MicroRNA-381 suppresses cell growth and invasion by targeting the liver receptor homolog-1 in hepatocellular carcinoma

Zhang, Qianqian; Zhao, Shixing; Pang, Xiaoli; Chi, Baorong

doi:10.3892/or.2015.4491

Cited by 44 publications

(31 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the reported expression patterns and roles of miR-381 in various types of cancer markedly differ. miR-381 has been shown to be downregulated in malignancies and exerts tumour suppressive effects on colon, breast and liver cancer and pituitary tumours (27,(37)(38)(39). In lung cancer, this miRNA has been shown to inhibit cell migration and invasion by targeting LRH-1, where it acts as a prognostic marker (40).…”

Section: Discussionmentioning

confidence: 99%

miR‑381 and miR‑489 suppress cell proliferation and invasion by targeting CUL4B via the Wnt/β‑catenin pathway in gastric cancer

et al. 2018

View full text Add to dashboard Cite

Accumulating evidence has highlighted the critical role of cullin 4B (CUL4B) in driving tumourigenesis in several malignancies, including gastric cancer (GC); however, the mechanisms underlying CUL4B upregulation remain unclear. The dysregulation of microRNAs (miRNAs or miRs) is known to be involved in tumourigenesis. In this study, we report that the expression of miR-381 and miR-489 is downregulated and is negatively correlated with that of CUL4B in GC tissues and cell lines. Further analysis verified that miR-381 and miR-489 directly targeted CUL4B. CUL4B silencing inhibited cell proliferation, migration and invasion by inactivating the Wnt/β-catenin pathway. miR-381/miR-489 overexpression recapitulated the effects of CUL4B silencing, while CUL4B restoration negated the suppressive effects induced by the ectopic expression of miR-381/miR-489. Furthermore, miR-381/miR-489 exerted tumour suppressive functions by inactivating the Wnt/β-catenin pathway through the targeting of CUL4B. Taken together, the findings of this study suggest that the miR-381/miR-489-mediated expression of CUL4B modulates the proliferation and invasion of GC cells via the Wnt/β-catenin pathway, which indicates that the miR-381/miR-489-CUL4B axis is critical in the control of GC tumourigenesis.

show abstract

Section: Discussionmentioning

confidence: 99%

miR‑381 and miR‑489 suppress cell proliferation and invasion by targeting CUL4B via the Wnt/β‑catenin pathway in gastric cancer

et al. 2018

View full text Add to dashboard Cite

show abstract

“…As one of the miRs, miR‐381 acts a suppressing or promoting role in different malignant tumors . Previous studies have suggested that miR‐381 serves as an oncogenic or tumor‐suppressive miRNA in many types of cancers, such as hepatocellular carcinoma and esophageal cancer cells . However, there is currently no substantial data that describes the protective effects of miR‐381 on angiogenesis after renal I/R injury in rats.…”

Section: Introductionmentioning

confidence: 99%

Retracted: MicroRNA‐381‐induced down‐regulation of CXCR4 promotes the proliferation of renal tubular epithelial cells in rat models of renal ischemia reperfusion injury

Zheng

Wen

Wang

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

This study aims to explore whether microRNA-381 (miR-381) mediating CXCR4 affects the renal tubular epithelial cells (RTEC) of renal ischemia reperfusion (I/R) injury. Forty-eight rats were assigned into the I/R (n = 24, successfully established as I/R model) and sham (n = 24) groups. After collecting kidney tissues, immunohistochemistry, and microvascular density (MVD) counting were conducted for CXCR4 positive expression and MVD numbers. RTECs were assigned into the sham, blank, negative control (NC), miR-381 mimics, miR-381 inhibitor, si-CXCR4, and miR-381 inhibitor + si-CXCR4 groups. RT-qPCR and Western blotting were performed for relative expressions in tissues and cells. Cell proliferation and apoptosis were measured by MTT assay and flow cytometry. Results showed that compared with the sham group, positive expression of CXCR4 and MVD number were higher in the I/R group, which exhibited decreased miR-381 and increased expression of CXCR4, stromal cell-derived factor-1 (SDF1), vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1 (HIF-1α) and Tie-2. Dual luciferase reporter gene assay verified that CXCR4 is a target gene of miR-381. MiR-381 expression was lower in the miR-381 inhibitor + si-CXCR4 and miR-381 inhibitor groups and higher in the miR-381 mimics group than the blank and NC groups. Compared with the blank and NC groups, the miR-381 mimics and si-CXCR4 groups exhibited higher cell proliferation but lower cell apoptosis and expression of CXCR4, SDF1, VEGF, HIF-1α, and Tie-2, whereas the miR-381 inhibitor group exhibited the opposite trend. In conclusion, miR-381 may promote RTEC proliferation in rats with renal I/R injury by down-regulating CXCR4.

show abstract

“…18 MiR-381 has been found to be involved in cancer progression, including chondrosarcoma, ovarian cancer, hepatocellular carcinoma, and colorectal cancer. 19, 20, 21, 22 However, the role of miR-381 in osteosarcoma is poorly understood.…”

mentioning

confidence: 99%

WISP-1 positively regulates angiogenesis by controlling VEGF-A expression in human osteosarcoma

et al. 2017

View full text Add to dashboard Cite

In recent years, much research has focused on the role of angiogenesis in osteosarcoma, which occurs predominantly in adolescents and young adults. The vascular endothelial growth factor-A (VEGF-A) pathway is the key regulator of angiogenesis and in osteosarcoma. VEGF-A expression has been recognized as a prognostic marker in angiogenesis. Aberrant WNT1-inducible signaling pathway protein-1 (WISP-1) expression is associated with various cancers. However, the function of WISP-1 in osteosarcoma angiogenesis is poorly understood. We demonstrate a positive correlation between WISP-1 and VEGF-A expression in human osteosarcoma. Moreover, we show that WISP-1 promotes VEGF-A expression in human osteosarcoma cells, subsequently inducing human endothelial progenitor cell (EPC) migration and tube formation. The focal adhesion kinase (FAK), Jun amino-terminal kinase (JNK), and hypoxia-inducible factor (HIF)-1α signaling pathways were activated after WISP-1 stimulation, while FAK, JNK, and HIF-1α inhibitors or small interfering RNA (siRNA) abolished WISP-1-induced VEGF-A expression and angiogenesis. In vitro and in vivo studies revealed down-regulation of microRNA-381 (miR-381) in WISP-1-induced VEGF-A expression and angiogenesis. Our findings reveal that WISP-1 enhances VEGF-A expression and angiogenesis through the FAK/JNK/HIF-1α signaling pathways, as well as via down-regulation of miR-381 expression. WISP-1 may be a promising target in osteosarcoma angiogenesis.

show abstract

MicroRNA-381 suppresses cell growth and invasion by targeting the liver receptor homolog-1 in hepatocellular carcinoma

Cited by 44 publications

References 56 publications

miR‑381 and miR‑489 suppress cell proliferation and invasion by targeting CUL4B via the Wnt/β‑catenin pathway in gastric cancer

miR‑381 and miR‑489 suppress cell proliferation and invasion by targeting CUL4B via the Wnt/β‑catenin pathway in gastric cancer

Retracted: MicroRNA‐381‐induced down‐regulation of CXCR4 promotes the proliferation of renal tubular epithelial cells in rat models of renal ischemia reperfusion injury

WISP-1 positively regulates angiogenesis by controlling VEGF-A expression in human osteosarcoma

Contact Info

Product

Resources

About