<i>MiR-130a-3p</i> inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

Chen, Xin; Yue, Bo; Zhang, Changming; Qi, Meihao; Qiu, Jianhua; Wang, Ye; Chen, Jun

doi:10.1042/bsr20160576

Cited by 33 publications

(28 citation statements)

References 42 publications

(53 reference statements)

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“…Abnormal expression of RPN2 has been reported in breast cancer, non-small cell lung cancer, gastric cancer, colorectal cancer, and prostatic carcinoma. 11 – 13 In the present study, we observed a marked increase in RPN2 expression in NPC tissues. The subsequent experiments were designed to explore the effect of siRNA-RPN2 treatment on tumor migration and invasion in NPC.…”

Section: Discussionsupporting

confidence: 66%

Downregulation of ribophorin II suppresses tumor growth, migration, and invasion of nasopharyngeal carcinoma

Hong

et al. 2018

OTT

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BackgroundIt has been reported that ribophorin II (RPN2) expression is increased in many cancers, but the role of RPN2 in nasopharyngeal carcinoma (NPC) remains unclear.Patients and methodsThis study found that the expression of RPN2 is increased dramatically in NPC tissues of patients compared with that in the adjacent normal tissues. This study attempted at understanding the effect of siRNA-RPN2 treatment on the migration and invasion of NPC cell lines CNE2 and HNE1.ResultsRT-PCR and Western blotting showed that RPN2 was highly expressed in CNE2 and HNE1 cells. siRNA-RPN2 treatment significantly inhibited cell viability at 24 and 48 h compared with the control group. Results of the transwell assay showed that, compared to the control groups, migration and invasion of the cells treated with siRNA-RPN2 decreased markedly. In addition, compared to the control groups, caspase-3, caspase-9, and E-cadherin expression levels increased and MMP 2 expression decreased significantly in the siRNA-RPN2-treated group. Phosphorylation of AKT and PI3K was also inhibited after siRNA-RPN2 treatment.ConclusionsiRNA-RPN2 can effectively inhibit the invasion and migration of human NPC cells via AKT/PI3K signaling. This can serve as a novel strategy for NPC treatment.

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Section: Discussionsupporting

confidence: 66%

Downregulation of ribophorin II suppresses tumor growth, migration, and invasion of nasopharyngeal carcinoma

Hong

et al. 2018

OTT

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“…The downregulation of BACH2 significantly inhibits the viability, migration and invasive ability of glioma cells and promotes glioma cell apoptosis, suggesting that BACH2 may act as an oncogene. Chen et al [32] found that BACH2 is upregulated in NPC, while its knockdown inhibits the proliferation, migration and invasion of NPC cells. BACH2 expression varies in different tumours; CD19+ B cells from mantle cell lymphoma patient samples showed reduced BACH2 levels.…”

Section: Discussionmentioning

confidence: 99%

Interaction of BACH2 with FUS promotes malignant progression of glioma cells via the TSLNC8–miR‐10b‐5p–WWC3 pathway

et al. 2020

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Glioma, a common malignant tumour of the human central nervous system, has poor prognosis and limited treatment options. Dissecting the biological mechanisms underlying glioma pathogenesis can facilitate the development of better therapies. Here, we investigated the endogenous expression of BTB and CNC homolog 2 (BACH2), fused in sarcoma (FUS), TSLNC8 and microRNA (miR)-10b-5p in glioma cells and tissues. We studied the interaction between BACH2 and FUS and its contribution to glioma progression. We demonstrated that the interaction between BACH2 and FUS promoted glioma progression via transcriptional inhibition of TSLNC8. Overexpression of TSLNC8 restrained glioma progression by suppressing miR-10b-5p. Binding of TSLNC8 to miR-10b-5p attenuated the suppression of WWC family member 3 (WWC3) by miR-10b-5p and activated the Hippo signalling pathway. Growth of subcutaneous xenografts could be inhibited by knockdown of BACH2 or FUS, by overexpressing TSLNC8 or a combination of the three, also leading to a prolonged survival in nude mice. Our results indicate that the BACH2 and FUS/TSLNC8/miR-10b-5p/WWC3 axis is responsible for glioma development and could serve as a potential target for the development of new glioma therapies.

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“…miR‐199b‐5p promotes cell aggregation, suppresses cell invasion and migration and inhibits TGF‐β‐induced EMT in hepatocellular carcinoma by inhibiting N‐cadherin . In several studies, miR‐130a‐3p was shown to decrease in cancer tissues and inhibit cell invasion, migration, and EMT . By contrast, miR‐130a‐3p is upregulated in some GC cases and promotes cell proliferation and migration in GC cells.…”

Section: Discussionmentioning

confidence: 99%

miR‐130a‐3p regulated TGF‐β1‐induced epithelial‐mesenchymal transition depends on SMAD4 in EC‐1 cells

Tian

Qian

et al. 2019

Cancer Medicine

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Metastasis and invasion are the primary causes of malignant progression in esophageal squamous cell carcinoma (ESCC). Epithelial‐mesenchymal transition (EMT) is crucial step of acquisition of "stemness" properties in tumor cells. However, the mechanism of esophageal cancer metastasis remains unclear. This research was designed to explore the role and mechanism of SMAD4 and miR‐130a‐3p in the progression of transforming growth factor‐β (TGF‐β)‐induced EMT in vivo and in vitro. The expression of miR‐130a‐3p in ESCC cell line and normal esophageal epithelial cell was determined by RT‐qPCR. The protein expression levels of TGF‐β‐induced changes in EMT were analyzed by western blotting and immunofluorescence. Dual‐luciferase report assays were used to validate the regulation of miR‐130a‐3p‐SMAD4 axis. The effect of miR‐130a‐3p and SMAD4 in TGF‐β‐induced migration, invasion in the ESCC cell line EC‐1 was investigated by wound healing assays and Transwell assays. Here we found that knocked down SMAD4 could partially reverse TGF‐β‐induced migration, invasion, and EMT progression in the ESCC cell line EC‐1. miR‐130a‐3p, which directly targets SMAD4, is down‐regulated in ESCC. miR‐130a‐3p inhibits the migration and invasion of EC‐1 cells both in vitro and in vivo. Finally, miR‐130a‐3p inhibits TGF‐β‐induced EC‐1 cell migration, invasion, and EMT progression in a SMAD4‐dependent way. In conclusion, this study provides new insights into the mechanism underlying ESCC metastasis. The TGF‐β/miR‐130a‐3p/SMAD4 pathway could be potential targets for clinical treatment of ESCC.

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MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

Cited by 33 publications

References 42 publications

Downregulation of ribophorin II suppresses tumor growth, migration, and invasion of nasopharyngeal carcinoma

Downregulation of ribophorin II suppresses tumor growth, migration, and invasion of nasopharyngeal carcinoma

Interaction of BACH2 with FUS promotes malignant progression of glioma cells via the TSLNC8–miR‐10b‐5p–WWC3 pathway

miR‐130a‐3p regulated TGF‐β1‐induced epithelial‐mesenchymal transition depends on SMAD4 in EC‐1 cells

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