miR-153 inhibits the migration and the tube formation of endothelial cells by blocking the paracrine of angiopoietin 1 in breast cancer cells

Liang, Hongjun; Ge, Fei; Xu, Yuhui; Xiao, Jianru; Zhou, Zhongmei; R, Liu; Chen, Ceshi

doi:10.1007/s10456-018-9630-9

Cited by 42 publications

(25 citation statements)

References 31 publications

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“…MicroRNAs (miRNAs or miRs) are a category of small non-coding RNAs approximately 20 nucleotides in length (15). Previous studies have indicated that miRNAs, such as miR-214, miR-153 and miR-146a-5p, play important roles during the progression of various types of cancer (16)(17)(18). As a type of miRNA, miR-197-3p has been reported to facilitate the proliferation of breast cancer cells (19).…”

Section: Introductionmentioning

confidence: 99%

TUSC8 inhibits the development of osteosarcoma by sponging miR‑197‑3p and targeting EHD2

et al. 2020

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Osteosarcoma (OS) is one of the most common malignant bone tumours and generally occurs in children and adolescents. Increasing evidence has demonstrated that dysregulated long non-coding RNAs (lncRNAs) play crucial roles in the progression of various human neoplasms. Among these, tumour suppressor candidate 8 (TUSc8) is a novel lncRNA and has been reported to function as a tumour suppressor in cervical cancer. However, the exact role of TUSc8 in OS remains largely unknown. In the present study, it was observed that TUSc8 was markedly downregulated in OS tissues and cell lines. Functional experiments demonstrated that the overexpression of TUSC8 significantly suppressed the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), whereas it accelerated the apoptosis of OS cells. Mechanistically, TUSc8 served as a sponge for miR-197-3p, and EH-domain containing 2 (EHd2) was identified as a downstream target molecule of miR-197-3p. Further investigations indicated that EHD2 knockdown significantly reversed the effects on OS cellular processes induced by TUSC8 overexpression. On the whole, these findings indicate that TUSc8 functions as a competing endogenous RNA (ceRNA) to suppress OS cell growth and EMT via the miR-197-3p/EHd2 axis. TUSc8 may thus function as a potential therapeutic target in OS treatment.

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Section: Introductionmentioning

confidence: 99%

TUSC8 inhibits the development of osteosarcoma by sponging miR‑197‑3p and targeting EHD2

et al. 2020

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“…Due to the complex nature of miRNAs, miR-153 can function as both tumor promotor and tumor suppressor in various human cancers. For example, as a tumor suppressor, miR-153 inhibits the migration and tuber formation of breast cancer cells by blocking angiopoietin 1 [33]. However, as an oncogene, miR-153 promotes the cell proliferation of prostate cancer via suppression of phosphatase and tensin homolog (PTEN), and upregulation of miR-153 is associated with a poor prognosis of prostate cancer patients [34].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of miR-153 ameliorates ischemia/reperfusion-induced cardiomyocytes apoptosis by regulating Nrf2/HO-1 signaling in rats

et al. 2020

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Background Previous in vitro studies demonstrated that suppression of microRNAs might protect cardiomyocytes and neurons against oxygen–glucose deprivation and reoxygenation (OGD/R)-induced cell apoptosis. However, whether the protective effect of miR-153-inhibition on cardiomyocytes can be observed in the animal model is unknown. We aimed to address this question using a rat model of ischemia–reperfusion (I/R). Methods Rats were received the intramyocardial injection of saline or adenovirus-carrying target or control gene, and the rats were subjected to ischemia/reperfusion (I/R) treatment. The effects of miR-153 on I/R-induced inflammatory response and oxidative stress in the rat model were assessed using various assays. Results We found that suppression of miR-153 decreased cleaved caspase-3 and Bcl-2-associated X (Bax) expression, and increased B cell lymphoma 2 (Bcl-2) expression. We further confirmed that Nuclear transcription factor erythroid 2-like 2 (Nrf2) is a functional target of miR-153, and Nrf2/Heme oxygenase-1 (HO-1) signaling was involved in miR-153-regulated I/R-induced cardiomyocytes apoptosis. Inhibition of miR-153 reduced I/R-induced inflammatory response and oxidative stress in rat myocardium. Conclusion Suppression of miR-153 exerts a cardioprotective effect against I/R-induced injury through the regulation of Nrf2/HO-1 signaling, suggesting that targeting miR-153, Nrf2, or both may serve as promising therapeutic targets for the alleviation of I/R-induced injury.

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“…Recent studies have reported that certain miRNAs may become involved in this procedure. Liang et al indicated that miR-153 suppresses the tube formation and the migration of endothelial cells by targeting angiopoietin 1 (ANG1) directly in breast cancer cells (10). miR-205 was found to significantly suppress angiogenesis and epithelial-mesenchymal transition (EMT) through the simultaneous targeting of vascular endothelial growth factor A (VEGFA), zinc finger e-box binding homeobox 1 (ZEB1), and downstream products in anaplastic thyroid carcinoma (11).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑218 inhibits tumor angiogenesis of human renal cell carcinoma by targeting GAB2

Guan

Tian

et al. 2020

Oncol Rep

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Renal cell carcinoma (RCC) is one of the most common malignant cancers in the adult urinary system worldwide. Tumor angiogenesis is a critical process during cancer progression, as it modulates carcinogenesis and metastasis. In recent years, microRNA-218 (miR-218) has been confirmed to play a crucial role in tumor suppression. However, the role of miR-218 in RCC angiogenesis remains unclear. In the present study, it was found that the expression of miR-218 was decreased in RCC tumor tissues and cell lines as detected by real-time PCR analysis. Tube formation assays and migration assays also confirmed that miR-218 inhibited the interaction between RCC cells and vascular endothelial cells by suppressing proangiogenic factor vascular endothelial growth factor A (VEGFA) in RCC cells. miR-218 also repressed the subcutaneous tumorigenesis of RCC cells in nude mice, and the corneal angiogenesis in rabbit eyes. The underlying molecular mechanism was elucidated; miR-218 targets GRB2-associated binding protein 2 (GAB2), thereby inhibiting the PI3K/AKT/mTOR/VEGFA pathway. These results provide new insights into the mechanism of RCC carcinogenesis and progression, suggesting that miRNA-218 may be a therapeutic target for the treatment of RCC.

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miR-153 inhibits the migration and the tube formation of endothelial cells by blocking the paracrine of angiopoietin 1 in breast cancer cells

Cited by 42 publications

References 31 publications

TUSC8 inhibits the development of osteosarcoma by sponging miR‑197‑3p and targeting EHD2

TUSC8 inhibits the development of osteosarcoma by sponging miR‑197‑3p and targeting EHD2

Inhibition of miR-153 ameliorates ischemia/reperfusion-induced cardiomyocytes apoptosis by regulating Nrf2/HO-1 signaling in rats

MicroRNA‑218 inhibits tumor angiogenesis of human renal cell carcinoma by targeting GAB2

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