RETRACTED: CCDC88A Post-Transcriptionally Regulates VEGF via miR-101 and Subsequently Regulates Hepatocellular Carcinoma

Hu, Qiongying; Li, Yuchen; Chen, Hongqing; Liao, Hongyan; He, Yong; Zheng, Qin

doi:10.3389/fimmu.2022.859331

Cited by 10 publications

(10 citation statements)

References 36 publications

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“…TEAD2 has been found to be relevant to tumor suppression by restricting proliferation and promoting apoptosis through the Hippo signaling pathway [42,43]. CCDC88A serves as a nonreceptor guanine nucleotide exchange factor which binds to and activates guanine nucleotide-binding protein G (i) alpha subunits, involved in multiple biological processes, such as cell migration and cellular immunity [44][45][46][47][48]. However, the specific role of these six genes in CLL has not been reported yet.…”

Section: Discussionmentioning

confidence: 99%

Identification of Six Diagnostic Biomarkers for Chronic Lymphocytic Leukemia Based on Machine Learning Algorithms

Zhu

Xin-jin

Qin

et al. 2022

Journal of Oncology

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Background. Chronic lymphocytic leukemia (CLL) is the most common type of leukemia in adults. Thus, novel reliable biomarkers need to be further explored to increase diagnostic, therapeutic, and prognostic effectiveness. Methods. Six datasets containing CLL and control samples were downloaded from the Gene Expression Omnibus database. Differential gene expression analysis, weighted gene coexpression network analysis (WGCNA), and the least absolute shrinkage and selection operator (LASSO) regression were applied to identify potential diagnostic biomarkers for CLL using R software. The diagnostic performance of the hub genes was then measured by the receiver operating characteristic (ROC) curve analysis. Functional analysis was implemented to uncover the underlying mechanisms. Additionally, correlation analysis was performed to assess the relationship between the hub genes and immunity characteristics. Results. A total number of 47 differentially expressed genes (DEGs) and 25 candidate hub genes were extracted through differential gene expression analysis and WGCNA, respectively. Based on the 14 overlapped genes between the DEGs and the candidate hub genes, LASSO regression analysis was used, which identified a final number of six hub genes as potential biomarkers for CLL: ABCA6, CCDC88A, PMEPA1, EBF1, FILIP1L, and TEAD2. The ROC curves of the six genes showed reliable predictive ability in the training and validation cohorts, with all area under the curve (AUC) values over 0.80. Functional analysis revealed an abnormal immune status in the CLL patients. A significant correlation was found between the hub genes and the immune-related pathways, indicating a possible tight connection between the hub genes and tumor immunity in CLL. Conclusion. This study was based on machine learning algorithms, and we identified six genes that could be possible CLL markers, which may be involved in CLL pathogenesis and progression through immune-related signal pathways.

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Section: Discussionmentioning

confidence: 99%

Identification of Six Diagnostic Biomarkers for Chronic Lymphocytic Leukemia Based on Machine Learning Algorithms

Zhu

Xin-jin

Qin

et al. 2022

Journal of Oncology

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“…The decreased miR-101 promotes cancer cell proliferation by increasing the expression of numerous oncogenes. In hepatocellular carcinoma, miR-101 is proven to specifically bind to vascular endothelial growth factor (VEGF) mRNA three prime untranslated region (3′-UTR) to decrease protein levels of VEGFA (one of the main isotypes of VEGF) [ 21 ] and inhibit VEGFR2 signaling pathway thereby impair the malignant behavior of HCC cells. MiR-101 could also inhibit the proliferation of liver cancer cells by targeting zinc finger protein 217 (ZNF217), mitogen-activated protein kinases (MAPK)/extracellular signal-regulated kinase (ERK) signaling pathways, and hepatocyte growth factor (HGF)/c-MET axis [ 22 , 23 , 24 ].…”

Section: Mir-101 Regulates Cancer Growth Metastasis and Therapeutic R...mentioning

confidence: 99%

“…By using the liver cancer model, Wang et al found that overexpression of miR-101 could significantly reduce the level of VEGF, and further studies confirmed that miR-101 affected the secretion of VEGF by inhibiting the expression of junB proto-oncogene/AP-1 transcription factor subunit (JunB) [ 73 ]. MiR-101 was found to target VEGF mRNA 3′-UTR to regulate its expression in hepatocellular carcinoma [ 21 ]. Moreover, the VEGF mRNA is also identified as the target of miR-101 in cholangiocarcinoma cells.…”

Section: Mir-101 Inhibits Cancer By Remodeling the Tumor Ecosystemmentioning

confidence: 99%

“…However, in breast cancer cells, we found that miR-101 can target and down-regulate VHL expression, which is a negative regulator of hypoxia-inducible factor 1 subunit alpha (HIF1α) to increase HIF-1α expression and HIF-1α downstream target VEGFA expression. MiR-101 could promote angiogenesis by indirectly promoting VEGFA gene expression [ 21 ]. As described above, miR-101 can improve blood perfusion in the ischemic hind limbs of mice, confirming that hypoxia-induced miR-101 plays an important role in angiogenesis and vascular remodeling after ischemia [ 122 ].…”

Section: Mir-101 Inhibits Cancer By Remodeling the Tumor Ecosystemmentioning

confidence: 99%

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MiR-101: An Important Regulator of Gene Expression and Tumor Ecosystem

Liu

Yang

Gao

et al. 2022

Cancers

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MiRNAs are small single-stranded non-coding RNAs. MiRNA contributes to the transcriptional and post-transcriptional regulation of mRNA in different cell types, including mRNA transcription inhibition and mRNA decay and phenotypes via the effect of several essential oncogenic processes and tumor microenvironment. MiR-101 is a highly conserved miRNA that was found to alter the expression in various human cancers. MiR-101 has been reported to have tumor oncogenic and suppressive effects to regulate tumorigenesis and tumor progression. In this review, we summarize the new findings about the roles of miR-101 in cancers and the underlying mechanisms of targeting genes degradation and microenvironment regulation, which will improve biological understanding and design of novel therapeutics.

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“…In these studies of HCC, many miRNAs have been proven to be involved in the regulation of tumor proliferation, invasion and metastasis [ 16 , 17 , 18 ]. For example, Qiongying Hu et al [ 19 ] confirmed that miR-101 can suppress HCC progression by decreasing the expression level of VEGF. MiRNAs may become novel breakthroughs or therapeutic targets for seeking new therapeutic methods for HCC.…”

Section: Introductionmentioning

confidence: 99%

Genistein Restricts the Epithelial Mesenchymal Transformation (EMT) and Stemness of Hepatocellular Carcinoma via Upregulating miR-1275 to Inhibit the EIF5A2/PI3K/Akt Pathway

Yang

Jiang

Kong

et al. 2022

Biology

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Purpose: Genistein is a natural phytoestrogen with various antitumor effects. In recent years, some microRNAs (miRNA) in cancer cells have been reported to be regulated by genistein. Our study focused on exploring the mechanisms of miRNA upregulation to inhibit the epithelial mesenchymal transformation (EMT) and stemness of hepatocellular carcinoma (HCC). Patients and Methods: MiR-1275 was discovered by the transcriptome sequencing of miRNA expression profiles in HepG2 cells treated with genistein or DMSO as a control. Then, we performed series functional experiments in vitro and vivo to explore the relationship between genistein and miR-1275 in HCC. The target gene (Eukaryotic initiation factor 5A2, EIF5A2) of miR-1275 was predicted by databases and finally determined by a dual luciferase reporter assay. The downstream signaling pathway of EIF5A2 was assessed by bioinformatics analysis and Western blot. Results: the inhibition of genistein on the viability of HCC cells was enhanced by the increase in treatment time and dose, but it had no obvious inhibitory effect on normal hepatocytes (QSG-7701). Through qRT-PCR and transcriptome sequencing, we discovered that miR-1275 was lowly expressed in HCC, and it can be raised by genistein. The overall survival (OS) and recurrence-free survival (RFS) of HCC patients with lowly expressed miR-1275 were lower than those of those with high expression levels. In vitro and vivo experiments exhibited that genistein and the overexpression of miR-1275 can both significantly suppress the proliferation, migration, invasion, metastasis, EMT and stemness of HCC. Moreover, the inhibition can be further enhanced when miR-1275 mimic and genistein exist together. Finally, we demonstrated that miR-1275 can inhibit the epithelial mesenchymal transformation (EMT) and stemness of HCC via inhibiting the EIF5A2/PI3K/Akt pathway. Conclusion: Our findings proved that genistein can inhibit the EIF5A2/PI3K/Akt pathway by upregulating miR-1275 so as to attenuate the EMT and stemness of HCC cells to restrict their progression and metastasis.

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RETRACTED: CCDC88A Post-Transcriptionally Regulates VEGF via miR-101 and Subsequently Regulates Hepatocellular Carcinoma

Cited by 10 publications

References 36 publications

Identification of Six Diagnostic Biomarkers for Chronic Lymphocytic Leukemia Based on Machine Learning Algorithms

Identification of Six Diagnostic Biomarkers for Chronic Lymphocytic Leukemia Based on Machine Learning Algorithms

MiR-101: An Important Regulator of Gene Expression and Tumor Ecosystem

Genistein Restricts the Epithelial Mesenchymal Transformation (EMT) and Stemness of Hepatocellular Carcinoma via Upregulating miR-1275 to Inhibit the EIF5A2/PI3K/Akt Pathway

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