Elevated microRNA-7 inhibits proliferation and tumor angiogenesis and promotes apoptosis of gastric cancer cells via repression of Raf-1

Lin, Jing; Liu, Zewa; Liao, Shasha; Li, E; Wu, Xiaohua; Zeng, Wanting

doi:10.1080/15384101.2020.1807670

Cited by 18 publications

(9 citation statements)

References 31 publications

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“…In tumour tissue, cell apoptosis was induced by inhibiting angiogenesis, 40 and cardiac fibrosis had a negative correlation with cardiac angiogenesis 36,37 ; in this study, we demonstrated KN-93 suppressed myocardial angiogenesis, thereby cardiomyocyte apoptosis and cardiac fibrosis were all aggravated by KN-93, and the results were consistent with the previous studies.…”

Section: Discussionsupporting

confidence: 91%

CaMKII inhibitor KN‐93 impaired angiogenesis and aggravated cardiac remodelling and heart failure via inhibiting NOX2/mtROS/p‐VEGFR2 and STAT3 pathways

Deng

Bai

et al. 2021

J Cellular Molecular Medi

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Persistent cardiac Ca2+/calmodulin‐dependent Kinase II (CaMKII) activation was considered to promote heart failure (HF) development, some studies believed that CaMKII was a target for therapy of HF. However, CaMKII was an important mediator for the ischaemia‐induced coronary angiogenesis, and new evidence confirmed that angiogenesis inhibited cardiac remodelling and improved heart function, and some conditions which impaired angiogenesis aggravated ventricular remodelling. This study aimed to investigate the roles and the underlying mechanisms of CaMKII inhibitor in cardiac remodelling. First, we induced cardiac remodelling rat model by ISO, pre‐treated by CaMKII inhibitor KN‐93, evaluated heart function by echocardiography measurements, and performed HE staining, Masson staining, Tunel staining, Western blot and RT‐PCR to test cardiac remodelling and myocardial microvessel density; we also observed ultrastructure of cardiac tissue with transmission electron microscope. Second, we cultured HUVECs, pre‐treated by ISO and KN‐93, detected cell proliferation, migration, tubule formation and apoptosis, and carried out Western blot to determine the expression of NOX2, NOX4, VEGF, VEGFR2, p‐VEGFR2 and STAT3; mtROS level was also measured. In vivo, we found KN‐93 severely reduced myocardial microvessel density, caused apoptosis of vascular endothelial cells, enhanced cardiac hypertrophy, myocardial apoptosis, collagen deposition, aggravated the deterioration of myocardial ultrastructure and heart function. In vitro, KN‐93 inhibited HUVECs proliferation, migration and tubule formation, and promoted apoptosis of HUVECs. The expression of NOX2, NOX4, p‐VEGFR2 and STAT3 were down‐regulated by KN‐93; mtROS level was severely reduced by KN‐93. We concluded that KN‐93 impaired angiogenesis and aggravated cardiac remodelling and heart failure via inhibiting NOX2/mtROS/p‐VEGFR2 and STAT3 pathways.

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Section: Discussionsupporting

confidence: 91%

CaMKII inhibitor KN‐93 impaired angiogenesis and aggravated cardiac remodelling and heart failure via inhibiting NOX2/mtROS/p‐VEGFR2 and STAT3 pathways

Deng

Bai

et al. 2021

J Cellular Molecular Medi

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“…Subsequently, the cell suspension was delivered by subcutaneous injection into the right axilla lesions of nude mice. The length (L), width (W) and height (H) of the nodule lesions were measured every week and the lesion volumes were calculated according to the following formula [ 15 ]: V = π/6 (L x W x H). On the 84th day after cell inoculation, the mice were euthanized.…”

Section: Methodsmentioning

confidence: 99%

Upregulated Talin1 synergistically boosts β-estradiol-induced proliferation and pro-angiogenesis of eutopic and ectopic endometrial stromal cells in adenomyosis

Wang

Duan

Wang

et al. 2021

Reprod Biol Endocrinol

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Adenomyosis (ADS) is an estrogen-dependent gynecological disease with unspecified etiopathogenesis. Local hyperestrogenism may serve a key role in contributing to the origin of ADS. Talin1 is mostly identified to be overexpressed and involved in the progression of numerous human carcinomas through mediating cell proliferation, adhesion and motility. Whether Talin1 exerts an oncogenic role in the pathogenesis of ADS and puts an extra impact on the efficacy of estrogen, no relevant data are available yet. Here we demonstrated that the adenomyotic eutopic and ectopic endometrial stromal cells (ADS_Eu_ESC and ADS_Ec_ESC) treated with β-estradiol (β-E2) presented stronger proliferative and pro-angiogenetic capacities, accompanied by increased expression of PCNA, Ki67, VEGFB and ANGPTL4 proteins. Meanwhile, these promoting effects were partially abrogated by Fulvestrant (ICI 182780, an estrogen-receptor antagonist). Aberrantly upregulation of Talin1 mRNA and protein level was observed in ADS endometrial specimens and stromal cells. Through performing functional experiments in vitro, we further determined that merely overexpression of Talin1 (OV-Talin1) also enhanced ADS stromal cell proliferation and pro-angiogenesis, while the most pronounced facilitating effects were found in the co-intervention group of OV-Talin1 plus β-E2 treatment. Results from the xenograft nude mice model showed that the hypodermic endometrial lesions from co-intervention group had the highest mean weight and volume, compared with that of individual OV-Talin1 or β-E2 treatment. The expression levels of PCNA, Ki67, VEGFB and ANGPTL4 in the lesions were correspondingly elevated the most in the co-intervention group. Our findings unveiled that overexpressed Talin1 might cooperate withβ-E2 in stimulating ADS endometrial stromal cell proliferation and neovascularization, synergistically promoting the growth and survival of ectopic lesions. These results may be beneficial to provide a new insight for clarifying the pathogenesis of ADS.

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“…miR-7-5p is the mature form of miR-7 and is closely related to the occurrence and development of tumors (34). For example, miR-7 inhibits the ability of gastric cancer cells to divide, migrate and invade, while promoting their apoptosis (35). circRNA circR-7 acts as a miR-7 sponge that inhibits its biological function (36).…”

Section: Biogenesis and Function Of Circrnamentioning

confidence: 99%

Underlying metastasis mechanism and clinical application of exosomal circular RNA in tumors (Review)

et al. 2021

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Circular RNA (circRNA) is a long non-coding RNA molecule with a closed loop structure lacking a 5'cap and 3'tail. circRNA is stable, difficult to cleave and resistant to RNA exonuclease or RNase R degradation. circRNA molecules have several clinical applications, especially in tumors. For instance, circRNA may be used for non-invasive diagnosis, therapy and prognosis. Exosomes play a crucial role in the development of tumors. Exosomal circRNA in particular has led to increased research interest into tumorigenesis and tumor progression. Additionally, exosomal circRNA plays a role in cell-cell communication. Exosomal circRNA facilitates tumor metastasis by altering the tumor microenvironment and the pre-metastatic niche. Additionally, studies have revealed the mechanism by which exosomal circRNA affects malignant progression through signal transduction. Moreover, exosomal circRNA promotes tumor metastasis by regulating gene expression, RNA transcription and protein translation. In this review, the biological features and clinical application of exosomal circRNA are described, highlighting the underlying mechanisms through which they regulate tumor metastasis. The application of circRNA as clinical diagnostic biomarkers and in the development of novel therapeutic strategies is also discussed.

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Elevated microRNA-7 inhibits proliferation and tumor angiogenesis and promotes apoptosis of gastric cancer cells via repression of Raf-1

Cited by 18 publications

References 31 publications

CaMKII inhibitor KN‐93 impaired angiogenesis and aggravated cardiac remodelling and heart failure via inhibiting NOX2/mtROS/p‐VEGFR2 and STAT3 pathways

CaMKII inhibitor KN‐93 impaired angiogenesis and aggravated cardiac remodelling and heart failure via inhibiting NOX2/mtROS/p‐VEGFR2 and STAT3 pathways

Upregulated Talin1 synergistically boosts β-estradiol-induced proliferation and pro-angiogenesis of eutopic and ectopic endometrial stromal cells in adenomyosis

Underlying metastasis mechanism and clinical application of exosomal circular RNA in tumors (Review)

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