SALL4 suppresses PTEN expression to promote glioma cell proliferation via PI3K/AKT signaling pathway

Liu, Chuanjin; Wu, Haibin; Li, Yanyan; Shen, Liang; Yu, Renchun; Yin, Hongwei; Sun, Ting; Sun, Chao; Du, Ziwei

doi:10.1007/s11060-017-2589-3

Cited by 40 publications

(37 citation statements)

References 46 publications

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“…Cell cycle analysis showed that the proportion of G1-phase cells was significantly increased, whereas the percentage of S-phase cells was significantly decreased with the increase ofAG1478 concentration. These results are consistent with previous reports [22][23][24], indicating that the main mechanism of action of AG1478 may be through its binding to EGFR, which then inhibits autophosphorylation, blocks EGFR-mediated signalling pathways, hinders cell cycle progression, inhibits cell proliferation and promotes apoptosis. The c-Myc protein, which has been proved to be an essential factor for cell proliferation, is also an accessory factor for reverse transcription that plays important roles in signal transduction, cell proliferation, differentiation, apoptosis and cell cycle control.…”

Section: Comparative Analysissupporting

confidence: 93%

Epidermal growth factor receptor inhibitor AG1478 affects HepG2 cell proliferation, cell cycle, apoptosis and c-Myc protein expression in a dose-dependent manner

Wang

Yan

Liu

et al. 2018

Biotechnology & Biotechnological Equipment

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The aim of this study was to observe the effect of AG1478, an inhibitor of the epidermal growth factor receptor, on cell proliferation, cell cycle and apoptosis of human hepatoma HepG2 cells. Cell counting kit-8 assay was employed to examine the survival rates of cultured HepG2 cells after treatments with different concentrations of AG1478 for 24 h. Flow cytometry was performed to determine the effect of AG1478 on cell cycle and apoptosis. Immunohistochemistry was used to measure the expression of c-Myc protein. The survival rates of human hepatoma HepG2 cells after

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Section: Comparative Analysissupporting

confidence: 93%

Epidermal growth factor receptor inhibitor AG1478 affects HepG2 cell proliferation, cell cycle, apoptosis and c-Myc protein expression in a dose-dependent manner

Wang

Yan

Liu

et al. 2018

Biotechnology & Biotechnological Equipment

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“…This results in enhanced translation of a subset of genes that are required for protein synthesis, as well as acceleration of cell proliferation, which finally lead to tumorigenesis. [22][23][24] Previous studies report that polyamines are involved in the inhibition of AKT phosphorylation in colorectal cancer cells. 25 In addition, knockdown of AOC1 suppressed the EMT process in human gastric cancer cells.…”

Section: Discussionmentioning

confidence: 99%

<p>AOC1 Contributes to Tumor Progression by Promoting the AKT and EMT Pathways in Gastric Cancer</p>

Xu¹,

Xu²,

Xiong³

et al. 2020

CMAR

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Background: AOC1 is a copper-containing amine oxidase that is responsible for catalyzing the deamination of polyamines, which produces reactive oxygen species. Previous studies have demonstrated that polyamines are involved in the regulation of proliferation, migration, and apoptosis of cells. However, very little is known about the functions and regulatory mechanisms of AOC1 in tumors. Methods: Based on GEPIA data, we found that AOC1 was significantly upregulated in human gastric cancer tissues. We knocked down AOC1 in human AGS and MKN45 cells using siRNA transfection, then utilized qRT-PCR assay and Western blot to verify the effectiveness of AOC1 knockdown in gastric cancer cells. Results: Function analysis demonstrated that knockdown of AOC1 inhibited the proliferation, invasion, and migration of human gastric cancer cells. Flow cytometry detection suggested that AOC1 knockdown induced apoptosis in human gastric cancer cells. Mechanism investigation suggested that AOC1 knockdown increased the ratio of Bax/ Bcl2 and induced activation of the caspase cascade. Furthermore, the AKT signaling pathway was inactivated when AOC1 was silenced, including downregulated phosphorylation level of AKT and expression of downstream effectors, Cyclin D1, and p70S6K. Finally, we found that knockdown of AOC1 inhibited the epithelial-mesenchymal transition (EMT) in human gastric cancer by increasing the expression of epithelial markers E-cadherin, as well as decreasing mesenchymal marker N-cadherin, SNAIL and Slug. Conclusion: Our study suggests that AOC1 functions as an oncogene in human gastric cancer by activating the AKT signaling pathway and EMT process and maybe a target of 6-mercaptopurine, which provides new insight in the clinical use of AOC1 in gastric cancer therapy.

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“…For example, E3 ubiquitin-protein ligase regulated PTEN/PI3K/AKT signaling to promote the cell growth and migration of hepatocellular carcinoma cells (29). Liu et al (30) reported that Sal-like protein 4 suppressed PTEN expression to promote glioma cell proliferation via the PI3K/AKT pathway. Another study revealed that miRNA-1297 contributed to tumor growth of human breast cancer by targeting the PTEN/PI3K/AKT signaling pathway (28).…”

Section: Discussionmentioning

confidence: 99%

miR‑494‑3p promotes the progression of endometrial cancer by regulating the PTEN/PI3K/AKT pathway

Zhu

Wang²,

Wang

et al. 2018

Mol Med Report

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MicroRNAs (miRs) are essential regulators in the development and progression of cancer. The role of miR-494-3p in endometrial cancer (EC) has not yet been investigated. In the present study, the expression levels of miR-494-3p were significantly upregulated in EC tissues compared with adjacent normal tissues. Furthermore, upregulation of miR-494-3p in patients with EC indicated poorer prognosis; miR-494-3p overexpression significantly promoted the proliferation, migration and invasion of HHUA and JEC cells in vitro. Consistently, inhibition of miR-494-3p in HHUA cells significantly suppressed tumor growth in vivo in a xenograft model. Additionally, phosphatase and tensin homolog (PTEN) was revealed to be a direct target of miR-494-3p in EC cells. Furthermore, overexpression of miR-494-3p inhibited PTEN expression and consequently activated the downstream phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signialing pathway. Restoration of PTEN or inhibition of PI3K/AKT pathway also abolished miR-494-3p-mediated proliferation, migration and invasion of HHUA and JEC cells. In summary, the results of the present study revealed the importance of the miR-494-3p/PTEN/PI3K/AKT axis in the progression of EC, which may provide novel insight into potential therapeutic targets for the treatment of EC.

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SALL4 suppresses PTEN expression to promote glioma cell proliferation via PI3K/AKT signaling pathway

Cited by 40 publications

References 46 publications

Epidermal growth factor receptor inhibitor AG1478 affects HepG2 cell proliferation, cell cycle, apoptosis and c-Myc protein expression in a dose-dependent manner

Epidermal growth factor receptor inhibitor AG1478 affects HepG2 cell proliferation, cell cycle, apoptosis and c-Myc protein expression in a dose-dependent manner

<p>AOC1 Contributes to Tumor Progression by Promoting the AKT and EMT Pathways in Gastric Cancer</p>

miR‑494‑3p promotes the progression of endometrial cancer by regulating the PTEN/PI3K/AKT pathway

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