analysis, and the dual luciferase reporter gene assay. Results We found that XIST lncRNA levels were increased in blood and tissue samples of WT patients, and this upregulation was significantly correlated with TNM staging and shorter survival time. Notably, we found that XIST upregulation correlated with miR-194-5p downregulation and YAP upregulation in WT tissues, suggesting that XIST regulates the miR-194-5p/YAP pathway. Conversely, XIST downregulation inhibited WT cell proliferation, migration, and invasion and induced apoptosis. Our study revealed the oncogenic role of the lncRNA XIST in WT and demonstrated its role as a competitive endogenous RNA that regulates the miR-194-5p/YAP pathway. Conclusion Our study demonstrates XIST’s potential as a clinical prognostic biomarker and therapeutic target for WT.

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Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA XIST Promotes Wilms Tumor Progression Through the miR-194-5p/YAP Axis

He¹,

Luo²,

Dong³

et al. 2021

CMAR

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“…The role of XIST in cancer has also been widely reported. Tian et al showed that XIST was highly expressed in melanoma cells 39 . Overexpression of XIST can promote the proliferation, migration, and invasion of melanoma cells.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis of lncRNA‑associated ceRNA network in melanoma

Ding¹,

Li²,

Tayier³

et al. 2021

J. Cancer

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Melanoma is an extremely malignant tumor with early metastasis and high mortality. Little is known about the process of by which melanoma occurs, as its mechanism is very complex and only limited data are available on its long non-coding RNA (lncRNA)-associated competing endogenous RNAs (ceRNAs). The purpose of this study was to screen out potential prognostic molecules and identify a ceRNA network related to the occurrence of melanoma. We screened 169 differentially expressed mRNAs (DEmRNAs) from E-MTAB-1862 and GSE3189; gene ontology (GO) enrichment analysis showed that these genes were closely related to the development of skin. In the protein-protein interaction network, we screened out a total of 19 hub genes. Furthermore, we predicted the microRNAs (miRNAs) that regulate hub genes using the miRWalk database and then intersected these with GSE35579, resulting in nine DEmiRNAs. We also predicted the lncRNAs that regulate the miRNAs using the LncBasev.2 database. According to the ceRNA hypothesis, and based on the intersection of the DElncRNAs with merged GTEx and TCGA data, we obtained 20 DElncRNAs. A total of four DEmRNAs, nine DEmiRNAs, and 20 DElncRNAs were included in the ceRNA network. Based on Cox stepwise regression and survival analysis, we identified five biomarkers, ZSCAN16-AS1, LINC00520, XIST, DTL, and let-7a-5p, and obtained risk scores. The results showed that most of the differentially expressed genes were related to epithelial-mesenchymal transition (EMT) in melanoma. Finally, we obtained a LINC00520/let-7a-5p/DTL molecular regulatory network. These results suggest that ceRNA networks have an important role in evaluating the prognosis of patients with melanoma and provide a new experimental basis for exploring the EMT process in the development of melanoma.

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“…miR-139-5p expression was significantly downregulated and positively correlated with ROCK1 expression during Ewing sarcoma progression ( 35 ). Moreover, the lncRNA X-inactive specific transcript was found to sponge miR-139-5p, thereby reducing the levels of ROCK1( 36 ). In the present study, miR-139-5p expression was reduced in the mice with sepsis-induced lung injury, whereas ROCK1 expression was significantly increased.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑139‑5p improves sepsis‑induced lung injury by targeting Rho‑kinase1

et al. 2021

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Sepsis-induced acute lung injury (ALI) is an inflammatory process that involves inflammatory cytokine production and cell apoptosis. In the present study, the regulatory role of microRNA (miR)-139-5p in sepsis-induced ALI was investigated using a murine model of cecal ligation puncture (CLP) and an in vitro model using lipopolysaccharide (LPS)-induced normal human bronchial epithelial cells (NHBEs). Sepsis-induced pathological changes in the lungs of ALI mice were detected using hematoxylin and eosin staining. Lung water content was determined, and the expression of proinflammatory cytokines in the bronchoalveolar lavage fluid and serum of sepsis-induced ALI mice were quantified using ELISA. The levels of oxidative stress in lung tissues were determined using commercial kits. The degree of apoptosis was determined using a TUNEL assay. The expression levels of miR-139-5p and Rho-kinase 1 (ROCK1) were determined using reverse transcription-quantitative PCR and western blot analyses. A dual-luciferase reporter assay was used to confirm the direct targeting of ROCK1 by miR-139-5p. NHBEs were co-transfected with vectors expressing ROCK1 (or empty vector) and miR-139-5p mimics or control mimics prior to LPS treatment. The transcriptional activity of caspase-3, the ratio of apoptotic cells, the expression levels of mucin 5AC, mucin 1, TNF-α, IL-1β, IL-6, NLR family pyrin domain containing 3, apoptosis-associated speck-like protein containing a CARD and caspase-1 were evaluated. Compared with the normal group, mice that underwent CLP exhibited abnormal lung morphology, enhanced production of TNF-α, IL-1β and IL-6, increased reactive oxygen species (ROS), malondialdehyde and lactate dehydrogenase levels, an increased proportion of apoptotic cells and increased ROCK1 expression. Superoxide dismutase, glutathione peroxidase and miR-139-5p levels were decreased following CLP. In the NHBEs, stimulation with LPS caused a marked increase in inflammatory cytokine levels and apoptosis compared with the untreated cells. Overexpression of miR-139-5p attenuated cell apoptosis and inflammation. Overexpression of ROCK1 in NHBEs restored the ROS levels and proinflammatory cytokine production inhibited by miR-139-5p. In conclusion, miR-139-5p alleviated sepsis-induced ALI via suppression of its downstream target, ROCK1, suggesting that miR-139-5p may hold promise in the treatment of sepsis-induced ALI.

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<p>Long Noncoding RNA X-Inactive Specific Transcript Facilitates Cellular Functions in Melanoma via miR-139-5p/ROCK1 Pathway</p>

Cited by 14 publications

References 29 publications

Long Non-Coding RNA XIST Promotes Wilms Tumor Progression Through the miR-194-5p/YAP Axis

Long Non-Coding RNA XIST Promotes Wilms Tumor Progression Through the miR-194-5p/YAP Axis

Bioinformatics analysis of lncRNA‑associated ceRNA network in melanoma

MicroRNA‑139‑5p improves sepsis‑induced lung injury by targeting Rho‑kinase1

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