Circ0001429 regulates progression of bladder cancer through binding miR-205-5p and promoting VEGFA expression

Cao, Weijun; Zhao, Youguang; Wang, Liang; Huang, Xiaoke

doi:10.3233/cbm-182380

Cited by 51 publications

(54 citation statements)

References 31 publications

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“…As a member of the growth factor family, VEGFA has a large capacity to stimulate the angiogenic milieu, as it can increases microvascular density and vascular permeability, which promotes tumour angiogenesis and metastasis and leads to the resistance of tumours to antiangiogenic therapy [98]. Similarly, circ0001429 was found to upregulate VEGFA expression by sponging miR-205-5p to promote the growth and metastasis of bladder cancer cells [99]. CircSCAF11 activates the VEGFA transcription via the miR-421/SP1/VEGFA axis, which stimulates angiogenesis and tumourigenesis of glioma [100].…”

Section: Promoting Angiogenesismentioning

confidence: 99%

Roles of circRNAs in the tumour microenvironment

et al. 2020

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The tumour microenvironment (TME) constitutes the area surrounding the tumour during its development and has been demonstrated to play roles in cancer-related diseases through crosstalk with tumour cells. Circular RNAs (circRNAs) are a subpopulation of endogenous noncoding RNAs (ncRNAs) that are ubiquitously expressed in eukaryotes and have multiple biological functions in the regulation of cancer onset and progression. An increasing number of studies have shown that circRNAs participate in the multifaceted biological regulation of the TME. However, details on the mechanisms involved have remained elusive until now. In this review, we analyse the effects of circRNAs on the TME from various perspectives, including immune surveillance, angiogenesis, hypoxia, matrix remodelling, exo-circRNAs and chemoradiation resistance. Currently, the enormous potential for circRNA use in targeted therapy and as noninvasive biomarkers have drawn our attention. We emphasize the prospect of targeting circRNAs as an essential strategy to regulate TME, overcome cancer resistance and improve therapeutic outcomes.

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Section: Promoting Angiogenesismentioning

confidence: 99%

Roles of circRNAs in the tumour microenvironment

et al. 2020

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“…7 In addition, we have identified some potential targets of miR-205-5p and their biological processes. 7,[11][12][13]47 Moreover, it has been suggested that miR-205-5p could interact indirectly via PI3K/AKT also involved in angiogenesis. In fact, it F I G U R E 5 VEGFA-mediated Vasculogenesis is regulated by miR-205-5p.…”

Section: Vegfa Mrna As a Mir-205-5p Targetmentioning

confidence: 99%

“…Statistically significant differences were set at *P < .05 is well documented that miR-205-5p acts as a tumour suppressor by regulating cell migration and proliferation. 7,[11][12][13]47 Moreover, it has been suggested that miR-205-5p could interact indirectly via PI3K/AKT also involved in angiogenesis. 13 In the present report, we have observed that VEGFA and miR-205-5p are inversely expressed ( Figure 3), inducing angiogenesis.…”

Section: Vegfa Mrna As a Mir-205-5p Targetmentioning

confidence: 99%

Oxidative stress‐induced angiogenesis is mediated by miR‐205‐5p

Oltra

Vidal-Gil

Maisto³

et al. 2019

J Cellular Molecular Medi

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miR‐205‐5p is known to be involved in VEGF‐related angiogenesis and seems to regulate associated cell signalling pathways, such as cell migration, proliferation and apoptosis. Therefore, several studies have focused on the potential role of miR‐205‐5p as an anti‐angiogenic factor. Vascular proliferation is observed in diabetic retinopathy and the ‘wet’ form of age‐related macular degeneration. Today, the most common treatments against these eye‐related diseases are anti‐VEGF therapies. In addition, both AMD and DR are typically associated with oxidative stress; hence, the use of antioxidant agents is accepted as a co‐adjuvant therapy for these patients. According to previous data, ARPE‐19 cells release pro‐angiogenic factors when exposed to oxidative insult, leading to angiogenesis. Matching these data, results reported here, indicate that miR‐205‐5p is modulated by oxidative stress and regulates VEGFA‐angiogenesis. Hence, miR‐205‐5p is proposed as a candidate against eye‐related proliferative diseases.

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“…For example, the low expression of miR‐199a‐5p inhibited the proliferation of scar fibroblasts by stagnating the cells at S stage or G2/M stage (Chen et al, ; Guo et al, ). Additionally, low expression of miR‐205‐5p inhibited VEGF pathway, which could damage keloid fibroblasts express activity obviously (Cao, Zhao, Wang, & Huang, ). Besides, other miRNAs with low expression or downregulation were miR‐7, miR‐451, miR‐720, and and so forth, they all play a role in the formation of HTS.…”

Section: The Epigenetic Mechanism Regulating the Formation Of Myofibrmentioning

confidence: 99%

Molecular mechanism of myofibroblast formation and strategies for clinical drugs treatments in hypertrophic scars

Zhu

Hou

et al. 2019

Journal Cellular Physiology

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Hypertrophic scars (HTS) commonly occurred after burn and trauma. It was characterized by the excessive deposition of extracellular matrix with the inadequate remodeling, which could result in severe physiological and psychological problems.However, the effective available prevention and treatment measures were still limited. The main pathological feature of HTS was the excessive formation of myofibroblasts, and they persist in the repaired tissue. To better understand the mechanics of this process, this review focused on the characteristics and formation of myofibroblasts, the main effector cells in HTS. We summarized the present theories and opinions on myofibroblasts formation from the perspective of related signaling pathways and epigenetic regulation, such as DNA methylation, miRNA/lncRNA/ ceRNA action, histone modification, and so forth for a better understanding on the development of HTS. This information might assist in developing effective experimental and clinical treatment strategies. Additionally, we also summarized currently known clinical strategies for HTS treatment, including traditional drugs, molecular medicine, stem cells, and exosomes. K E Y W O R D S epigenetic mechanism, extracellular matrix, hypertrophic scars, myofibroblast, stem cells

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Circ0001429 regulates progression of bladder cancer through binding miR-205-5p and promoting VEGFA expression

Cited by 51 publications

References 31 publications

Roles of circRNAs in the tumour microenvironment

Roles of circRNAs in the tumour microenvironment

Oxidative stress‐induced angiogenesis is mediated by miR‐205‐5p

Molecular mechanism of myofibroblast formation and strategies for clinical drugs treatments in hypertrophic scars

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