miR-597 inhibits breast cancer cell proliferation, migration and invasion through FOSL2

He, Jiangtu; Mai, Jieying; Li, Yan; Chen, Linyi; Xu, Hui; Zhu, Xiaofei; Pan, Qiuhui

doi:10.3892/or.2017.5558

Cited by 41 publications

(41 citation statements)

References 31 publications

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“…FOSL2 belongs to the activator protein 1 (activator protein, l, APl) transcription factor family 37 , 38 . FOSL2 is widespread in human tissues and plays an important role in mammalian growth, reproductive traits, and immune response 39 , 40 . The expression products of FOSL2 are related to cell adhesion, movement, invasion, metastasis and cell growth 37 .…”

Section: Discussionmentioning

confidence: 99%

“…The expression products of FOSL2 are related to cell adhesion, movement, invasion, metastasis and cell growth 37 . Studies have shown that over-expression of FOSL2 is associated with a higher invasive association with breast cancer and involved in breast cancer progression 39 . In addition, FOSL2 also plays a role in the TGF- beta signaling pathway, and is essential for TGF- beta1 to induce cell migration.…”

Section: Discussionmentioning

confidence: 99%

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miR-143-3p inhibits the proliferation, migration and invasion in osteosarcoma by targeting FOSL2

Sun

Dai

et al. 2018

Sci Rep

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Osteosarcoma (OS) is the most common type of primary malignant bone tumor and mainly occurs in children and adolescent. Because of its early migration and invasion, OS has a poor prognosis. It has been reported that mircoRNAs (miRNAs) play a crucial role in the occurrence and development of multiple tumors. In this study, we identified the aberrant-expression of miR-143-3p in osteosarcoma and examined the role of miR-143-3p in OS development. Further, we searched the miR-143-3p target gene and verified its accuracy by luciferase experiments. Finally, we explored the relationship between miR-143-3p and FOS-Like antigen 2 (FOSL2). Our data indicated that miR-143-3p expression was substantially lower in OS tissues and cell-line compared with normal tissues, and was lower in patients with poor prognosis. In addition miR-143-3p inhibited OS cell proliferation and metastasis while promoting apoptosis. We next showed that FOSL2 was directly targeted by miR-143-3p and could reverse the inhibition caused by miR-143-3p. Finally, we found FOSL2 expression in OS cells was significantly higher compared with normal cells and negatively correlated with miR-143-3p. Thus, miR-143-3p directly and negatively targets FOSL2 to affect OS characteristics. This provides a new target for the treatment of OS and deserves further study.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

miR-143-3p inhibits the proliferation, migration and invasion in osteosarcoma by targeting FOSL2

Sun

Dai

et al. 2018

Sci Rep

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“…The reaction was completed at 37°C for 60 min with PolyA primer, then the reaction solution was added to RT RNAase Free H 2 O to a total volume of 50 µl. Quantitative detection was completed according to the manufacturer's protocol as previously described ( 18 ) (miScript SYBR-Green PCR kit; Qiagen AB). The system included the following: 10 µl qRT-PCR-Mix, 0.5 µl forward primers and 0.5 µl reverse primers, 5 µl cDNA and 4 µl ddH 2 O.…”

Section: Methodsmentioning

confidence: 99%

Molecular mechanism of miR-181b in heart disease due to pregnancy-induced hypertension syndrome

Gao

Wang

et al. 2017

Experimental and Therapeutic Medicine

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The present study aimed to investigate the molecular mechanisms of microRNA (miR)-181b in heart disease due to hypertensive disorders complicating pregnancy (HDCP) through regulating the expression of metallopeptidase inhibitor 3 (TIMP3). miR-181b expression was detected by reverse transcription-quantitative polymerase chain reaction in peripheral blood samples from patients with HDCP. These samples were analyzed for clinical pathological characteristics. The primary cardiomyocytes of rats were cultured in hypoxic conditions for 24 h, in which miR-181b expression was detected at different time points. The expression of TIMP3 was assessed in normal rat cardiomyocytes following transfection with miR-181b mimics by western blot analysis. The TIMP3 protein was also detected in cardiomyocytes following transfection with TIMP3 short interfering-RNA. The apoptosis rate of transfected cardiomyocytes was detected by flow cytometry following 24 h of culture in a hypoxic environment. Luciferase assay was applied to validate whether miR-181b binds to the 3′ untranslated region of TIMP3 mRNA. miR-181b expression was significantly downregulated in the peripheral blood of patients with HDCP and the miR-181b expression was negatively associated with the grades of hypertension (P<0.05). The results of luciferase assay indicated that miR-181b directly targets TIMP3. The apoptosis rates of rat cardiomyocytes in the group transfected with miR-181b or TIMP3 siRNA was significantly lower than the normal control group (P<0.05). miR-181b may inhibit apoptosis of cardiomyocytes to protect myocardial cells through directly targeting TIMP3 genes, which serve important roles in HDCP.

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“…18 Studies have shown that overexpression of FOSL2 is associated with higher migratory and invasive abilities in breast cancer, colon cancer, and hepatocellular carcinoma. [18][19][20] Very recent data have indicated that FOSL2 participates in OS cell proliferation, migration, and invasion. 21 Moreover, it has been reported that several miRNAs play a regulatory role by directly inhibiting target FOSL2 in cancers.…”

Section: Lncrna Linc00313 Knockdown Inhibits Tumorigenesis and Metastmentioning

confidence: 99%

LncRNA LINC00313 Knockdown Inhibits Tumorigenesis and Metastasis in Human Osteosarcoma by Upregulating FOSL2 through Sponging miR-342-3p

et al. 2020

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Purpose: Osteosarcoma (OS) is the most common primary bone tumor, with high morbidity in infants and adolescents. Long noncoding RNA LINC00313 has been found to modulate papillary thyroid cancer tumorigenesis and to be dysregulate in lung cancer. However, the role of LINC00313 in OS has not yet been addressed. Materials and Methods: We evaluated mRNA and protein expression using real-time quantitative PCR and Western blotting. Cell proliferation was evaluated using MTT; apoptosis and autophagy were assessed with flow cytometry, Western blotting, and/or GFP-LC3 assay. Transwell assay was conducted to measure cell migration and invasion. Potential target sites for LINC00313 and miR-342-3p were predicted with starBase v.2.0 and TargetScan Human, and verified using luciferase reporter assay, RNA immunoprecipitation, and RNA pull-down assay. In vivo, xenogeneic tumors were induced with U2OS and MG-63 cells, separately. Results: LINC00313 was upregulated and miR-342-3p was downregulated in OS tissues and cells. High expression of LINC00313 was associated with shorter overall survival. FOSL2 downregulation and miR-342-3p overexpression suppressed cell proliferation and migratory and invasive abilities while promoting apoptosis and autophagy, all of which were consistent with the effects of LINC00313 knockdown. miR-342-3p, sponged by LINC00313, inversely modulated FOSL2 by targeting MG-63 cells, and FOSL2 expression was positively controlled by LINC00313. LINC00313 knockdown suppressed tumor growth in vivo. Conclusion: LINC00313 is upregulated in OS, and LINC00313 knockdown plays a vital anti-tumor role in OS cell progression through a miR-342-3p/FOSL2 axis. Our study suggests that LINC00313 may be a novel, promising biomarker for diagnosis and prognosis of OS.

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miR-597 inhibits breast cancer cell proliferation, migration and invasion through FOSL2

Cited by 41 publications

References 31 publications

miR-143-3p inhibits the proliferation, migration and invasion in osteosarcoma by targeting FOSL2

miR-143-3p inhibits the proliferation, migration and invasion in osteosarcoma by targeting FOSL2

Molecular mechanism of miR-181b in heart disease due to pregnancy-induced hypertension syndrome

LncRNA LINC00313 Knockdown Inhibits Tumorigenesis and Metastasis in Human Osteosarcoma by Upregulating FOSL2 through Sponging miR-342-3p

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