PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways

Jia, Mengmeng; Chen, Xiaoyun; Liu, Jili

doi:10.3892/mmr.2017.7912

Cited by 11 publications

(11 citation statements)

References 38 publications

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“…Caspase-3 is widely recognized as a pro-apoptosis factor [22]. Meanwhile, AKT signaling pathway is closely associated with cell growth [23,24]. In the current study, we found the protein content of cleaved caspase-3 was upregulated in miR-338-5p mimic transfected cells.…”

Section: Mir-338-5p Overexpression Suppressed the Growth And Invasionsupporting

confidence: 48%

miR-338-5p Targets Epidermal Growth Factor-Containing Fibulin-Like Extracellular Matrix Protein 1 to Inhibit the Growth and Invasion of Trophoblast Cells in Selective Intrauterine Growth Restriction

Wen

Chen

et al. 2020

Reprod. Sci.

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Selective intrauterine growth restriction (sIUGR) is a disorder of monochorionic (MC) twin pregnancies. However, the underlying mechanism remains largely unknown. Trophoblast cells are the major component of the placenta. Dysfunction of trophoblast cells is associated with placental dysfunction. Our previous study identified miR-338-5p is downregulated in placenta tissues sharing larger twins of sIUGR. In the present study, we aimed to investigate the role of miR-338-5p in trophoblast cells and explored its target. Our results further indicated that miR-338-5p was downregulated in placental tissues supporting larger twins of sIUGR, whereas epidermal growth factor-containing fibulin-like extracellular matrix protein 1 (EFEMP1) was upregulated. Moreover, miR-338-5p overexpression suppressed the growth and invasion of trophoblast cells. Importantly, results from luciferase reporter assay demonstrated that miR-338-5p bound on the 3′-UTR of EFEMP1. miR-338-5p suppressed the growth and invasion of trophoblast cells via targeting EFEMP1. Further, miR-338-5p/EFEMP1 might disrupt the function of trophoblast cells via inhibiting the phosphorylation of AKT.

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Section: Mir-338-5p Overexpression Suppressed the Growth And Invasionsupporting

confidence: 48%

miR-338-5p Targets Epidermal Growth Factor-Containing Fibulin-Like Extracellular Matrix Protein 1 to Inhibit the Growth and Invasion of Trophoblast Cells in Selective Intrauterine Growth Restriction

Wen

Chen

et al. 2020

Reprod. Sci.

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“…Previous report has demonstrated that PTEN accelerates cell apoptosis via PI3/AKT pathway [28]. Moreover, TRIM27 has enhanced the phosphorylation of AKT pathway in colorectal cancer [5].…”

Section: Discussionmentioning

confidence: 99%

TRIM27 promotes the development of esophagus cancer via regulating PTEN/AKT signaling pathway

Yao

Chen

et al. 2019

Cancer Cell Int

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Background: Tripartite motif-containing 27 (TRIM27) belongs to the TRIM protein family, which is closely related to the progression of some certain human cancers. Nevertheless, the biological function of TRIM27 in esophageal squamous cell carcinoma (ESCC) is still not clear. The aim of present research is to examine the function of TRIM27 in ESCC cells. Methods: In the present study, RNA interference (RNAi) and lentiviral vector were used to knockdown and overexpression of TRIM27 in ESCC cells respectively. qRT-PCR and western blot were used to examine the expression of TRIM27 in ESCC cells. Cell counting kit-8 (CCK-8) assay was performed to determine the proliferation of cells. Results: Our analyses indicated that TRIM27 was a pro-proliferation factor in ESCC cells. Moreover, overexpression of TRIM27 deeply suppressed the apoptosis of ESCC cells and accelerated its glucose uptake. In addition, an AKT inhibitor LY294002 was used to determine the connection between TRIM27 and AKT in ESCC cells. Our results demonstrated that TRIM27 has involved in the PI3/AKT signaling pathway. Moreover, TRIM27 interacted with PTEN and mediated its poly-ubiquitination in ESCC cells. Importantly, the glycolysis inhibitor 3-BrPA also inhibited the effect of TRIM27 on ESCC cells. Hence, TRIM27 also participated in the regulation of energy metabolism in ESCC cells. Conclusions: This research not only gained a deep insight into the biological function of TRIM27 but also elucidated its potential target and signaling pathway in human ESCC cells.

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“…Based on this knowledge, it is important to investigate whether mitophagy is involved in inflammatory injury in nasal epithelial cells. In addition to mitophagy, phosphatase and tensin homolog (PTEN) is the intrinsic defender of nasal and sinus inflammatory injury (25,26). PTEN functions as a tumor suppressor involving in the regulation of the cell growth and differentiation (27).…”

Section: Pten Enhances Nasal Epithelial Cell Resistance To Tnfα-inducmentioning

confidence: 99%

PTEN enhances nasal epithelial cell resistance to TNFα‑induced inflammatory injury by limiting mitophagy via repression of the TLR4‑JNK‑Bnip3 pathway

Xiang

Shouchuan

2018

Mol Med Report

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Nasal epithelial cell inflammatory injury is associated with chronic obstructive pulmonary disease development. However, the mechanism by which inflammation triggers nasal epithelial cell damage remains unclear. In the present study, tumor necrosis factor (TNF)α was used to induce an inflammatory injury and explore the underlying pathogenesis for nasal epithelial cell apoptosis in vitro, with a focus on mitochondrial homeostasis. Then, cellular apoptosis was detected via a terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling assay and western blotting. Mitochondrial function was evaluated via JC‑1 staining, mPTP opening measurement and western blotting. The results demonstrated that TNFα treatment induced nasal epithelial cell apoptosis, proliferation arrest and migration inhibition via downregulating phosphatase and tensin homolog (PTEN) levels. Increased PTEN expression was associated with reduce Toll‑like receptor (TLR)4‑c‑Jun kinase (JNK)‑Bcl2‑interacting protein 3 (Bnip3) pathway signaling, leading to reductions in mitophagy activity. Excessive mitophagy resulted in ATP deficiencies, mitochondrial dysfunction, caspase‑9 activation and cellular apoptosis. By contrast, PTEN overexpression in nasal epithelial cells alleviated the mitochondrial damage and cellular apoptosis via inhibiting the TLR4‑JNK‑Bnip3 pathway, favoring the survival of nasal epithelial cells under inflammatory injury. Therefore, this data uncovered a potential molecular basis for nasal epithelial cell apoptosis in response to inflammatory injury, and PTEN was identified as the endogenous defender of nasal epithelial cell survival via controlling lethal mitophagy by inhibiting the TLR4‑JNK‑Bnip3 pathway, suggesting that this pathway may be a potential target for clinically treating chronic nasal and sinus inflammatory injury.

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PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways

Cited by 11 publications

References 38 publications

miR-338-5p Targets Epidermal Growth Factor-Containing Fibulin-Like Extracellular Matrix Protein 1 to Inhibit the Growth and Invasion of Trophoblast Cells in Selective Intrauterine Growth Restriction

miR-338-5p Targets Epidermal Growth Factor-Containing Fibulin-Like Extracellular Matrix Protein 1 to Inhibit the Growth and Invasion of Trophoblast Cells in Selective Intrauterine Growth Restriction

TRIM27 promotes the development of esophagus cancer via regulating PTEN/AKT signaling pathway

PTEN enhances nasal epithelial cell resistance to TNFα‑induced inflammatory injury by limiting mitophagy via repression of the TLR4‑JNK‑Bnip3 pathway

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