Cofilin promotes vasculogenic mimicry by regulating the actin cytoskeleton in human breast cancer cells

Nakajima, Minami; Kawahara, Ryota; Simizu, Siro

doi:10.1002/1873-3468.14594

Cited by 3 publications

(2 citation statements)

References 40 publications

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“…To examine the function of DPY19L3 in VM genesis, we sought to establish HT1080 cell lines with deleted human DPY19L3 gene using CRISPR/Cas9 system, because we have reported that DPY19L3 is expressed in HT1080 cells [ 8 ] and HT1080 cells have enough VM formation capability [ 21 ]. Guide RNA sequences were designed at 2 close positions in exon 6 of DPY19L3 ( Figs.…”

Section: Resultsmentioning

confidence: 99%

“…VM-like network formation assay HT1080 and MDA-MB-231 cells, suspended in culture medium, were seeded at 3.2 × 10 3 and 2.0 × 10 4 cells/well, respectively, in a 96-well plate that was precoated with 40 µL/well Matrigel (Corning Inc., Somerville, MA, USA). The seeded cells were cultured at 37°C and photographed under a phase-contrast microscope (Leica DMi1; Leica Microsystems GmbH, Wetzlar, Germany) [21].…”

Section: Mtt Assaymentioning

confidence: 99%

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DPY19L3 promotes vasculogenic mimicry by its C-mannosyltransferase activity

BAYDOUN,

KATO,

KAMO

et al. 2024

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C -mannosylation is a post-translational modification that occurs intracellularly in the endoplasmic reticulum. In humans, biosynthesis of C -mannosylation in proteins containing thrombospondin type 1 repeat is catalyzed by the DPY19 family; nonetheless, biological functions of protein C -mannosylation are not yet fully understood, especially in tumor progression. Vasculogenic mimicry (VM) is the formation of fluid-conducting channels by highly invasive and genetically deregulated tumor cells, enabling the tumors to form matrix-embedded vasculogenic structures, containing plasma and blood cells to meet the metabolic demands of rapidly growing tumors. In this study, we focused on DPY19L3, a C -mannosyltransferase, and aimed to unravel its role in VM. Knockout of DPY19L3 inhibited the formation of VM in HT1080 human fibrosarcoma cells. Re-expression of wild-type DPY19L3 recovered VM formation; however, DPY19L3 isoform2, an enzymatic activity-defect mutant, did not restore it, suggesting that the C -mannosyltransferase activity of DPY19L3 is crucial to its function. Furthermore, the knockdown of DPY19L3 in MDA-MB-231 breast cancer cells hindered its network formation ability. Altogether, our findings suggest that DPY19L3 is required for VM formation and stipulate the relevance of C -mannosylation in oncogenesis.

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Section: Resultsmentioning

confidence: 99%

Section: Mtt Assaymentioning

confidence: 99%

DPY19L3 promotes vasculogenic mimicry by its C-mannosyltransferase activity

BAYDOUN,

KATO,

KAMO

et al. 2024

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Verteporfin regulates corneal neovascularization through inhibition of YAP protein activation

Lin,

Zheng,

et al. 2024

Experimental Eye Research

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Identification of C-mannosylation in a receptor tyrosine kinase AXL

Mori,

Suzuki,

Waki

et al. 2024

Glycobiology

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C-mannosylation is a unique type of glycosylation in which a mannose is added to tryptophan in a protein. However, the biological function of C-mannosylation is still largely unknown. AXL is a receptor tyrosine kinase, and its overexpression contributes to tumor malignancy. The role of AXL in cancer cells is broad, including invasion, drug resistance, and vasculogenic mimicry formation. Although Trp320 of AXL was predicted to be C-mannosylated, it has not been confirmed. Here, we demonstrated that Trp320 of AXL is C-mannosylated, measured by mass spectrometry of recombinant AXL purified from various cancer cells. Furthermore, re-expression of C-mannosylation-deficient AXL in human breast cancer MDA-MB-231 cells lacking AXL by the CRISPR/Cas9 system resulted in reduction of vasculogenic mimicry formation. Interestingly, phosphorylation levels of AKT in C-mannosylation-deficient AXL re-expressing cells were comparable to those of parental and wild-type AXL re-expressing cells. These results represent the first discovery of C-mannosylation in a receptor tyrosine kinase and the possibility that C-mannosylation may affect AXL function, distinct from its downstream signaling in cancer cells.

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Cofilin promotes vasculogenic mimicry by regulating the actin cytoskeleton in human breast cancer cells

Cited by 3 publications

References 40 publications

DPY19L3 promotes vasculogenic mimicry by its C-mannosyltransferase activity

DPY19L3 promotes vasculogenic mimicry by its C-mannosyltransferase activity

Verteporfin regulates corneal neovascularization through inhibition of YAP protein activation

Identification of C-mannosylation in a receptor tyrosine kinase AXL

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