Down-regulation of miR-489 contributes into NSCLC cell invasion through targeting SUZ12

Xie, Zongtao; Cai, Liming; R, Li; Zheng, Jinyu; Wu, Hongyan; Yang, Xiaoqi; Hu, Li; Wang, Zhiqiang

doi:10.1007/s13277-015-3340-3

Cited by 35 publications

(22 citation statements)

References 25 publications

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“…Moreover, miR-489 regulates ovarian cancer cell survival, growth and apoptosis via suppression of Akt3 [18]. miR-489 loss promotes invasion and epithelial-mesenchymal transition (EMT) events of lung cancer cells [30]. Recently, the expression miR-489 is found to be down-regulated in HCC tissues, especially in early recurrent cases, and miR-489 underexpression contributes to migration and invasion of HCC cells [20, 31].…”

Section: Discussionmentioning

confidence: 99%

LncRNA CHRF-induced miR-489 loss promotes metastasis of colorectal cancer via TWIST1/EMT signaling pathway

et al. 2017

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microRNA-489 (miR-489) is a novel cancer-related miRNAs and functions as a tumor suppressor in human cancers. While, the clinical significance of miR-489 and its role in colorectal cancer (CRC) remain rarely known. Here, we found that the levels of miR-489 in CRC tissues were significantly lower than those in matched tumor-adjacent tissues. Furthermore, decreased levels of miR-489 also observed in CRC cell lines compared to HIEC cells. Clinicopathological analysis revealed that miR-489 underexpression was positively correlated with advanced pT stage, pN stage and AJCC stage. Moreover, miR-489 low expressing CRC patients showed a obvious shorter survival. Functionally, miR-489 restoration inhibited cell migration and invasion as well as epithelial-mesenchymal transition (EMT) in HCT116 cells, while miR-489 loss facilitated these cellular processes in SW480 cells. In vivo experiments revealed that miR-489 overexpression reduced the number of metastatic nodules in nude mice liver. Notably, TWIST1 was recognized as a direct downstream target of miR-489 in CRC cells. Interestingly, TWIST1 restoration abrogated the effects of miR-489 on CRC cells with enhanced cell migration, invasion and EMT process. Furthermore, overexpression of long noncoding RNA cardiac hypertrophy-related factor (lncRNA CHRF) was inversely correlated with miR-489 expression in CRC tissues. CHRF knockdown increased the expression of miR-489 and suppressed EMT events of HCT116 cells, while CHRF overexpression showed opposite effects on miR-489 expression and EMT in SW480 cells. Taken together, this work support the first evidence that lncRNA CHRF-induced miR-489 loss facilitates metastasis and EMT process of CRC cells probably via TWIST1/EMT signaling pathway.

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Section: Discussionmentioning

confidence: 99%

LncRNA CHRF-induced miR-489 loss promotes metastasis of colorectal cancer via TWIST1/EMT signaling pathway

et al. 2017

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“…MiR‐489‐3p was originally reported that it might regulate early osteogenic differentiation in human mesenchymal stem cells, and has critical roles in osteogenesis . Although reduced expression levels of miR‐489‐3p is associated with several types of cancer metastasis , its role in OS metastasis has not been reported. In this study, we found that miR‐489‐3p expression was downregulated in OS cells and was also significantly decreased in metastatic lesions compared with their corresponding primary tumor samples, indicating miR‐489‐3p may be involved in OS metastasis.…”

Section: Discussionmentioning

confidence: 99%

“…It is worth mentioning that several proteins associated with tumor progression, such as protein tyrosine phosphatase PTPN11 , Akt3 , Smad3 and SUZ12 , had been identified as downstream effectors of miR‐489‐3p. It is not clear yet whether these proteins are also involved in invasion and metastasis of OS regulated by miR‐489‐3p.…”

Section: Discussionmentioning

confidence: 99%

Loss of MicroRNA‐489‐3p promotes osteosarcoma metastasis by activating PAX3‐MET pathway

Liu

Yang

Qian

2016

Molecular Carcinogenesis

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Osteosarcoma (OS) remains one deadly disease for many affected patients. MicroRNAs (miRNAs) are thought to have an important role in tumor metastasis by regulating diverse cellular pathways. Here, we describe the function and regulation network of miR-489-3p in osteosarcoma (OS) metastasis. MiR-489-3p expression was downregulated in OS cells especially in high metastatic potential cells and was also significantly decreased in metastatic lesions compared with their corresponding primary tumor samples. Both gain- and loss-of-function studies confirmed that miR-489-3p significantly suppressed OS cell invasion and metastasis both in vitro and in vivo. Mechanistically, paired box gene 3 (PAX3) was identified as a functional target of miR-489-3p in OS cells. MiR-489-3p inhibited OS metastasis by negatively regulating expression of PAX3. In addition, PAX3 expression was markedly higher in OS tissues than in adjacent non-cancerous tissues. Transwell assays and in vivo metastasis assays demonstrated that overexpression of PAX3 significantly promoted the invasiveness and pulmonary metastasis of OS cells. On the other hand, downregulation of PAX3 markedly reduced cell metastatic potential. Mechanistic investigations indicated that prometastasis function of PAX3 was mediated by upregulating downstream target MET tyrosine kinase receptor. In conclusion, our results reveal that miR-489-3p-PAX3-MET signaling is critical to OS metastasis. Targeting the pathway described here may open new therapeutic prospects to restrict the metastatic potential of OS. © 2016 Wiley Periodicals, Inc.

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“…One of these miRs, miR-133, has been shown to play a role in tumor suppression in a variety of cancers, including inhibiting breast cancer cell migration and invasion, gastric cancer cell growth and migration, and liver fibrosis (Esquela- Kerscher and Slack, 2006;Cheng et al, 2012;Liu et al, 2014;Mei et al, 2014;Wang et al, 2014;Yongchun et al, 2014;Xie et al, 2015;Zhang et al, 2015). Recent studies have shown that miRs may be a new regulatory mechanism involved in the onset of pituitary adenoma, providing a new method for the diagnosis and treatment of pituitary adenoma (Trivellin et al, 2012;Gadelha et al, 2013;Di Ieva et al, 2014;Leone et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

miR-133 inhibits pituitary tumor cell migration and invasion via down-regulating FOXC1 expression

Wang¹,

Zhang²,

Zhang³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Many studies have shown that microRNA (miR)-133 functions as a tumor suppressor in a variety of metastatic cancers, including breast cancer, gastric cancer, and liver fibrosis. However, the influence of miR-133 on pituitary tumor malignancy has not yet been reported. The purpose of this study was to explore the role of miR-133 in pituitary tumor cell migration and invasive ability and the molecular mechanisms involved. Our findings suggest that in pituitary adenoma cell lines, through direct targeting and negative control of forkhead box C1 (FOXC1), miR-133 can inhibit pituitary adenoma cell migration and invasion. In addition, epithelialto-mesenchymal transition can be induced by miR-133. Additionally, a negative correlation was found between FOXC1 and miR-133 expression when comparing their expression levels between cancerous tissue and adjacent normal tissue. This suggests that miR-133 can inhibit cell migration and invasion by directly targeting FOXC1, implying that miR-133 could be a potential therapeutic target for treatment of invasive pituitary adenoma.

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Down-regulation of miR-489 contributes into NSCLC cell invasion through targeting SUZ12

Cited by 35 publications

References 25 publications

LncRNA CHRF-induced miR-489 loss promotes metastasis of colorectal cancer via TWIST1/EMT signaling pathway

LncRNA CHRF-induced miR-489 loss promotes metastasis of colorectal cancer via TWIST1/EMT signaling pathway

Loss of MicroRNA‐489‐3p promotes osteosarcoma metastasis by activating PAX3‐MET pathway

miR-133 inhibits pituitary tumor cell migration and invasion via down-regulating FOXC1 expression

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