Implication of 4E-BP1 protein dephosphorylation and accumulation in pancreatic cancer cell death induced by combined gemcitabine and TRAIL

Elia, Androulla; Henry-Grant, Ricky; Adiseshiah, Charlotte; Marboeuf, Catherine; Buckley, R.; Clemens, Michael J.; Mudan, Satvinder; Pyronnet, Stéphane

doi:10.1038/s41419-017-0001-z

Cited by 15 publications

(9 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, 4EBP1 can slow tumor progression in phosphatase and tensin homolog (PTEN)-driven prostate cancer ( 37 ). Significant upregulation and dephosphorylation of 4EBP1 serve an important role in the promotion of pancreatic cancer cell death ( 38 ). The results from these studies suggest that 4EBP1 might serve as a tumor suppressor factor and inhibit the migratory and invasive abilities of various cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Arctigenin inhibits human breast cancer cell proliferation, migratory and invasive abilities and epithelial to mesenchymal transition by targeting 4EBP1

et al. 2021

View full text Add to dashboard Cite

Breast cancer (BC) is one of the most common types of cancer with the highest morbidity rate amongst all cancers in women worldwide. Arctigenin is isolated from the seeds of Asteraceae lappa and exhibits anti-inflammatory and anti-viral effects. The present study aimed to investigate the effect of arctigenin on BC cells and to explore the regulation of arctigenin on eukaryotic translation initiation factor 4E binding protein 1 (4EBP1) expression. To do so, MDA-MB-231 and BT549 cells were treated with arctigenin at various concentrations (0, 5, 10, 20 and 40 µM). Cells treated with 40 µM arctigenin were transfected with pcDNA3.1-4EBP1 or NC control. Cell Counting Kit-8 assay was used to determine cell proliferation, reverse transcription quantitative PCR was used to evaluate the transfection efficiency, western blotting was used to detect relative protein expression and Transwell assays were performed to evaluate the migratory and invasive abilities of BC cells. The results demonstrated that arctigenin could inhibit the proliferation, migratory and invasive abilities, and epithelial to mesenchymal transition (EMT) of MDA-MB-231 and BT549 cells. Furthermore, arctigenin downregulated the expression of 4EBP1 in MDA-MB-231 and BT549 cells, whereas 4EBP1 overexpression could reverse the inhibiting effect of arctigenin on proliferation, migratory and invasive abilities, and EMT in MDA-MB-231 and BT549 cells. The findings suggested that arctigenin may inhibit human BC cell proliferation, migratory and invasive abilities, and EMT by targeting 4EBP1.

show abstract

Section: Discussionmentioning

confidence: 99%

Arctigenin inhibits human breast cancer cell proliferation, migratory and invasive abilities and epithelial to mesenchymal transition by targeting 4EBP1

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Inhibition of mTORC1 has been suggested to provide wide-ranging clinical benefits, including as a treatment for cancer, epilepsy, neurodegenerative diseases, and aging ( 14 , 72 – 76 ). The recent development of new pharmacological inhibitors for mTORC1 inhibition, based around rapamycin, have focused on identifying “rapalogues” without the toxicity associated with rapamycin ( 68 ).…”

Section: Discussionmentioning

confidence: 99%

Decanoic acid inhibits mTORC1 activity independent of glucose and insulin signaling

Warren

Dooves

Lugarà

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Low-glucose and -insulin conditions, associated with ketogenic diets, can reduce the activity of the mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway, potentially leading to a range of positive medical and health-related effects. Here, we determined whether mTORC1 signaling is also a target for decanoic acid, a key component of the medium-chain triglyceride (MCT) ketogenic diet. Using a tractable model system, Dictyostelium, we show that decanoic acid can decrease mTORC1 activity, under conditions of constant glucose and in the absence of insulin, measured by phosphorylation of eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1). We determine that this effect of decanoic acid is dependent on a ubiquitin regulatory X domain-containing protein, mediating inhibition of a conserved Dictyostelium AAA ATPase, p97, a homolog of the human transitional endoplasmic reticulum ATPase (VCP/p97) protein. We then demonstrate that decanoic acid decreases mTORC1 activity in the absence of insulin and under high-glucose conditions in ex vivo rat hippocampus and in tuberous sclerosis complex (TSC) patient-derived astrocytes. Our data therefore indicate that dietary decanoic acid may provide a new therapeutic approach to down-regulate mTORC1 signaling.

show abstract

“…Eukaryotic translation initiation factor 4E-BP1 is a highly conserved low-molecular-weight protein 45 . 4E-BP1 is regulated by several signaling pathways, such as PI3K/AKT/ mTOR and MEK/ERK/MAPK.…”

Section: Effects On Obs Differentiation and Inhibited Apoptosismentioning

confidence: 99%

Effects of Antibacterial Co‐Cr‐Mo‐Cu Alloys on Osteoblast Proliferation, Differentiation, and the Inhibition of Apoptosis

Duan

Yang

Wang

2022

Orthopaedic Surgery

View full text Add to dashboard Cite

Objectives To investigate the effects of antibacterial Co‐Cr‐Mo‐Cu alloys with different Cu contents on osteoblast proliferation, differentiation, and the inhibition of apoptosis to optimize the selection of surgical implantation. Methods Microstructure, phase structure, and ion release were evaluated using X‐ray diffraction, scanning electron microscopy (SEM), and inductively coupled plasma (ICP) spectrometry. The effects on osteoblast proliferation, differentiation, and apoptosis were characterized by cell proliferation assay, alkaline phosphatase (ALP) activity assay, and western blotting, respectively. Results Compared to the original Co‐Cr‐Mo alloys, the released Cu ions from Co‐Cu alloys promoted osteoblast proliferation and differentiation and inhibited apoptosis. It can be noted that the optical density (OD490) and the ALP activity have increased to 1.237 and 1.053, respectively, in Co‐2Cu alloy (0.604 and 0.171 for original Co‐Cr‐Mo alloy). Meanwhile, these effects were evaluated through the upregulation of ROS levels and 4E‐binding protein 1 (4E‐BP1) expression and the downregulation of adenosine 5′‐monophosphate (AMP)‐activated protein kinase (AMPK) and p‐AMPK. Moreover, the antibacterial properties of the Co‐Cu alloys were also enhanced, as demonstrated by the strong antibacterial activity of Cu phases in Co‐Cu alloys incubated with Staphylococcus aureus, in which more than 99.8% of the bacteria has been killed. Conclusions The addition of Cu element in the Co‐Cr‐Mo alloys could induce OB proliferation and differentiation and inhibited OB apoptosis. Meanwhile, it can be recognized that the Co‐Cu alloys with 2wt% Cu exhibit the highest performance among all the samples, indicating that the effects of osteoblast differentiation and the inhibition of apoptosis are highly dependent on the adding of Cu elements. Co‐Cr‐Mo‐Cu alloys with an excellent antibacterial property could be used as a tool to improve osteogenic ability and antibacterial properties in orthopaedic implant operations.

show abstract

Implication of 4E-BP1 protein dephosphorylation and accumulation in pancreatic cancer cell death induced by combined gemcitabine and TRAIL

Cited by 15 publications

References 64 publications

Arctigenin inhibits human breast cancer cell proliferation, migratory and invasive abilities and epithelial to mesenchymal transition by targeting 4EBP1

Arctigenin inhibits human breast cancer cell proliferation, migratory and invasive abilities and epithelial to mesenchymal transition by targeting 4EBP1

Decanoic acid inhibits mTORC1 activity independent of glucose and insulin signaling

Effects of Antibacterial Co‐Cr‐Mo‐Cu Alloys on Osteoblast Proliferation, Differentiation, and the Inhibition of Apoptosis

Contact Info

Product

Resources

About