LncRNA HCG11/miR‐26b‐5p/QKI5 feedback loop reversed high glucose‐induced proliferation and angiogenesis inhibition of HUVECs

Du, Jianxiu; Han, Ruijuan; Li, Yihua; Liu, Xiaolin; Liu, Shurong; Cai, Zhenyu; Xu, Zhao-Long; Li, Ya; Yuan, Xiaoyi; Guo, Xin; Lü, Bin; Sun, Kai

doi:10.1111/jcmm.16040

Cited by 15 publications

(14 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, suppression of miR-214 expression may be a possible treatment for atherosclerotic CVDs. Other miRNAs, such as miR-26b-5p, miR-17-5p, and miR-181-5p, show inhibitory effects on TCF7L2 expression similar to those of miR-217 (122,123). Moreover, miR-26b-5p and miR-17-5p can promote adipogenic differentiation by downregulating TCF7L2 expression (124).…”

Section: Therapeutic Strategies To Promote Tcf7l2 Expressionmentioning

confidence: 93%

Transcription Factor-7-Like-2 (TCF7L2) in Atherosclerosis: A Potential Biomarker and Therapeutic Target

Zhou

Ouyang

et al. 2021

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

Transcription factor-7-like-2 (TCF7L2), a vital member of the T-cell factor/lymphoid enhancer factor (TCF/LEF) family, plays an important role in normal human physiological and pathological processes. TCF7L2 exhibits multiple anti-atherosclerotic effects through the activation of specific molecular mechanisms, including regulation of metabolic homeostasis, macrophage polarization, and neointimal hyperplasia. A single-nucleotide substitution of TCF7L2, rs7903146, is a genetic high-risk factor for type 2 diabetes and indicates susceptibility to cardiovascular disease as a link between metabolic disorders and atherosclerosis. In this review, we summarize the anti-atherosclerosis effect and novel mechanisms underlying the function of TCF7L2 to elucidate its potential as an anti-atherosclerosis biomarker and provide a novel therapeutic target for cardiovascular diseases.

show abstract

Section: Therapeutic Strategies To Promote Tcf7l2 Expressionmentioning

confidence: 93%

Transcription Factor-7-Like-2 (TCF7L2) in Atherosclerosis: A Potential Biomarker and Therapeutic Target

Zhou

Ouyang

et al. 2021

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

show abstract

“…LINC00657 represses miR-26b-5p and enhances COMMD8 expression to promote NSCLC progression [ 27 ]. In addition, lncRNA HCG11 participates in the regulation of HUVEC proliferation by suppressing miR-26b-5p on QKI-5 expression [ 28 ]. These results support the idea that miR-26b-5p is implicated in the negative regulation of cell growth, which is consistent with our findings.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-26b-5p suppresses the proliferation of tongue squamous cell carcinoma via targeting proline rich 11 (PRR11)

Liu

et al. 2021

Bioengineered

View full text Add to dashboard Cite

MicroRNAs (miRNAs) have been proved to be involved in many biological processes during tumorigenesis and progression, including cell proliferation and cell cycle progression. However, the potential role of miR-26b-5p in tongue squamous cell carcinoma (TSCC) remains unclear. In the present study, we demonstrated that miR-26b-5p was decreased in TSCC tissues in both TCGA-TSCC subset and eight paired samples from TSCC patients, while Proline Rich 11 (PRR11) was obviously increased. Transfection of miR-26b-5p mimics inhibited CALL7 cell proliferation by arresting the cells at the S/G2 transition. Meanwhile, miR-26b-5p inhibitor had the opposite biological functions. The results of luciferase activity and RNA-pulldown assays indicated that miR-26b-5p directly targeted the PRR11 3 -untranslated region in CAL27 cells. Furthermore, the effects of miR-26b-5p on cell cycle regulation were reversed after treatment with siRNA against PRR11. In summary, our findings indicate that miR-26b-5p induce cell cycle arrest in TSCC by targeting PRR11. Hence, targeting miR-26b-5p could be a promising therapeutic strategy for the treatment of TSCC.

show abstract

“…It has been reported that the main transcription products of QKI include QKi-5, QKi-6, and QKi-7, which have relatively conservative sequences, and the different sequences mainly exist in the C-terminal. These three QKI allosteric proteins all existed in vascular endothelial cells, and QKI-5 has the highest expression abundance [ 18 ]. Both QKI-5 and QKI-6 have a favorable impact on angiogenesis, but they play a different role in different cell types, showing the key influence of the unique C-terminal sequence on its function.…”

Section: Introductionmentioning

confidence: 99%

Regulation of the Proliferation of Diabetic Vascular Endothelial Cells by Degrading Endothelial Cell Functional Genes with QKI‐7

Zhao

Zhang

et al. 2022

Contrast Media & Molecular Imaging

View full text Add to dashboard Cite

Background. Diabetes has emerged as one of the most serious and common chronic diseases of our times, causing life-threatening, disabling and costly complications, and reducing life expectancy. Studies have shown that cardiovascular morbidity is 1–3 times higher in diabetic patients than in normal people. There are many clinical and experimental data that prove that most of the complications of diabetes are related to atherosclerosis, which suggests that chronic hyperglycemia may induce an imbalance in the proliferation of vascular endothelial cells. Purpose. This study aims to explore the relationship between QKI-7 and vascular endothelial cell dysfunction and lay a foundation for further clarifying the molecular mechanism of endothelial cell damage in the process of diabetes with atherosclerosis. Methods. We chose blood samples and pluripotent stem cells and vascular endothelial cells of hospitalized patients with diabetes and diabetes atherosclerosis as research subjects. The expression levels of endothelial cell proliferation and genes related to endothelial cell proliferation were analyzed by RT-qPCR and Western blot, to study the influence of QKi-7 on the physiological state of endothelial cells. Through gene knockdown experiment, the effects of QKi-7 knockdown on functional genes and physiological functions of endothelial cells were analyzed. Finally, RNA immunoprecipitation was used to test the mutual effect among QKI-7 and the transcription level of functional genes, and the mRNA attenuation experiment proved that QKI-7 participated in the degradation process of functional genes. Results. The findings of the RT-qPCR and Western blot tests revealed that QKI-7 was highly expressed in blood samples of diabetic patients and atherosclerosis as well as in endothelial cells induced by human pluripotent stem cells and human vascular endothelial cells after high-glucose treatment. Overexpression and high glucose of QKI-7 resulted in inhibiting expressed function genes CD144, NLGN1, and TSG6 and upregulation of inflammatory factors TNF-α, IL-1β, and IFN-γ, leading to excessive proliferation of endothelial cells. After QKI-7 gene knockdown, the expression levels of CD144, NLGN1, and TSG6, inflammatory factors TNF-α, IL-1β, and IFN-γ, and the cell proliferation rate all returned to normal levels. RNA immunoprecipitation showed that QKi-7 interacted with CD144, NLGN1, and TSG6 mRNAs and was involved in the transcriptional degradation of functional genes through their interactions. Conclusion. This research initially revealed the relevant molecular mechanism of QKI-7 leading to the excessive proliferation of endothelial cells in diabetic and atherosclerotic patients. In view of the role of QKI-7 in diabetic vascular complications, we provided a potential target for clinical diabetes treatment strategies in the future.

show abstract

LncRNA HCG11/miR‐26b‐5p/QKI5 feedback loop reversed high glucose‐induced proliferation and angiogenesis inhibition of HUVECs

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 15 publications

References 42 publications

Transcription Factor-7-Like-2 (TCF7L2) in Atherosclerosis: A Potential Biomarker and Therapeutic Target

Transcription Factor-7-Like-2 (TCF7L2) in Atherosclerosis: A Potential Biomarker and Therapeutic Target

MicroRNA-26b-5p suppresses the proliferation of tongue squamous cell carcinoma via targeting proline rich 11 (PRR11)

Regulation of the Proliferation of Diabetic Vascular Endothelial Cells by Degrading Endothelial Cell Functional Genes with QKI‐7

Contact Info

Product

Resources

About