MiR‐125b suppresses the carcinogenesis of osteosarcoma cells via the MAPK‐STAT3 pathway

Xiao, Tao; Li, Hui; Xiong, Liang; Wang, Jing; Wang, Zhihua; Liu, Li‑Hong

doi:10.1002/jcb.27568

Cited by 15 publications

(14 citation statements)

References 43 publications

(112 reference statements)

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“…In recent, accumulating evidence demonstrated that several miRNAs were dysregulated in types of tumors, and the oncogenic or anti-cancer roles of miRNA were obvious in various cancers [24–26]. For example, miR-125b has been found to play a vital role in the development of malignant tumors [3]. MiR-590 regulated the chemoresistance of osteosarcoma by targeting wild-type p53-induced phosphatase 1 (WIP1) [27].…”

Section: Discussionmentioning

confidence: 99%

“…Osteosarcoma (OS) is regarded as the most prevalent malignant bone cancer, which generally appears in the long bones of limbs as well as the growth plate nearby the metaphyseal [1, 2]. According to the reports, OS is usually observed in young adults and adolescents, and accounts for about 2.4% of all malignant tumors in children and exceeds about 20% of all primary bone cancers [3]. According to the reports, the morbidity of OS has reached approximately one to three cases annually per million all over the world [4].…”

Section: Introductionmentioning

confidence: 99%

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miR-328-3p mediates the anti-tumor effect in osteosarcoma via directly targeting MMP-16

Shi

Guan

et al. 2019

Cancer Cell Int

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Background: Increasing reports demonstrated that dysregulated expression of microRNAs (miRNAs) leads to the progression of various tumors. Previous studies revealed that miR-328-3p exhibited dysregulated expression in various types of tumors. However, its function and underlying mechanism in osteosarcoma (OS) are still unexplored. Methods:The expression of miR-328-3p in the tissues and OS cell lines was detected by qRT-PCR analysis. The effects of miR-328-3p in the proliferation were analyzed by MTT assay. The proliferation and apoptosis of OS cells were examined by colony formation assay and TUNEL staining respectively. The migration and tumor formation ability of OS cells were measured by wound healing assay and xenograft in vivo mice assay. Furthermore, the regulatory roles of miR-328-3p/MMP16 were determined by western blot and luciferase reporter assay. Results:The expression of miR-328-3p was significantly decreased in OS tissues and cell lines. Furthermore, overexpression of miR-328-3p inhibited the cell proliferation and migration, but promoted the apoptosis of OS cells in vitro. Moreover, the analysis in vivo showed that miR-328-3p effectively suppressed the formation of tumors. According to the results of western blot analysis and luciferase reporter assay, we identified matrix metalloproteinase-16 (MMP-16) acted as a direct target of miR-328-3p. Moreover, the expression level of MMP-16, which participates in the occurrence and development of many cancers, was negatively correlated with the miR-328-3p expression in OS cells.Conclusion: miR-328-3p inhibited the proliferation, migration but accelerated the apoptosis of OS by directly inhibiting MMP-16. And miR-328-3p/MMP-16 axis may be one of the mechanisms of OS development and a novel potential method for the treatment of OS in clinic.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

miR-328-3p mediates the anti-tumor effect in osteosarcoma via directly targeting MMP-16

Shi

Guan

et al. 2019

Cancer Cell Int

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“…MAPKs are also involved in numerous diseases. Xiao proved that miR-125b attenuates the carcinogenic progression of osteosarcoma cells by regulating the MAPK-STAT3 signaling pathway [25], and Han et al confirmed that micro-RNA-128 contributed to gastric carcinoma progression by activating GAREM-mediated MAPK signaling [26]. In the hypoxia/reoxygenation injury model, antiphospholipid antibody can affect the apoptosis of neonatal rat cardiomyocytes by regulating the p38 MAPK signaling pathway [27].…”

Section: Electronic Supplementary Materialsmentioning

confidence: 98%

Astragaloside IV protects human cardiomyocytes from hypoxia/reoxygenation injury by regulating miR-101a

Fan

Chen³

et al. 2020

Mol Cell Biochem

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Astragaloside IV (AS/IV) is one of the extracted components from the traditional Chinese medicine Astragalus which has been demonstrated to have potential capacity for anti-inflammation activity and for treating cardiovascular disease. Our purpose was to determine the function and underlying molecular mechanism of AS/IV in hypoxia/reoxygenation (H/R) injured in cardiomyocytes. Differentially expressed genes (DEGs) were screened using bioinformatic analysis, and the molecular targeting relationship was verified by the dual-luciferase report system. H/R injured cardiomyocytes were employed to explore the effect of AS/IV. QRT-PCR and Western blot analysis were applied to detect the expression of mRNA and proteins, respectively. Additionally, superoxide dismutase (SOD), lactic dehydrogenase (LDH) and MDA (malondialdehyde) levels were detected to determine the oxidative damage. Cell viability was assessed by CCK-8, and flow cytometry was used to evaluate cell apoptosis ratio. TGFBR1 and TLR2 were selected as DEGs. Additionally, AS/IV could enhance cell proliferation and upregulated miR-101a expression, which suppressed TGFBR1 and TLR2 expression in H/R injured cardiomyocytes. Moreover, the results of Western blot exhibited that the downstream genes (p-ERK and p-p38) in the MAPK signaling pathway were suppressed, which meant AS/IV could inhibit this pathway in H/R injured cardiomyocytes. Overall, this study demonstrated AS/IV could attenuate H/R injury in human cardiomyocytes via the miR-101a/TGFBR1/TLR2/ MAPK signaling pathway axis, which means that it could serve as a possible alternate for H/R treatment.

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“…miR-143 and miR-125b directly targets MAPK7 and suppresses MAPK7 expression in OS cells. These miRNAs suppress cell growth and invasion and migration [67,68]. Cyclin-dependent kinase 4 (CDK4) and mouse double minute 2 homolog (MDM2) are genes located in 12q13–q14.…”

Section: The Functions Of Mirna and Exosomes In Sarcomamentioning

confidence: 99%

An Insight into the Roles of MicroRNAs and Exosomes in Sarcoma

Kohama

Kosaka

Chikuda

et al. 2019

Cancers

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Sarcomas are rare solid tumors, but at least one-third of patients with sarcoma die from tumor-related disease. MicroRNA (miRNA) is a noncoding RNA that regulates gene expression in all cells and plays a key role in the progression of cancers. Recently, it was identified that miRNAs are transferred between cells by enclosure in extracellular vesicles, especially exosomes. The exosome is a 100 nm-sized membraned vesicle that is secreted by many kinds of cells and contains miRNA, mRNA, DNA, and proteins. Cancer uses exosomes to influence not only the tumor microenvironment but also the distant organ to create a premetastatic niche. The progression of sarcoma is also regulated by miRNAs and exosomes. These miRNAs and exosomes can be targeted as biomarkers and treatments. In this review, we summarize the studies of miRNA and exosomes in sarcoma.

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MiR‐125b suppresses the carcinogenesis of osteosarcoma cells via the MAPK‐STAT3 pathway

Cited by 15 publications

References 43 publications

miR-328-3p mediates the anti-tumor effect in osteosarcoma via directly targeting MMP-16

miR-328-3p mediates the anti-tumor effect in osteosarcoma via directly targeting MMP-16

Astragaloside IV protects human cardiomyocytes from hypoxia/reoxygenation injury by regulating miR-101a

An Insight into the Roles of MicroRNAs and Exosomes in Sarcoma

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