Bmi‐1 regulates the migration and invasion of glioma cells through p16

Liang, Jun; Wang, Peng; Xie, Shao; Wang, Weifeng; Zhou, Xiuping; Hu, Jinxia; Shi, Qiong; Zhang, Xianli; Yu, Rutong

doi:10.1002/cbin.10390

Cited by 5 publications

(5 citation statements)

References 38 publications

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“…Bmi1 is highly elevated in glioma tissues and patients with high levels of Bmi1 show a poor survival rate (52). Bmi1 promotes glioma cell migration and invasion via nuclear factor kappa B and p16 (25,28,53). Consistently, our results showed that the inhibition of Bmi1 by miR-194 significantly suppressed the glioma cell migration, invasion and EMT, further implying that Bmi1 can serve as a therapeutic target for preventing glioma metastasis.…”

Section: Discussionsupporting

confidence: 83%

“…Notably, a recent study has shown that Bmi1 plays an important role in inducing EMT (22)(23)(24). Bmi1 plays an important role in glioma tumorigenesis through promoting the invasion, migration, angiogenesis and proliferation of glioma cells (25)(26)(27)(28). Therefore, targeted therapy on Bmi1 may have promising and potential therapeutic values on glioma treatment.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-194 represses glioma cell epithelial-to-mesenchymal transition by targeting Bmi1

et al. 2017

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MicroRNA-194 (miR-194) is frequently dysregulated in many types of cancer. However, the function of miR-194 in glioma remains unknown. In the present study, we aimed to investigate the biological functions of miR-194 in glioma and the potential molecular mechanism of miR-194 involved in glioma progression. We found that miR-194 expression was significantly reduced in glioma specimens and cell lines, as detected by real-time quantitative polymerase chain reaction (RT-qPCR) analysis. The overexpression of miR-194 inhibited while the suppression of miR-194 promoted cell migration, invasion and epithelial mesenchymal transition (EMT) in glioma cells. Bioinformatics analysis showed that the B cell-specific moloney murine leukemia virus insertion site 1 (Bmi1) was a direct target of miR-194, which was validated by dual-luciferase reporter assay, RT-qPCR and western blot analysis. The restoration of Bmi1 expression significantly abrogated the suppressive effect of miR-194 on glioma cell EMT. Taken together, the present study suggests that miR-194 inhibits glioma cell EMT by targeting Bmi1 providing novel insights into understanding the pathogenesis of glioma. The restoration of miR-194 may be a potential therapeutic strategy for glioma treatment.

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Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

MicroRNA-194 represses glioma cell epithelial-to-mesenchymal transition by targeting Bmi1

et al. 2017

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“…Recently, Nayak (26) reported that nuclear VAV3 served an important role in B-cell lymphoblastic leukemogenesis through regulation of nuclear Bmi1 phosphorylation and polycomb repression complex-1 (PRC1) activity. the role of BMI 1 in the regulation of glioblastoma migration, invasion and stem cell renewal has been reported by numerous previous studies (27)(28)(29)(30). Therefore, VaV3 could regulate glioblastoma migration, invasion and stem cell stemness via regulation of the PI3K-AKT signaling pathway or PRC1 activity.…”

Section: Discussionmentioning

confidence: 54%

VAV3 regulates glioblastoma cell proliferation, migration, invasion and cancer stem‑like cell self‑renewal

et al. 2023

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Glioblastoma multiforme (GBM; World Health Organization grade IV) is one of the most common and aggressive malignant brain tumors and has no effective treatment. Therefore, elucidation of the molecular mechanism of glioma development is very important for finding new therapeutic strategies. The present study evaluated the expression level of Vav guanine nucleotide exchange factor 3 (VAV3) using bioinformatics analysis and demonstrated that VAV3 was overexpressed in human glioblastoma and associated with patient survival. Knock down of VAV3 using shRNA in glioblastoma cells significantly inhibited glioblastoma cell migration, invasion and proliferation. Furthermore, downregulation of VAV3 expression inhibited the stem cell self-renewal capacity and decreased the expression levels of the stem cell markers Nestin and Sox2. Bioinformatic analysis demonstrated that VAV3 was a target gene of miR-218. Furthermore, overexpression of VAV3 markedly reversed the tumor suppressor effect of miR-218 in glioblastoma cell. These findings suggested that VAV3 could be a potential biomarker and therapeutic target for glioblastoma.

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“…The results are consistent with those from a study by Chintala et al (12), which demonstrated that restoring wild-type P16 activity into P16-null SNB19 glioma cells significantly inhibited tumor cell invasion, thus, suggesting the P16 gene may inhibit the invasion of multiple tumor cell types. Liang et al (20) also demonstrated that reduced glioma cell invasion due to decreased BMI-1 proto-oncogene was rescued by P16 downregulation, and that BMI-1 enhances to the motility of glioma cells by regulating the expression of P16, indicating that P16 is important during tumor cell invasion (20).…”

Section: Discussionmentioning

confidence: 99%

Adenovirus with p16 gene exerts antitumor effect on laryngeal carcinoma Hep2 cells

Yang

et al. 2016

Molecular Medicine Reports

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Laryngeal cancer is an uncommon form of cancer. The tumor suppressor P16, known to be mutated or deleted in various types of human tumor, including laryngeal carcinoma, is involved in the formation and development of laryngeal carcinoma. It has been previously reported that the inactivation or loss of P16 is associated with the acquisition of malignant characteristics. The current study hypothesized that restoring wild‑type P16 activity into P16‑null malignant Hep2 cells may exert an antitumor effect. A recombinant adenovirus carrying the P16 gene (Ad‑P16) was used to infect and express high levels of P16 protein in P16‑null Hep2 cells. Cell proliferation and invasion assays and polymerase chain reaction were performed to evaluate the effects of the P16 gene on cell proliferation and the antitumor effect on Hep2 cells. The results demonstrated that the Hep2 cells infected with Ad‑P16 exhibited significantly reduced cell proliferation, invasion and tumor volume compared with untreated or control adenovirus cells. Furthermore, the expression of laryngeal carcinoma‑associated genes, EGFR, survivin and cyclin D1, were measured in Ad‑P16‑infected cells and were significantly reduced compared with control groups. The results of the current study demonstrate that restoring wild‑type P16 activity into P16-null Hep2 cells exerts an antitumor effect.

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Bmi‐1 regulates the migration and invasion of glioma cells through p16

Cited by 5 publications

References 38 publications

MicroRNA-194 represses glioma cell epithelial-to-mesenchymal transition by targeting Bmi1

MicroRNA-194 represses glioma cell epithelial-to-mesenchymal transition by targeting Bmi1

VAV3 regulates glioblastoma cell proliferation, migration, invasion and cancer stem‑like cell self‑renewal

Adenovirus with p16 gene exerts antitumor effect on laryngeal carcinoma Hep2 cells

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