The SHIP2 interactor Myo1c is required for cell migration in 1321 N1 glioblastoma cells

Edimo, William’s Elong; Ramos, António Manuel Pinho; Ghosh, Somadri; Vanderwinden, Jean‐Marie; Erneux, Christophé

doi:10.1016/j.bbrc.2016.05.154

Cited by 14 publications

(10 citation statements)

References 33 publications

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“…The effect is transient, suggesting that SHIP2 is only active at the plasma membrane for a short time, probably due to its localization upon stimulation to a fraction of the cell where PI(3,4,5)P 3 is also present. This could be secondary to SHIP2 interaction with cytoskeletal proteins [actin-binding proteins such as filamin (19) or myosin 1c (32)] in plasma membrane-associated platforms and scaffold proteins (33). Furthermore, the stimulation of PI(3,4,5)P 3 in response to EGF was very much amplified in cells in which both PTEN and SHIP2 were deleted (10).…”

Section: Fig 3 Pi(345)p 3 and Pi(34)p 2 Levels In Ship2mentioning

confidence: 99%

The impact of phosphoinositide 5-phosphatases on phosphoinositides in cell function and human disease

Ramos

Ghosh

Erneux

2019

Journal of Lipid Research

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Phosphoinositides (PIs) are recognized as major signaling molecules in many different functions of eukaryotic cells. PIs can be dephosphorylated by multiple phosphatase activities at the 5-, 4- and 3- positions. Human PI 5-phosphatases belong to a family of 10 members. Except for INPP5A, they all catalyze the dephosphorylation of PI(4,5)P2 and/or PI(3,4,5)P3 at the 5- position. PI 5-phosphatases thus directly control the levels of PI(3,4,5)P3 and also participate in fine-tuning regulatory mechanisms of PI(3,4)P2 and PI(4,5)P2. Second messenger functions have been demonstrated for PI(3,4)P2 in invadopodium maturation and in lamellipodia formation. PI 5-phosphatases can use several substrates on isolated enzymes, and it has been challenging to establish their real substrate in vivo. PI(4,5)P2 has multiple functions in signaling, including interaction with scaffold proteins, ion channels, and cytoskeleton proteins. PI 5-phosphatase isoenzymes have been individually implicated in human diseases, such as the oculocerebrorenal syndrome of Lowe, through mechanisms which include lipid-controlling. Oncogenic and tumor suppressive functions of PI 5-phosphatases have also been reported in different cell contexts. The mechanisms responsible for genetic diseases and for tumor suppressor or oncogenic functions are not fully understood. The regulation of PI 5-phosphatases is thus crucial in understanding cell functions.

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Section: Fig 3 Pi(345)p 3 and Pi(34)p 2 Levels In Ship2mentioning

confidence: 99%

The impact of phosphoinositide 5-phosphatases on phosphoinositides in cell function and human disease

Ramos

Ghosh

Erneux

2019

Journal of Lipid Research

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“…(27) SHIP2 localizes to the focal contacts and lamellipodia, (27,28) and it inhibits cell migration in PTEN-null 1321 N1 glioblastoma cells through de-phosphorylation of PI(4,5)P 2. (29,30) In contrast, a number of studies have suggested that SHIP2 is often amplified in human cancer cells, (31)(32)(33) whereas the tumor suppressors PTEN and INPP4B are often mutated or deleted, which leads to sustained activation of PIP 3 -dependent Akt signaling in these cells. However, it is not clear how amplification of SHIP2 is involved in the malignancy of cancer cells, though this event is expected to lead to decreased PIP 3 levels.…”

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PI(3,4)P₂ plays critical roles in the regulation of focal adhesion dynamics of MDA‐MB‐231 breast cancer cells

2017

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Phosphoinositides play pivotal roles in the regulation of cancer cell phenotypes. Among them, phosphatidylinositol 3,4‐bisphosphate (PI(3,4)P2) localizes to the invadopodia, and positively regulates tumor cell invasion. In this study, we examined the effect of PI(3,4)P2 on focal adhesion dynamics in MDA‐MB‐231 basal breast cancer cells. Knockdown of SHIP2, a phosphatidylinositol 3,4,5‐trisphosphatase (PIP 3) 5‐phosphatase that generates PI(3,4)P2, in MDA‐MB‐231 breast cancer cells, induced the development of focal adhesions and cell spreading, leading to the suppression of invasion. In contrast, knockdown of PTEN, a 3‐phosphatase that de‐phosphorylates PIP 3 and PI(3,4)P2, induced cell shrinkage and increased cell invasion. Interestingly, additional knockdown of SHIP2 rescued these phenotypes. Overexpression of the TAPP1 PH domain, which binds to PI(3,4)P2, and knockdown of Lpd, a downstream effector of PI(3,4)P2, resulted in similar phenotypes to those induced by SHIP2 knockdown. Taken together, our results suggest that inhibition of PI(3,4)P2 generation and/or downstream signaling could be useful for inhibiting breast cancer metastasis.

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“…A total of 193 and 543 genes are significantly associated with better and worse survival, respectively, leveraging clinical information and RNA-seq data of TCGA GBM samples (Additional file 1 : Table S6 for complete list). We identified 20 GSC-upregulated miRNA-targeted genes associated with significantly reduced 5-year survival in GBM patients, including previously identified glioma-promoting genes HMGA2 [ 20 ], MYO1C [ 21 ], RGS4 [ 22 ], and several novel targets, such as HPCAL1, IMPDH1, and YWHAG (Additional file 1 : Table S5, orange-colored genes, Additional file 2 : Figure S2F). Therefore, deregulation of miRNAs in GSCs may contribute to poor outcome in part through modulating expression of these miRNA-targeted loci.…”

Section: Resultsmentioning

confidence: 99%

Distinctive epigenomes characterize glioma stem cells and their response to differentiation cues

Zhou

Alver

et al. 2018

Genome Biol

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BackgroundGlioma stem cells (GSCs) are a subpopulation of stem-like cells that contribute to glioblastoma (GBM) aggressiveness, recurrence, and resistance to radiation and chemotherapy. Therapeutically targeting the GSC population may improve patient survival, but unique vulnerabilities need to be identified.ResultsWe isolate GSCs from well-characterized GBM patient-derived xenografts (PDX), characterize their stemness properties using immunofluorescence staining, profile their epigenome including 5mC, 5hmC, 5fC/5caC, and two enhancer marks, and define their transcriptome. Fetal brain-derived neural stem/progenitor cells are used as a comparison to define potential unique and common molecular features between these different brain-derived cells with stem properties. Our integrative study reveals that abnormal expression of ten-eleven-translocation (TET) family members correlates with global levels of 5mC and 5fC/5caC and may be responsible for the distinct levels of these marks between glioma and neural stem cells. Heterogenous transcriptome and epigenome signatures among GSCs converge on several genes and pathways, including DNA damage response and cell proliferation, which are highly correlated with TET expression. Distinct enhancer landscapes are also strongly associated with differential gene regulation between glioma and neural stem cells; they exhibit unique co-localization patterns with DNA epigenetic mark switching events. Upon differentiation, glioma and neural stem cells exhibit distinct responses with regard to TET expression and DNA mark changes in the genome and GSCs fail to properly remodel their epigenome.ConclusionsOur integrative epigenomic and transcriptomic characterization reveals fundamentally distinct yet potentially targetable biologic features of GSCs that result from their distinct epigenomic landscapes.Electronic supplementary materialThe online version of this article (10.1186/s13059-018-1420-6) contains supplementary material, which is available to authorized users.

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The SHIP2 interactor Myo1c is required for cell migration in 1321 N1 glioblastoma cells

Cited by 14 publications

References 33 publications

The impact of phosphoinositide 5-phosphatases on phosphoinositides in cell function and human disease

The impact of phosphoinositide 5-phosphatases on phosphoinositides in cell function and human disease

PI(3,4)P₂ plays critical roles in the regulation of focal adhesion dynamics of MDA‐MB‐231 breast cancer cells

Distinctive epigenomes characterize glioma stem cells and their response to differentiation cues

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The SHIP2 interactor Myo1c is required for cell migration in 1321 N1 glioblastoma cells

Cited by 14 publications

References 33 publications

The impact of phosphoinositide 5-phosphatases on phosphoinositides in cell function and human disease

The impact of phosphoinositide 5-phosphatases on phosphoinositides in cell function and human disease

PI(3,4)P2 plays critical roles in the regulation of focal adhesion dynamics of MDA‐MB‐231 breast cancer cells

Distinctive epigenomes characterize glioma stem cells and their response to differentiation cues

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PI(3,4)P₂ plays critical roles in the regulation of focal adhesion dynamics of MDA‐MB‐231 breast cancer cells