miR‐134 inhibits osteosarcoma cell invasion and metastasis through targeting <scp>MMP</scp>1 and <scp>MMP</scp>3 <i>in vitro</i> and <i>in vivo</i>

Chen, Chenglong; Zhang, Long; Jiao, Yurui; Zhou, Yi; Ge, Qiaofeng; Li, Pengcui; Sun, Xiaojuan

doi:10.1002/1873-3468.13387

Cited by 44 publications

(34 citation statements)

References 54 publications

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“…We found that in addition to KLF4 and BMI1, miR-135a also inhibited the expression of MMP2 and MMP9, as shown by Western blot, and inhibited MMP activation, as shown by the decrease in the intensity of MMPSense in FMT, which plays important roles in promoting tumor invasion and metastasis. These data are consistent with our previously published study (8). Meanwhile, Zheng et al (38) showed that the decrease in MMP2 and MMP9 protein levels induced by DANCR silencing was partially increased by the miR-135a-5p inhibitor, which supports our result that miR-135a inhibits MMP2 and MMP9.…”

Section: Discussionsupporting

confidence: 93%

“…MicroRNAs (miRNAs) are a family of small, noncoding RNA molecules that regulate gene expression at the posttranscriptional level through either mRNA cleavage or translational repression through direct binding to the 3′ untranslated region (3′-UTR) (25,26). Our previous studies indicated that upregulation of some miRNAs could intensely restrain the growth, invasion, and metastasis in OS xenograft tumors and attenuate angiogenesis (8,27). We also found that the level of miRNA-135 (miR-135a-5p) was reduced in OS tissues from patients in whom BMI1, KLF4, and MMP expression was upregulated.…”

Section: Introductionmentioning

confidence: 99%

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miR-135a Reduces Osteosarcoma Pulmonary Metastasis by Targeting Both BMI1 and KLF4

et al. 2021

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Because of the modest response rate after surgery and chemotherapy, treatment of osteosarcoma (OS) remains challenging due to tumor recurrence and metastasis. miR-135a has been reported to act as an anticarcinogenic regulator of several cancers. However, its expression and function in osteosarcoma remain largely unknown. Here, we reported that abridged miR-135a expression in OS cells and tissues, and its expression is inversely correlated with the expression of BMI1 and KLF4, which are described as oncogenes in several cancers. Ectopic expression of miR-135a inhibited cell invasion and expression of BMI1 and KLF4 in OS cells. In vivo investigation confirmed that miR-135a acts as a tumor suppressor in OS to inhibit tumor growth and lung metastasis in xenograft nude mice. BMI1 and KLF4 were revealed to be direct targets of miR-135a, and miR-135a had a similar effect as the combination of si-BMI1 and si-KLF4 on inhibiting tumor progression and the expression of BMI1 and KLF4 in vivo. Altogether, our results demonstrate that the targeting of BMI1/KLF4 with miR-135a may provide an applicable strategy for exploring novel therapeutic approaches for OS.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

miR-135a Reduces Osteosarcoma Pulmonary Metastasis by Targeting Both BMI1 and KLF4

et al. 2021

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“…Several mechanisms have been reported in context of miR-134 mediated tumour regulation. In osteosarcoma, the upregulation of miR-134 reportedly inhibits cell invasion and metastasis via the suppression of MMP1 and MMP3 expression [26]. In addition, miR-134 is reported to impede EMT and reduce the invasive potential of NSCLC cells [27] and inhibit the growth of NSCLC by targeting the epidermal growth factor receptor [28].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: MicroRNA-134 prevents the progression of esophageal squamous cell carcinoma via the PLXNA1-mediated MAPK signalling pathway

et al. 2019

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Background: MicroRNAs (miRNAs) are involved in oncogenesis of esophageal squamous cell carcinoma (ESCC). miR-134 is reported to have a tumour-suppressive role but its role in ESCC is not known. The present study was designed to examine whether miR-134 inhibits ESCC development and further explored relevant underlying mechanisms. Methods: Differentially expressed genes related to ESCC were identified from microarray gene expression profiles. Immunohistochemical staining and RT-qRCR assays identified elevated PLXNA1 expression levels and low miR-134. The relationship between miR-134 and PLXNA1 was predicted and further verified by a dualluciferase reporter assay. The expression levels of miR-134 and PLXNA1 in ESCC cells were modified by miR-134 mimic/inhibitor and siRNA against PLXNA1, respectively. Thereafter, the expression of MAPK signalling pathway-related proteins, as well as the viability, migration, invasion, cell cycle and cell apoptosis of ESCC cells was investigated. Findings: The results showed that miR-134 could block the MAPK signalling pathway by downregulating PLXNA1. When miR-134 was overexpressed or PLXNA1 was silenced, cell apoptosis was enhanced, the cell cycle was retarded, and the cell proliferation, migration and invasion were suppressed. In vivo experiments confirmed that miR-134 overexpression or PLXNA1 silencing restrained tumour growth and lymph node metastasis. Interpretation: These findings demonstrate that cancer cell proliferation, migration, invasion, and tumour metastasis of ESCC can be suppressed by overexpression of miR-134 through downregulating PLXNA1, which subsequently blocks the MAPK signalling pathway. These results provide new potential targets and strategies for the treatment of ESCC.

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“…MiR-134-5p can also be targeted and regulated by lncRNA [32, 33]. Studies have found that miR-134-5p exerts anti-tumour effects by affecting target gene expression in osteosarcoma [34–36]. This study demonstrated that miR-134-5p was regulated by lncRNA TTN-AS1 to inhibit osteosarcoma growth and apoptosis.…”

Section: Discussionmentioning

confidence: 81%

LncRNA TTN-AS1 regulates osteosarcoma cell apoptosis and drug resistance via the miR-134-5p/MBTD1 axis

et al. 2019

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Aim: To explore the mechanism by which long non-coding RNA (lncRNA) TTN-AS1 regulates osteosarcoma cell apoptosis and drug resistance via the microRNA miR-134-5p/malignant brain tumour domain containing 1 (MBTD1) axis.Results: The lncRNA TTN-AS1 was highly expressed in osteosarcoma and was associated with poor prognosis. The lncRNA TTN-AS1 promoted cell viability and inhibited apoptosis. MiR-134-5p targeted MBTD1, which was regulated by lncRNA TTN-AS1. MBTD1 was highly expressed in osteosarcoma and was associated with poor prognosis. MBTD1 promoted cell viability and inhibited apoptosis, and knockdown of MBTD1 reversed the cancer-promoting effects of lncRNA TTN-AS1. Downregulation of lncRNA TTN-AS1 reduced drug resistance.Conclusion: In osteosarcoma, lncRNA TTN-AS1 promoted the expression of MBTD1 by targeting miR-134-5p and regulated cell growth, apoptosis and drug resistance.Methods: The expression characteristics of genes in osteosarcoma patients were analysed using bioinformatics. Plasmid transfection technology was applied to silence or overexpress lncRNA TTN-AS1, miR-134-5p and MBTD1. Western blotting and quantitative polymerase chain reaction (qPCR) were used to detect protein and RNA, respectively. A cell counting kit 8 (CCK-8) and flow cytometry were used to detect cell viability and apoptosis. The effects of lncRNA TTN-AS1 and MBTD1 on osteosarcoma in vivo were studied by using a tumour burden assay.

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miR‐134 inhibits osteosarcoma cell invasion and metastasis through targeting MMP1 and MMP3 in vitro and in vivo

Cited by 44 publications

References 54 publications

miR-135a Reduces Osteosarcoma Pulmonary Metastasis by Targeting Both BMI1 and KLF4

miR-135a Reduces Osteosarcoma Pulmonary Metastasis by Targeting Both BMI1 and KLF4

RETRACTED: MicroRNA-134 prevents the progression of esophageal squamous cell carcinoma via the PLXNA1-mediated MAPK signalling pathway

LncRNA TTN-AS1 regulates osteosarcoma cell apoptosis and drug resistance via the miR-134-5p/MBTD1 axis

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