&lt;p&gt;Simultaneous Treatment with Soluble Forms of GAS1 and PTEN Reduces Invasiveness and Induces Death of Pancreatic Cancer Cells&lt;/p&gt;

Daniel-García, Lizbeth; Vergara, Paula; Navarrete, Araceli; González, Rosa O.; Segovia, José

doi:10.2147/ott.s260671

Cited by 4 publications

(3 citation statements)

References 29 publications

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“…One investigation found that PTEN expression was reduced under continuous hypoxic stimulation [ 33 ]. Combined treatment of pancreatic cancer with GAS1 and PTEN inhibited cell invasion promoting cell death [ 34 ]. The reduced expression of Tp53 and PTEN promotes the progression of pleural and peritoneal malignant mesotheliomas [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Hypoxic Microenvironment-Induced Reduction in PTEN-L Secretion Promotes Non-Small Cell Lung Cancer Metastasis through PI3K/AKT Pathway

Song

Shi

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Objective. Lung cancer is the leading cause of cancer-related deaths worldwide. The aim of this study was to investigate the effects of hypoxic microenvironment on PTEN-L secretion and the effects of PTEN-L on the metastasis of non-small cell lung cancer (NSCLC) and the potential mechanisms. Methods. The expression levels of PTEN-L in NSCLC tissues, cells, and cell culture media were detected. The transfection of PTEN-L overexpression construct or HIF-1α-siRNAs was conducted to manipulate the expression of PTEN-L or HIF-1α. NSCLC cells were introduced into 200 μM CoCl2 medium for 72 hours under 37°C to simulate hypoxia. The proliferation and apoptosis of the A549 cells were determined by the Cell Counting Kit-8 assay and Annexin V-FITC/PI-stained flow cytometry assay, respectively. Wound healing assay and transwell invasion assay were used to measure the migration and invasion of A549 cells. The protein expression of PTEN, PTEN-L, PI3K/AKT pathway-related proteins, and HIF-1α was detected by Western blot. Results. PTEN and PTEN-L are downregulated in lung cancer tissues and cells. The protein expression of PTEN-L in the culture medium of lung cancer cell lines is decreased. The hypoxic microenvironment inhibits PTEN-L secretion. The low level of PTEN-L promotes cell proliferation, migration, and invasion, as well as inhibits apoptosis of A549 cells. The overexpression of PTEN-L attenuated the activation of the PI3K/AKT pathway by the hypoxic microenvironment. The knockdown of HIF-1α upregulates PTEN-L secretion under hypoxia. Conclusions. The hypoxic microenvironment inhibits PTEN-L secretion and thus activates PI3K/AKT pathway to induce proliferation, migration, and invasion promotion, and apoptosis inhibition in NSCLC cells.

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Section: Discussionmentioning

confidence: 99%

Hypoxic Microenvironment-Induced Reduction in PTEN-L Secretion Promotes Non-Small Cell Lung Cancer Metastasis through PI3K/AKT Pathway

Song

Shi

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…11836170001). Samples containing 50 μg of total protein per condition, were separated in either 8% or 10% SDS-PAGE gels and transferred onto the polyvinylidene-difluoride (PVDF) membranes [ 48 ] (Bio-Rad, cat. #1620177), which were subsequently blocked for 1 h at room temperature with a solution of 3% non-fat milk in Tris buffered saline (TBS) 1% and then incubated overnight at 4 °C with primary antibodies against p21 (Cell Signaling, USA; cat.…”

Section: Methodsmentioning

confidence: 99%

Combined treatments with AZD5363, AZD8542, curcumin or resveratrol induce death of human glioblastoma cells by suppressing the PI3K/AKT and SHH signaling pathways

Mejía-Rodríguez

Romero-Trejo

González

et al. 2023

Biochemistry and Biophysics Reports

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“…Furthermore, PTEN is subject to a range of regulatory mechanisms (e.g., PTMs, PTEN‐interacting proteins, dimerization, and secretion) that ultimately govern its protein levels, activity, and function [ 14 ]. Recently, the inhibition of PTEN expression has been shown to promote cell proliferation [ 15 ], cancer metastasis [ 16 ], invasion [ 17 ], tumorigenesis and progression [ 18 ], and drug resistance [ 19 ] in pancreatic cancer. Therefore, mechanistic exploration is needed regarding the regulation of PTEN expression in pancreatic cancer.…”

Section: Introductionmentioning

confidence: 99%

USP22‐mediated deubiquitination of PTEN inhibits pancreatic cancer progression by inducing p21 expression

Ren

Sun

et al. 2021

Molecular Oncology

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Phosphatase and tensin homolog deleted on chromosome ten (PTEN) is a dual lipid and protein phosphatase. Multiple mechanisms contributing to the regulation of PTEN levels have been identified thus far, including post‐translational modifications, epigenetic mechanisms, and transcriptional mechanisms. In the present study, we identified ubiquitin‐specific peptidase 22 (USP22) as a novel deubiquitination‐modifying enzyme of PTEN. Furthermore, by inducing deubiquitination and inhibiting the degradation of PTEN, USP22 could induce cyclin‐dependent kinase inhibitor 1A (CDKN1A, also symboled as p21) expression in pancreatic cancer. Besides, MDM2 proto‐oncogene (MDM2) inhibitor enhanced the antipancreatic cancer effects of USP22 overexpression. In addition to its regulation of MDM2‐tumor protein p53 (p53) signaling, we found that PTEN could induce p21 expression by interacting with ankyrin repeat and KH domain containing 1 (ANKHD1) and inhibiting ANKHD1 binding to the p21 promoter. Taken together, our results indicate that ANKHD1 and MDM2 might be novel therapeutic targets in pancreatic cancer.

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<p>Simultaneous Treatment with Soluble Forms of GAS1 and PTEN Reduces Invasiveness and Induces Death of Pancreatic Cancer Cells</p>

Cited by 4 publications

References 29 publications

Hypoxic Microenvironment-Induced Reduction in PTEN-L Secretion Promotes Non-Small Cell Lung Cancer Metastasis through PI3K/AKT Pathway

Hypoxic Microenvironment-Induced Reduction in PTEN-L Secretion Promotes Non-Small Cell Lung Cancer Metastasis through PI3K/AKT Pathway

Combined treatments with AZD5363, AZD8542, curcumin or resveratrol induce death of human glioblastoma cells by suppressing the PI3K/AKT and SHH signaling pathways

USP22‐mediated deubiquitination of PTEN inhibits pancreatic cancer progression by inducing p21 expression

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