miR‐454 is down‐regulated in osteosarcomas and suppresses cell proliferation and invasion by directly targeting c‐Met

Niu, Guangfeng; Li, Bin; Sun, Juan; Sun, Li

doi:10.1111/cpr.12187

Cited by 62 publications

(56 citation statements)

References 41 publications

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“…Osteosarcoma is the most prevalent malignant tumor of bone and is usually observed in young adults and adolescents [1][2][3][4][5]. Despite the recent advances in the treatment of osteosarcoma such as radiation therapy, adjuvant chemotherapy and surgery that have been achieved, the relative 5-year survival rate of osteosarcoma patients remains discontent [6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

miR-423-5p Inhibits Osteosarcoma Proliferation and Invasion Through Directly Targeting STMN1

Wang¹,

Peng²,

Gong³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Increasing evidences suggest that dysregulated expression of miRNAs contributes to the progression of various tumors. However, the underlying function of miR-423-5p in osteosarcoma remains unexplored. Methods: The expression of miR-423-5p and STMN1 were determined in osteosarcoma samples and cell lines via quantitative real-time PCR. Colony formation and Cell Counting Kit-8 (CCK-8) assays were performed to measure cell proliferation ability and transwell analysis was used to detect cell invasion, and dual luciferase reporter assay was perform to analysis the interaction between the miR-423-5p and STMN1. Results: The expression levels of miR-423-5p and STMN1 in the osteosarcoma tissues and cell lines were measured by qRT-PCR. Cell viability was determined using the clone formation and CCK-8 assays. A dual-luciferase reporter and Western blot were performed to stdudy the target gene of miR-423-5p. Here, we showed that miR-423-5p expression was downregulated in osteosarcoma tissues and cell lines. However, the expression of stathmin1 (STMN1) was downregulated in osteosarcoma tissues and cell lines. Moreover, STMN1 expression level was negatively correlated with the miR-423-5p expression in the osteosarcoma tissues. We identified STMN1 was a direct target gene of miR-423-5p in osteosarcoma cell. Overexpression of miR-423-5p inhibited osteosarcoma cell proliferation, colony formation and invasion. Furthermore, we demonstrated that STMN1 was involved in miR-423-5p-mediated cell behavior such as cell proliferation, colony formation and invasion in the osteosarcoma cell. Conclusion: Our present study indicated that miR-423-5p acted as a tumor suppressor gene in osteosarcoma partly through inhibiting STMN1 expression.

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Section: Introductionmentioning

confidence: 99%

miR-423-5p Inhibits Osteosarcoma Proliferation and Invasion Through Directly Targeting STMN1

Wang¹,

Peng²,

Gong³

et al. 2018

Cell Physiol Biochem

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“…Increasing studies have showed that miRNAs play pivotal roles in cell proliferation, metabolism, differentiation, invasion and migration [18–24]. More importantly, miRNAs play important roles in cancer progression and initiation and function as tumor suppressors or oncogenes [25–27]. Abnormal expressions of miRNAs are associated with various cancers such as gastric cancer, renal cell carcinoma, breast cancer, ovarian carcinoma and osteosarcoma [28–32].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-300 inhibited glioblastoma progression through ROCK1

Zhou

et al. 2016

Oncotarget

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Glioblastoma is a common type of brain aggressive tumors and has a poor prognosis. MicroRNAs (miRNAs) are a class of small, endogenous and non-coding RNAs that play crucial roles in cell proliferation, survival and invasion. Deregulated expression of miR-300 has been studied in a lot of cancers. However, the role of miR-300 in glioblastoma is still unknown. In this study, we demonstrated that miR-300 expression was downregulated in glioblastoma tissues compared with the normal tissues. Lower expression level of miR-300 was observed in thirty cases (75 %, 30/40) of glioblastoma samples compared with the normal samples. Moreover, the overall survival of glioblastoma patients with lower miR-300 expression level was shorter than those with higher miR-300 expression level. In addition, miR-300 expression was also downregulated in glioblastoma cell lines. Overexpression of miR-300 inhibited cell proliferation, cell cycle and invasion in glioblastoma cell line U87 and U251. Moreover, we identified ROCK1 as a direct target of miR-300 in U87 and U251 cells. Overexpression of ROCK1 partially rescued the miR-300-mediated cell growth. ROCK1 expression levels in glioblastoma tissues were higher than that in normal tissues. ROCK1 expression levels were higher in thirty-one cases of glioblastoma samples than their normal samples. Furthermore, the expression level ROCK1 was inversely correlated with the expression level of miR-300. Importantly, overexpression of miR-300 suppressed glioblastoma progression in an established xenograft model. In conclusion, we revealed that miR-300 might act as a tumor suppressor gene through inhibiting ROCK1 in glioblastoma.

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“…The remaining 11 miRNAs have never been studied in liver cancer (Table III). Among the 11 differentially dysregulated miRNAs, the function of miR-374a, miR-188-5p, miR-1183, miR-454, miR-324-3p, miR-484, miR-3188, and miR-216b have been studied in human cancers (27,(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43); however, the exact function of miR-4271, miR-1471 and miR-3610 remains unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have demonstrated that miR-454 acts as an oncogene or tumor suppressor in cancer (39)(40)(41). miR-454 has been reported to be decreased in tissue of patients with esophageal cancer compared with normal tissue, which may perform as novel molecular markers of esophageal cancer (39).…”

Section: Discussionmentioning

confidence: 99%

“…miR-454 has been reported to be decreased in tissue of patients with esophageal cancer compared with normal tissue, which may perform as novel molecular markers of esophageal cancer (39). Niu et al (40) demonstrated that miR-454 expression was downregulated in osteosarcoma tissues, acting as a tumor suppressor gene in osteosarcoma. The miR-454 expression was increased in colorectal cancer (CRC) tissues and CRC cells.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA expression profiling in patients with hepatocellular carcinoma of familial aggregation and hepatitis B virus infection

Zhang

et al. 2017

Oncology Letters

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Abstract. Numerous studies have suggested that microRNAs (miRNAs) potently affect hepatocarcinogenesis. However, the miRNA expression profiling in patients with hepatocellular carcinoma (HCC) of familial aggregation and hepatitis B virus (HBV) infection has not been elucidated. In the present study, the plasma miRNA expression profiles of 3 patients with HCC with familial aggregation of HCC and HBV infection and 1 healthy volunteer were examined by microarray analysis, in order to identify relevant miRNAs involved in the pathogenesis of HCC with familial aggregation and HBV infection. The results indicated that 26 miRNAs exhibited a ≥20-fold increase or decrease in the plasma of patients with HCC, compared with the healthy control (24 upregulated and 2 downregulated). Among these altered miRNAs, 15 of them have been reported in HCC. The other 11 miRNAs have never been reported in HCC. These differentially-expressed miRNAs may be potential molecular markers for HCC pathogenesis and development.

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miR‐454 is down‐regulated in osteosarcomas and suppresses cell proliferation and invasion by directly targeting c‐Met

Abstract: Reduced-expression of miR-454 in osteosarcoma cells promoted tumour growth by targeting c-Met, thus miR-454 may be a potential therapy target for this tumour.

Cited by 62 publications

References 41 publications

miR-423-5p Inhibits Osteosarcoma Proliferation and Invasion Through Directly Targeting STMN1

miR-423-5p Inhibits Osteosarcoma Proliferation and Invasion Through Directly Targeting STMN1

MicroRNA-300 inhibited glioblastoma progression through ROCK1

MicroRNA expression profiling in patients with hepatocellular carcinoma of familial aggregation and hepatitis B virus infection

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