BRCA1-associated protein inhibits glioma cell proliferation and migration and glioma stem cell self-renewal via the TGF-β/PI3K/AKT/mTOR signalling pathway

Wang, Bo; Cao, Chen; Liu, Xi; He, Xin; Zhuang, Hao; Wang, Dong; Chen, Budong

doi:10.1007/s13402-019-00482-8

Cited by 27 publications

(19 citation statements)

References 36 publications

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“…In gliomas, the PI3K/AKT/mTOR pathway helps to induce invasion and angiogenesis in cells, and patients with activated PI3K/AKT/mTOR pathway have a worse prognosis than those without carcinogenic activation of the pathway [ 39 , 40 ]. In addition, BRCA1-associated proteins inhibit glioma cell proliferation and migration through the TGF- AKT/PI3K/mTOR signaling pathway [ 41 ] To some extent, the above research [ 13 ]. Besides in gliomas, this pathway was involved in the pathological mechanism of other cancer.…”

Section: Discussionmentioning

confidence: 99%

M2 macrophage-derived exosomal microRNAs inhibit cell migration and invasion in gliomas through PI3K/AKT/mTOR signaling pathway

et al. 2021

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Background Glioma, the most common primary brain tumor, account Preparing figures for 30 to 40% of all intracranial tumors. Herein, we aimed to study the effects of M2 macrophage-derived exosomal microRNAs (miRNAs) on glioma cells. Methods First, we identified seven differentially expressed miRNAs in infiltrating macrophages and detected the expression of these seven miRNAs in M2 macrophages. We then selected hsa-miR-15a-5p (miR-15a) and hsa-miR-92a-3p (miR-92a) for follow-up studies, and confirmed that miR-15a and miR-92a were under-expressed in M2 macrophage exosomes. Subsequently, we demonstrated that M2 macrophage-derived exosomes promoted migration and invasion of glioma cells, while exosomal miR-15a and miR-92a had the opposite effects on glioma cells. Next, we performed the target gene prediction in four databases and conducted target gene validation by qRT-PCR, western blot and dual luciferase reporter gene assays. Results The results revealed that miR-15a and miR-92a were bound to CCND1 and RAP1B, respectively. Western blot assays demonstrated that interference with the expression of CCND1 or RAP1B reduced the phosphorylation level of AKT and mTOR, indicating that both CCND1 and RAP1B can activate the PI3K/AKT/mTOR signaling pathway. Conclusion Collectively, these findings indicate that M2 macrophage-derived exosomal miR-15a and miR-92a inhibit cell migration and invasion of glioma cells through PI3K/AKT/mTOR signaling pathway.

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Section: Discussionmentioning

confidence: 99%

M2 macrophage-derived exosomal microRNAs inhibit cell migration and invasion in gliomas through PI3K/AKT/mTOR signaling pathway

et al. 2021

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“…PI3K/AKT pathway is an important signaling pathway involved in tumorigenesis, which demonstrates its antiapoptotic effect mainly by affecting multiple effector molecules. 14,18,19 In this research, we found that the expression levels of p-PI3K, p-AKT and p-STAT3 were remarkably downregulated after MALAT1 knockdown in GC cells, while the protein levels of p-PI3K, p-AKT and p-STAT3 were significantly upregulated after MALAT1 overexpression in GC cells, indicating that MALAT1 contributes to proliferation and metastasis in GC via the PI3K/AKT pathway. Furthermore, we hypothesized the underlying role of MALAT1 in chemotherapy resistance of GC.…”

Section: Discussionmentioning

confidence: 63%

“…PI3K/AKT pathway has been confirmed to regulate cellular functions, including cell migration and invasion. 14,18,19 Therefore, we hypothesized whether MALAT1 contributes to GC development through PI3K/AKT pathway. Western blot analysis demonstrated that protein levels of p-PI3K, p-AKT and p-STAT3 were downregulated after MALAT1 knockdown in GC cells ( Figure 4A).…”

Section: Malat1 Regulates Pi3k/akt Pathwaymentioning

confidence: 99%

<p>LncRNA MALAT1 Regulates the Cell Proliferation and Cisplatin Resistance in Gastric Cancer via PI3K/AKT Pathway</p>

Dai¹,

Zhang²,

Li³

2020

CMAR

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Background: Many studies showed that long non-coding RNA MALAT1 is served as an oncogene. However, the specific role of MALAT1 in gastric cancer is not fully elucidated. The aim of this study is to elucidate the regulatory effects of MALAT1 on tumor development and cisplatin resistance in gastric cancer. Methods: TCGA database was applied to investigate the expression levels of MALAT1 in GC tissues and normal gastric tissues and its correlation with GC patients' survival. Univariate and multivariate analysis were performed to investigate whether MALAT1 expression is an independent risk for overall survival of gastric cancer patients. The expression of MALAT1 was detected by Quantitative real-time PCR. After knockdown or overexpression of MALAT1, the cellular functions of GC cells were detected by cell-proliferation, flow cytometry, transwell assay and colony formation assays, respectively. Western blot analysis was performed to detect the protein levels of Bcl-2 and key genes in the PI3K/AKT pathway in GC cells. Finally, CCK-8 assay was performed to explore the effect of MALAT1 on cisplatin resistance of GC cells. Results: Higher expression of MALAT1 was detected in GC tissues than that of adjacent normal tissues, high MALAT1 expression is an independent risk for overall survival of gastric cancer patients. Knockdown of MALAT1 inhibited proliferation, migration and invasion of GC cells, while overexpression of MALAT1 Overexpression of MALAT1 yielded opposite results. Western blot results showed that protein expressions of p-PI3K, p-AKT and p-STAT3 were downregulated after MALAT1 knockdown in GC cells, while these proteins were upregulated after MALAT1 overexpression. Additionally, the IC 50 in MGC803/CDDP cells transfected with si-MALAT1 was lower than in those transfected with si-NC. The apoptotic rate in MGC803 cells transfected with pcDNA-MALAT1 was remarkably lower than those transfected with NC. Conclusion: We demonstrated that MALAT1 is highly expressed in GC, high MALAT1 expression is an independent risk factor for OS among GC patients. Moreover, MALAT1 promotes malignant progression of GC and contributes to cisplatin resistance of GC cells, indicating MALAT1 may serve as a biological hallmark for predicting the prognosis of GC.

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“…So, revealing interaction between TGF-β and autophagy can be of importance for developing therapeutics. The interesting point is that TGF-β can affect various molecular pathways in disease development including mTOR ( Chen et al, 2020c ), PI3K/Akt ( Wang et al, 2020a ), Wnt ( Liu et al, 2019 ), and STAT3 ( Dees et al, 2020 ). There are also molecular pathways that can function as upstream mediators of TGF-β in pathological events.…”

Section: Transforming Growth Factor-beta Signaling Pathway: From Basimentioning

confidence: 99%

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

et al. 2020

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Immune response, proliferation, migration and angiogenesis are juts a few of cellular events that are regulated by transforming growth factor-β (TGF-β) in cells. A number of studies have documented that TGF-β undergoes abnormal expression in different diseases, e.g., diabetes, cancer, fibrosis, asthma, arthritis, among others. This has led to great fascination into this signaling pathway and developing agents with modulatory impact on TGF-β. Curcumin, a natural-based compound, is obtained from rhizome and roots of turmeric plant. It has a number of pharmacological activities including antioxidant, anti-inflammatory, anti-tumor, anti-diabetes and so on. Noteworthy, it has been demonstrated that curcumin affects different molecular signaling pathways such as Wnt/β-catenin, Nrf2, AMPK, mitogen-activated protein kinase and so on. In the present review, we evaluate the potential of curcumin in regulation of TGF-β signaling pathway to corelate it with therapeutic impacts of curcumin. By modulation of TGF-β (both upregulation and down-regulation), curcumin ameliorates fibrosis, neurological disorders, liver disease, diabetes and asthma. Besides, curcumin targets TGF-β signaling pathway which is capable of suppressing proliferation of tumor cells and invading cancer cells.

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BRCA1-associated protein inhibits glioma cell proliferation and migration and glioma stem cell self-renewal via the TGF-β/PI3K/AKT/mTOR signalling pathway

Cited by 27 publications

References 36 publications

M2 macrophage-derived exosomal microRNAs inhibit cell migration and invasion in gliomas through PI3K/AKT/mTOR signaling pathway

M2 macrophage-derived exosomal microRNAs inhibit cell migration and invasion in gliomas through PI3K/AKT/mTOR signaling pathway

<p>LncRNA MALAT1 Regulates the Cell Proliferation and Cisplatin Resistance in Gastric Cancer via PI3K/AKT Pathway</p>

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

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