RASA1 inhibits the progression of renal cell carcinoma by decreasing the expression of miR-223-3p and promoting the expression of <i>FBXW7</i>

Zhang, Ruili; Aimudula, Ainiwaer; Bao, Yongxing

doi:10.1042/bsr20194143

Cited by 17 publications

(14 citation statements)

References 42 publications

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“…The results revealed miR-223-3p could bind directly to solute carrier family 4, member 4 (SLC4A4) mRNA, and reduced SLC4A4 mRNA and protein expression, which was associated with KRAS signaling and epithelial-mesenchymal transition [ 36 ]. Besides, Zhang et al's study confirmed the carcinogenesis of miR-223-3p and found RASA1 may play a key role in the progression of RCC by decreasing miR-223-3p and subsequently increasing FBXW7 expression [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Deciphering a Novel Necroptosis-Related miRNA Signature for Predicting the Prognosis of Clear Cell Renal Carcinoma

Bao

Lin

et al. 2022

Analytical Cellular Pathology

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Clear cell renal cell carcinoma (ccRCC) is the most common histological and devastating subtype of renal cell carcinoma. Necroptosis is a form of programmed cell death that causes prominent inflammatory responses. miRNAs play a significant role in cancer progression through necroptosis. However, the prognostic value of necroptosis-related miRNAs remains ambiguous. In this study, 39 necroptosis-related miRNAs (NRMs) were extracted and 17 differentially expressed NRMs between normal and tumor samples were identified using data form The Cancer Genome Atlas (TCGA). After applying univariate Cox proportional hazard regression analysis and LASSO Cox regression model, six necroptosis-related miRNA signatures were identified in the training cohort and their expression levels were verified by qRT-PCR. Using the expression levels of these miRNAs, all patients were divided into the high- and low-risk groups. Patients in the high-risk group showed poor overall survival ( P < 0.0001 ). Time-dependent ROC curves confirmed the good performance of our signature. The results were verified in the testing cohort and the entire TCGA cohort. Univariate and multivariate Cox regression models demonstrated that the risk score was an independent prognostic factor. Additionally, a predictive nomogram with good performance was constructed to enhance the implementation of the constructed signature in a clinical setting. We then employed miRBD, miRTarBase, and TargetScan to predict the target genes of six necroptosis-related miRNAs. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses indicated that 392 potential target genes were enriched in cell proliferation-related biological processes. Six miRNAs and 59 differentially expressed target genes were used to construct an miRNA–mRNA interaction network, and 11 hub genes were selected for survival and tumor infiltration analysis. Drug sensitivity analysis revealed potential drugs that may contribute to cancer management. Hence, necroptosis-related genes play an important role in cancer biology. We developed, for the first time, a necroptosis-related miRNA signature to predict ccRCC prognosis.

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Section: Discussionmentioning

confidence: 99%

Deciphering a Novel Necroptosis-Related miRNA Signature for Predicting the Prognosis of Clear Cell Renal Carcinoma

Bao

Lin

et al. 2022

Analytical Cellular Pathology

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“…RASA1 inhibits renal tissue brosis by reducing myo broblasts proliferation 19 . In kidney carcinoma, RASA1 reduces miR-223-3p expression to inhibit the proliferation and differentiation of renal cell carcinoma 20 . YT521-B homology domain containing 2(YTHDC2) is an m6A reader that expedites messenger ribonucleic acid (mRNA) decay.…”

Section: Discussionmentioning

confidence: 99%

Identification of Ferroptosis-Related Genes and Pathways in Diabetic Kidney Disease Using Bioinformatics Analysis

Liu

Zhou

et al. 2022

Preprint

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Diabetic kidney disease (DKD) is a major public health issue because of its refractory nature. Ferroptosis is a newly coined programmed cell death characterized by the accumulation of lipid reactive oxygen species (ROS). However, the prognostic and diagnostic value of ferroptosis-related genes (FRGs) and their biological mechanisms in DKD remain elusive. The gene expression profiles GSE96804, GSE30566, GSE99339 and GSE30528 were obtained and analyzed. We constructed a reliable prognostic model for DKD consisting of eight FRGs (SKIL, RASA1, YTHDC2, SON, MRPL11, HSD17B14, DUSP1 and FOS). The receiver operating characteristic (ROC) curves showed that the ferroptosis-related model had predictive power with an area under the curve (AUC) of 0.818. Gene functional enrichment analysis showed significant differences between the DKD and normal groups, and ferroptosis played an important role in DKD. Consensus clustering analysis showed four different ferroptosis types, and the risk score of type four was significantly higher than that of other groups. Immune infiltration analysis indicated that the expression of macrophages M2 increased significantly, while that of neutrophils decreased significantly in the high-risk group. Our study identified and validated the molecular mechanisms of ferroptosis in DKD. FRGs could serve as credible diagnostic biomarkers and therapeutic targets for DKD.

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“…PFKL-WT or PFKL-MUT was co-transfected with miR-185-3p mimic into H1299/ER or A549/ER cells. After transfection for 48 h, H1299/ER and A549/ER cells were evaluated using the Reporter Vector System (AM5795, Invitrogen, CA, United States) using a GloMax 20/20 Luminometer (Promega, WI, United States) ( Zhang et al, 2020 ).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of miR-185-3p Confers Erlotinib Resistance Through Upregulation of PFKL/MET in Lung Cancers

Zhu

Yuan

2021

Front. Cell Dev. Biol.

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Erlotinib (ER), as an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), has a significant therapeutic effect in lung cancers. However, EGFR TKI resistance inevitably occurs after treatment for approximately 12 months, which weakens its antitumor effect. Here, we identified miR-185-3p as a significantly downregulated microRNA responsible for acquired EGFR TKI resistance in cells and patients with lung cancer. qRT-PCR and Western Blot were performed to determine the relative expression of miR-185-3p in ER-resistant tumor tissues and cells. The viability and apoptosis of lung cancer cells were evaluated by Cell Counting Kit-8 (CCK8) assay and flow cytometry, respectively. The binding between miR-185-3p and liver-type phosphofructokinase (PFKL) was verified by dual luciferase assay. It was found that overexpression of miR-185-3p conferred ER sensitivity in lung cancer cell lines. MiR-185-3p was downregulated in ER-resistant lung cancer cells (H1299/ER and A549/ER). MiR-185-3p inhibited proliferation and induced cell apoptosis in ER-resistant cells. Mechanistically, miR-185-3p downregulation contributed to ER resistance through upregulating the PFKL. Moreover, Mesenchymal to epithelial transition (MET) oncoprotein promoted EGFR-TKI resistance by regulating miR-185-3p and PFKL. These findings revealed a novel mechanism in which downregulation of miR-185-3p may induce overexpression of PFKL and MET and confer ER resistance in lung cells. Combination of PFKL/MET inhibitors and EGFR TKIs could be a rational therapeutic approach for lung cancer patients with EGFR mutation.

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RASA1 inhibits the progression of renal cell carcinoma by decreasing the expression of miR-223-3p and promoting the expression of FBXW7

Cited by 17 publications

References 42 publications

Deciphering a Novel Necroptosis-Related miRNA Signature for Predicting the Prognosis of Clear Cell Renal Carcinoma

Deciphering a Novel Necroptosis-Related miRNA Signature for Predicting the Prognosis of Clear Cell Renal Carcinoma

Identification of Ferroptosis-Related Genes and Pathways in Diabetic Kidney Disease Using Bioinformatics Analysis

Inhibition of miR-185-3p Confers Erlotinib Resistance Through Upregulation of PFKL/MET in Lung Cancers

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