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

Liu, Qifei; Yang, Guochun; Qian, Yuying

doi:10.1002/mc.22593

Cited by 46 publications

(42 citation statements)

References 42 publications

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“…Since the obtained data showed that overexpression of miR-1 acted on p21 and induced cell cycle arrest via a p53independent pathway, we focused on PAX3, one of the target genes of miR-1, as a potential p21-regulating gene ( Figure 3A, Table I) (20), as well as in the regulation of cell cycle via p21 (21). In osteosarcoma, high expression of PAX3 was found to promote cell migration and invasion (22). However, there have been no studies examining cell proliferation in osteosarcoma.…”

Section: Overexpression Of Mir-1 Down-regulated Pax3 Expressionmentioning

confidence: 99%

MiR-1 Suppresses Proliferation of Osteosarcoma Cells by Up-regulating p21 via PAX3

Fujii

Osaka

Sato

et al. 2018

Cancer Genomics Proteomics

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Background/Aim: miRNA-1(miR-1) is downregulated in various cancer cells including osteosarcoma cells. This study was conducted to analyze the function of miR-1 in osteosarcoma cells. Materials and Methods: miR-1 expression in osteosarcoma cells was evaluated by qRT-PCR. Cell proliferation was evaluated after transfecting miR-1 by WST8 assay and FACS analysis, both in vitro and in vivo. Results: Overexpression of miR-1 suppressed cell proliferation and induced cell-cycle arrest in the G 0-G 1 phase by increasing p21 levels via a p53-independent pathway. Overexpression of miR-1 down-regulated PAX3, a potential p21-regulating gene. Moreover, knockdown of PAX3 suppressed cell proliferation by increasing p21 levels, and induced arrest at the G 0 /G 1 phase. Administration of miR-1 showed an in vivo antitumor effect. Conclusion: Overexpression of miR-1 suppressed cell proliferation and induced arrest in the G 0 /G 1 phase by increasing p21 levels via a p53-independent pathway through PAX3 suppression. These results indicate that miR-1 could be a therapeutic target for osteosarcoma. Osteosarcoma is a primary bone malignancy that usually occurs in the metaphyseal region of long bones in children and adolescents, producing immature osteoids and bones. Previously, amputation of the extremities, concurrent with detection, was the conventional therapy for osteosarcoma and the 5-year survival rate was extremely poor, less than 20%, due to the inability to inhibit pulmonary metastases (1). Recently, the survival rate has increased to 60-80% through the application of combination treatments using surgery and 71 This article is freely accessible online.

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Section: Overexpression Of Mir-1 Down-regulated Pax3 Expressionmentioning

confidence: 99%

MiR-1 Suppresses Proliferation of Osteosarcoma Cells by Up-regulating p21 via PAX3

Fujii

Osaka

Sato

et al. 2018

Cancer Genomics Proteomics

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“…Previous research has shown that miR-489-3p was sponged by LINC01446 and targeted TPT1 to regulate glioblastoma progression [25]. In osteosarcoma, miR-489-3p signi cantly suppressed cell invasion and metastasis both in vitro and in vivo [26]. In the present study, we rstly proposed that miR-489-3p might be a target of LINC00115.…”

Section: Discussionmentioning

confidence: 52%

Long non-coding RNA LINC00115 contributes to the progression of colorectal cancer by targeting miR-489-3p via PI3K/AKT/mTOR pathway

Feng

Wang

et al. 2020

Preprint

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Background Long noncoding RNAs (lncRNAs) are tumor-related regulators and have been found to be involved in the underlying molecular mechanisms of colorectal cancer (CRC). However, the role of lncRNA LINC00115 during CRC progression is not entirely elucidated. Methods The expression of LINC00115 was analyzed in paired CRC tissue samples and its clinical significance was evaluated. The biological effects on CRC cells proliferation, apoptosis, migration, invasion and PI3K/AKT/mTOR signaling were assessed by Cell Counting Kit-8 assay, Transwell assay, flow cytometry analysis and Western blot, respectively. The regulatory relationship between LINC00115 and miR-489-3p was determined by dual-luciferase reporter assays. Results LINC00115 was significantly overexpressed in CRC and its overexpression predicted poor outcome of the patients. Downregulation of LINC00115 markedly inhibited CRC cell proliferation, increased cell apoptosis, and suppressed cell migration and invasion. Moreover, downregulation of LINC00115 led to the inactivation of PI3K/AKT/mTOR signaling. Bioinformatics analysis identified miR-489-3p as a candidate target of LINC00115. Furthermore, we revealed an inverse correlation between LINC00115 and miR-489-3p in CRC tissues. miR-489-3p might directly target LINC00115 and downregulation of miR-489-3p could rescue the biological effects induced by the absence of LINC0015. Conclusion LINC00115 serves as an excellent oncogene of CRC metastasis, the deeper understanding of LINC00115/miR-489-3p axis might provide potential therapeutic targets for CRC metastasis.

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“…The role of MiRNAs in tumors is extensive. The miR-489-3p found in this study is known to inhibit the growth of a variety of tumors, such as bladder cancer [28], renal cell carcinoma [29], and osteosarcoma [17]. However, its relationship with pancreatic cancer is unclear.…”

Section: Discussionmentioning

confidence: 77%

“…Meanwhile, literatures also have found multiple micro RNAs like miR-135 [13], miR-124 [16]and others have been implicated in metabolic reprogramming of pancreatic cancer. And miR-489-3p has been reported to inhibit tumor progression [17,18]. Therefore, we hypothesized that it can also inhibit the progression of pancreatic cancer, and it is inversely related to the glycolysis that can promote tumor progression.…”

Section: Introductionmentioning

confidence: 97%

MiR-489-3p reduced pancreatic cancer proliferation and metastasis by targeting PKM2 and LDHA involving glycolysis

Zhang

Shen

et al. 2020

Preprint

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Background: Malignant proliferation and chemotherapy resistance are some of the causes of high mortality in pancreatic cancer. MicroRNAs have long been a hot spot in cancer research and are involved in tumor formation and metabolic stress responses. miR-489-3p is involved in inhibiting the growth of many tumors, but its relationship with the growth and metabolism of pancreatic cancer is not clear. Methods：We used RNA in situ hybridization to analyze the differential expression of miR-489-3p in pancreatic cancer tissues and adjacent tissues. The qRT-PCR experiment detected the content of miR-489-3p in pancreatic cancer cell lines and ordinary pancreatic ductal epithelial cells. Then we did experiments in vivo (subcutaneous tumor formation in nude mice) and in vitro (plate cloning, transwell, glycolysis related experiments) experiments to verify that miR-489-3p can continue the invasion and metastasis of pancreatic cancer and glucose metabolism. Furthermore, we confirmed that LDHA and PKM2 are the two targets of miR-489-3p through dual luciferase reporter gene experiments. Finally, several reply experiments were done to verify the regulation mechanism of miR-489-3p.Results: We determined that miR-489-3p is under-expressed in pancreatic cancer tissues by RNA in situ hybridization, and the function acquisition and deletion experiments and glycolysis experiments confirmed that miR-489-3p can inhibit the proliferation and invasion of Glycolysis. We then analyzed the website to find that miR-489-3p can target LDHA and PKM, and then we verified this finding with a luciferase report experiment. Therefore, we proceeded with recovery experiments on LDHA and PKM2, and concluded that miR-489-3p performs its function by targeting LDHA and PKM2. Finally, in vivo experiments confirmed that highly expressed miR-489-3p inhibited the growth of pancreatic cancer. Conclusion: In short, we identified miR-489-3p as a novel chemotherapy target for pancreatic cancer, and its diagnostic value deserves further study.

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

Cited by 46 publications

References 42 publications

MiR-1 Suppresses Proliferation of Osteosarcoma Cells by Up-regulating p21 via PAX3

MiR-1 Suppresses Proliferation of Osteosarcoma Cells by Up-regulating p21 via PAX3

Long non-coding RNA LINC00115 contributes to the progression of colorectal cancer by targeting miR-489-3p via PI3K/AKT/mTOR pathway

MiR-489-3p reduced pancreatic cancer proliferation and metastasis by targeting PKM2 and LDHA involving glycolysis

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