miR-106b exerts tumor suppressive functions in ovarian carcinoma by directly targeting ZBTB7A

Yue, Ruiqin; Chen, Yuzhong; Wei, Lai; Wei, Wei

doi:10.23736/s0026-4806.20.06475-7

Cited by 5 publications

(3 citation statements)

References 4 publications

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“…reported that a novel inhibitor that served as a suicide substrate for MIF could effectively inhibit motility and growth of lung cancer cells ( 38 ). MiR-608 could suppress LUAD invasion and migration by directly targeting MIF ( 40 ). These results suggested that MIF could be a potential prognostic biomarker and therapeutic target for LUAD.…”

Section: Discussionmentioning

confidence: 99%

Construction of a Novel Ferroptosis-Related Gene Signature for Predicting Survival of Patients With Lung Adenocarcinoma

Song

Wang

et al. 2022

Front. Oncol.

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Lung adenocarcinoma (LUAD) is the most diagnosed subtype of lung cancer; ferroptosis is widely involved in the pathological cell death associated with various cancers, including lung cancer. However, the comprehensive relationship between ferroptosis and LUAD is little known in molecular levels until now. In the present study, 513 LUAD patients could be aggregated into three clusters by consensus clustering based on RNA sequencing data of 291 ferroptosis-related genes (FRGs) in The Cancer Genome Atlas (TCGA) database; cluster2 had significant survival advantage compared to the other two clusters. A novel prognostic model of 8 differential FRGs was constructed to effectively divide LUAD patients into high- or low-risk group according to the risk scores by the Cox and LASSO regression analyses. The overall survival of LUAD patients in the high-risk group was significantly worse in the TCGA and GEO cohorts. Moreover, patients with radiation therapy or high clinical stage had obviously higher risk scores. We validated the differential mRNA and protein expression of four FRGs in paired tumor and normal samples from our clinical cohort. Our study constructed a novel FRG signature to predict the prognosis of LUAD patients, which might provide a new prognostic tool and potential therapeutic targets for LUAD.

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Section: Discussionmentioning

confidence: 99%

Construction of a Novel Ferroptosis-Related Gene Signature for Predicting Survival of Patients With Lung Adenocarcinoma

Song

Wang

et al. 2022

Front. Oncol.

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“…At the transcriptional level, various non-coding microRNAs (miRNAs) regulate MIF expression by binding to its 3 ′ -untranslated region. Negative regulators of MIF and downregulated miRNAs include miRNA-451 (prostate cancer, neuroblastoma, gastric carcinoma, and hepatocellular carcinoma) [34][35][36][37], miRNA-144 and miRNA-1228 (hepatocellular carcinoma and gastric carcinoma) [37,38], and miRNA-608 (lung adenocarcinoma and glioblastoma) [39,40]. In contrast, MIF is positively regulated by miRNA-451 (colorectal carcinoma) and miRNA-301b (pancreatic carcinoma) [41][42][43].…”

Section: Mif and Ddt Structure And Regulationmentioning

confidence: 99%

Macrophage Migration Inhibitory Factor (MIF) and D-Dopachrome Tautomerase (DDT): Pathways to Tumorigenesis and Therapeutic Opportunities

Valdez,

Sánchez-Zuno,

Bucala

et al. 2024

IJMS

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Discovered as inflammatory cytokines, MIF and DDT exhibit widespread expression and have emerged as critical mediators in the response to infection, inflammation, and more recently, in cancer. In this comprehensive review, we provide details on their structures, binding partners, regulatory mechanisms, and roles in cancer. We also elaborate on their significant impact in driving tumorigenesis across various cancer types, supported by extensive in vitro, in vivo, bioinformatic, and clinical studies. To date, only a limited number of clinical trials have explored MIF as a therapeutic target in cancer patients, and DDT has not been evaluated. The ongoing pursuit of optimal strategies for targeting MIF and DDT highlights their potential as promising antitumor candidates. Dual inhibition of MIF and DDT may allow for the most effective suppression of canonical and non-canonical signaling pathways, warranting further investigations and clinical exploration.

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“…As a result, several target miRNAs that may interact with GS1-11520.1 were identified (Table S8). hsa-miR-608 has been confirmed to play a significant part in the apoptosis of NSCLC cells via the regulation of migration inhibitor factor (MIF), Akt serine/ threonine kinase 2 (AKT2) and transcription factor activation enhancer binding protein 4 (TFAP4) [47][48][49][50]; Dong et al found that hsa-miR-105-5p could be a biomarker for early diagnosis of NSCLC [51]; Zheng and other researchers found that hsa-miR-4651 elicited a negative effect on the progression of NSCLC via targeting bromodomain-containing protein 4 (BRD4) [52]; from a study by Wang's group, lncRNA LIFR-AS1 could inhibit NSCLC cell invasion and migration by serving as a sponge for hsa-miR-942-5p [53]; in patients suffering from anaplastic lymphoma kinase (ALK)-positive NSCLC, decreased hsa-miR-362-5p was accompanied by longer progression-free survival [54]. Therefore, we speculate that GS1-115G20.1 may interact with the above miRNAs to have an influence on the phenotype, treatment, and prognosis of NSCLC, but further validation of molecular experiments is still needed.…”

Section: Crucial Prognosis-related Lncrna Gs1-115g201 Is An Independe...mentioning

confidence: 99%

RYR2mutation in non‐small cell lung cancer prolongs survival via down‐regulation ofDKK1and up‐regulation ofGS1‐115G20.1: A weighted gene Co‐expression network analysis and risk prognostic models

Ren

Chen

et al. 2021

IET Systems Biology

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RYR2 mutation is clinically frequent in non‐small cell lung cancer (NSCLC) with its function being elusive. We downloaded lung squamous cell carcinoma and lung adenocarcinoma samples from the TCGA database, split the samples into RYR2 mutant group (n = 337) and RYR2 wild group (n = 634), and established Kaplan‐Meier curves. The results showed that RYR2 mutant group lived longer than the wild group (p = 0.027). Weighted gene co‐expression network analysis (WGCNA) of differentially expressed genes (DEGs) yielded prognosis‐related genes. Five mRNAs and 10 lncRNAs were selected to build survival prognostic models with other clinical features. The AUCs of 2 models are 0.622 and 0.565 for predicting survival at 3 years. Among these genes, the AUCs of DKK1 and GS1‐115G20.1 expression levels were 0.607 and 0.560, respectively, which predicted the 3‐year survival rate of NSCLC sufferers. GSEA identified an association of high DKK1 expression with TP53, MTOR, and VEGF expression. Several target miRNAs interacting with GS1‐115G20.1 were observed to show the relationship with the phenotype, treatment, and survival of NSCLC. NSCLC patients with RYR2 mutation may obtain better prognosis by down‐regulating DKK1 and up‐regulating GS1‐115G20.1.

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miR-106b exerts tumor suppressive functions in ovarian carcinoma by directly targeting ZBTB7A

Cited by 5 publications

References 4 publications

Construction of a Novel Ferroptosis-Related Gene Signature for Predicting Survival of Patients With Lung Adenocarcinoma

Construction of a Novel Ferroptosis-Related Gene Signature for Predicting Survival of Patients With Lung Adenocarcinoma

Macrophage Migration Inhibitory Factor (MIF) and D-Dopachrome Tautomerase (DDT): Pathways to Tumorigenesis and Therapeutic Opportunities

RYR2mutation in non‐small cell lung cancer prolongs survival via down‐regulation ofDKK1and up‐regulation ofGS1‐115G20.1: A weighted gene Co‐expression network analysis and risk prognostic models

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