miR-32-5p Inhibits the Proliferation, Migration and Invasion of Thyroid Cancer Cells by Regulating Twist1

Liu, Qing; Ouyang, Liang; Zhou, Chi; Wang, Yu; He, Chunxue; Li, Silei; Lu, Lu; Chen, Jidong

doi:10.21203/rs.3.rs-552882/v1

Cited by 3 publications

(3 citation statements)

References 2 publications

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“…POLE3 and POLE4 are the other two smaller subunits with relative molecular masses of 17,000 and 12,000, respectively. POLE 4 was observed to be associated with tumor proliferation and invasion in neuroblastoma [20]. MiR-7-5p inhibits tumor cell proliferation, migration and invasion by targeting different genes [21].…”

Section: Discussionmentioning

confidence: 98%

Functional characterization of the Polε protein family in hepatocellular carcinoma

Zhang

Liu

et al. 2023

Preprint

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Background: Numerous genetic sequencing projects have demonstrated that alterations in Polε (DNA polymerase epsilon ) due to various causes are associated with the development of multiple human cancers. However, the biological functions of its four core genes, POLE1/2/3/4/, in the occurrence, progression, and prognosis of hepatocellular carcinoma(HCC) remain poorly understood to date. Methods: Multi-omics, multi-level deep mining of HCC data from TCGA and other publicly available databases by using online analysis tools from GEPIA2, TIMER2.0, DAVID, Kaplan-Meier plotter, cBioPortal and MethSurv databases, as well asthe R package to assess Polε family members in HCC for their potential biological functions. Results: We found that the four target genes were significantly upregulated in HCC (P<0.001), their high expression was associated with a lower survival rate (P<0.05), and both diagnostic ROC curves and disease-specific survival time-dependent ROC curves suggested that POLE2/3 showed better disease predictive efficacy, and the four genes were significantly associated with immune infiltration, and drug sensitivity analysis suggested that the high expression groups of four target genes showed higher drug sensitivity in some chemotherapeutic drugs(P<0.001). Conclusion: The POLE1/2/3/4are potential prognostic predictive molecules for HCC and correlate with immune infiltration,and high expression of POLE may serve as a potential predictor of the effect of targeted therapies. POLE2/3 may be the potential diagnostic biomarkers for HCC, and the expression level of POLE3 may serve as a biological predictive target for HCC chemotherapy sensitivity.

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Section: Discussionmentioning

confidence: 98%

Functional characterization of the Polε protein family in hepatocellular carcinoma

Zhang

Liu

et al. 2023

Preprint

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“…In evaluation of studies and researches over the past decade it was discovered that miR-32 plays a wide range of regulatory roles in biological events, especially in tumorigenesis by targeting proteins such as E2F transcription factor 5, phosphatase and tensin homolog (PTEN), F-Box and WD repeat domain containing 7 (FBXW7), SRY-Box Transcription Factor 9 (Sox9), and Twist (Xu et al 2019 ; Yan et al 2015 ; Liu et al 2021 ; Yang et al 2019 ; Xia et al 2017 ).Based on the regulatory role of miR-32 in human cancer and the conserved sequence of miR-32 between humans and hamsters ( Crisetulus griseus) as well as its effects on cell proliferation, growth, and viability we hypothesized that overexpression of miR-32 in our CHO-VEGF-trap cells may increase the cell viability and the recombinant protein yield.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of miR-32 in Chinese hamster ovary cells increases production of Fc-fusion protein

et al. 2023

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The demand for industrial genetically modified host cells were increased with the growth of the biopharmaceutical market. Numerous studies on improving host cell productivity have shown that altering host cell growth and viability through genetic engineering can increase recombinant protein production. During the last decades, it was demonstrated that overexpression or downregulation of some microRNAs in Chinese Hamster Ovary (CHO) cells as the host cell in biopharmaceutical manufacturing, can improve their productivity. The selection of microRNA targets has been based on their previously identified role in human cancers. MicroRNA-32 (miR-32), which is conserved between humans and hamsters (Crisetulus griseus), was shown to play a role in the regulation of cell proliferation and apoptosis in some human cancers. In this study, we investigated the effect of miR-32 overexpression on the productivity of CHO-VEGF-trap cells. Our results indicated that stable overexpression of miR-32 could dramatically increase the productivity of CHO cells by 1.8-fold. It also significantly increases cell viability, batch culture longevity, and cell growth. To achieve these results, following the construction of a single clone producing an Fc-fusion protein, we transfected cells with a pLexJRed-miR-32 plasmid to stably produce the microRNA and evaluate the impact of mir-32 overexpression on cell productivity, growth and viability in compare with scrambled control. Our findings highlight the application of miRNAs as engineering tools and indicated that miR-32 could be a target for engineering CHO cells to increase cell productivity.

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“…Ophiopogonin B (OP-B), a saponin compound isolated from Ophiopogon japonicus (Thunb. ), has multi-target antitumor characteristics ( 21 – 23 ). In this study, analyses of the protein Gene Ontology (GO) terms and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways both exhibited OP-B as affecting the binding of intracellular ferric iron and regulating the gene expression in the ferroptosis-related pathway.…”

Section: Introductionmentioning

confidence: 99%

Induction of Ferroptosis by Ophiopogonin-B Through Regulating the Gene Signature AURKA in NSCLC

Gao

Wang

et al. 2022

Front. Oncol.

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Ferroptosis is a new type of iron-dependent programmed cell death. In recent years, its role in the diagnosis and treatment of multiple tumors, including non-small cell lung cancer (NSCLC), has been continuously observed. The relationship between the ferroptosis-related genes and the prognosis of patients with NSCLC needs to be clarified. In this study, The Cancer Genome Atlas (TCGA) and the Gene Expression Synthesis database (Gene Expression Omnibus, GEO) were used to build a model of ferroptosis-related differentially expressed genes (DEGs). A total of 101 ferroptosis-related DEGs were screened using R language, and a 12-gene signature was finally established through univariate Cox regression analysis and least absolute shrinkage and selection operator (LASSO)-penalized Cox regression analysis. According to the risk scores, the patients were divided into a high-risk or a low-risk group, with patients in the low-risk group showing better prognosis. AURKA, one of the genes in the 12-gene signature, was found to be highly expressed in tumors. In addition, further study verified AURKA to be a negative regulator of ferroptosis in NSCLC cells. Ophiopogonin B (OP-B) had been reported to induce apoptosis, mitotic catastrophe, and autophagy in NSCLC cells. Herein, proteomic sequencing analysis and OP-B administration revealed the upregulation of AURKA and the downregulation of PHKG2 and SLC7A5 in the 12-gene signature, indicating that OP-B induced ferroptosis in NSCLC. Determination of the concentrations of malondialdehyde (MDA), glutathione (GSH), and intracellular iron and the mitochondrial membrane potential (MMP) confirmed the induction of ferroptosis by OP-B in vitro. Furthermore, transmission electron microscopy (TEM) examination of lung cancer xenotransplantation in nude mice confirmed that OP-B induced ferroptosis in vivo. Further study of the molecular mechanism showed that the ferroptosis effect caused by OP-B can be partially reversed by the overexpression of AURKA. Overall, our study established a new ferroptosis-related risk prediction model for the prognosis of patients with NSCLC, revealed the enrichment pathways of ferroptosis in NSCLC, and discovered the negative regulation of AURKA in ferroptosis. On this basis, we demonstrated that OP-B can induce ferroptosis in NSCLC and clarified the specific molecular mechanism of OP-B inducing ferroptosis by regulating the expression of AURKA.

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miR-32-5p Inhibits the Proliferation, Migration and Invasion of Thyroid Cancer Cells by Regulating Twist1

Cited by 3 publications

References 2 publications

Functional characterization of the Polε protein family in hepatocellular carcinoma

Functional characterization of the Polε protein family in hepatocellular carcinoma

Overexpression of miR-32 in Chinese hamster ovary cells increases production of Fc-fusion protein

Induction of Ferroptosis by Ophiopogonin-B Through Regulating the Gene Signature AURKA in NSCLC

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