23 research outputs found
Optically Stable Biocompatible Flame-Made SiO<sub>2</sub>-Coated Y<sub>2</sub>O<sub>3</sub>:Tb<sup>3+</sup> Nanophosphors for Cell Imaging
Nanophosphors are light-emitting materials with stable optical properties that represent promising tools for bioimaging. The synthesis of nanophosphors, and thus the control of their surface properties, is, however, challenging. Here, flame aerosol technology is exploited to generate Tb-activated Y<sub>2</sub>O<sub>3</sub> nanophosphors (∼25 nm) encapsulated <i>in situ</i> by a nanothin amorphous inert SiO<sub>2</sub> film. The nanocrystalline core exhibits a bright green luminescence following the Tb<sup>3+</sup> ion transitions, while the hermetic SiO<sub>2</sub>-coating prevents any unspecific interference with cellular activities. The SiO<sub>2</sub>-coated nanophosphors display minimal photobleaching upon imaging and can be easily functionalized through surface absorption of biological molecules. Therefore, they can be used as bionanoprobes for cell detection and for long-term monitoring of cellular activities. As an example, we report on the interaction between epidermal growth factor (EGF)-functionalized nanophosphors and mouse melanoma cells. The cellular uptake of the nanophosphors is visualized with confocal microscopy, and the specific activation of EGF receptors is revealed with biochemical techniques. Altogether, our results establish SiO<sub>2</sub>-coated Tb-activated Y<sub>2</sub>O<sub>3</sub> nanophosphors as superior imaging tools for biological applications
A Nanoprinted Model of Interstitial Cancer Migration Reveals a Link between Cell Deformability and Proliferation
Metastatic
progression of tumors requires the coordinated dissemination
of cancerous cells through interstitial tissues and their replication
in distant body locations. Despite their importance in cancer treatment
decisions, key factors, such as cell shape adaptation and the role
it plays in dense tissue invasion by cancerous cells, are not well
understood. Here, we employ a 3D electrohydrodynamic nanoprinting
technology to generate vertical arrays of topographical pores that
mimic interstitial tissue resistance to the mesenchymal migration
of cancerous cells, in order to determine the effect of nuclear size,
cell deformability, and cell-to-substrate adhesion on tissue invasion
efficiency. The high spatial and temporal resolution of our analysis
demonstrates that the ability of cells to deform depends on the cell
cycle phase, peaks immediately after mitosis, and is key to the invasion
process. Increased pore penetration efficiency by cells in early G1
phase also coincided with their lower nuclear volume and higher cell
deformability, compared with the later cell cycle stages. Furthermore,
artificial decondensation of chromatin induced an increase in cell
and nuclear deformability and improved pore penetration efficiency
of cells in G1. Together, these results underline that along the cell
cycle cells have different abilities to dynamically remodel their
actin cytoskeleton and induce nuclear shape changes, which determines
their pore penetration efficiency. Thus, our results support a mechanism
in which cell proliferation and pore penetration are functionally
linked to favor the interstitial dissemination of metastatic cells
A Nanoprinted Model of Interstitial Cancer Migration Reveals a Link between Cell Deformability and Proliferation
Metastatic
progression of tumors requires the coordinated dissemination
of cancerous cells through interstitial tissues and their replication
in distant body locations. Despite their importance in cancer treatment
decisions, key factors, such as cell shape adaptation and the role
it plays in dense tissue invasion by cancerous cells, are not well
understood. Here, we employ a 3D electrohydrodynamic nanoprinting
technology to generate vertical arrays of topographical pores that
mimic interstitial tissue resistance to the mesenchymal migration
of cancerous cells, in order to determine the effect of nuclear size,
cell deformability, and cell-to-substrate adhesion on tissue invasion
efficiency. The high spatial and temporal resolution of our analysis
demonstrates that the ability of cells to deform depends on the cell
cycle phase, peaks immediately after mitosis, and is key to the invasion
process. Increased pore penetration efficiency by cells in early G1
phase also coincided with their lower nuclear volume and higher cell
deformability, compared with the later cell cycle stages. Furthermore,
artificial decondensation of chromatin induced an increase in cell
and nuclear deformability and improved pore penetration efficiency
of cells in G1. Together, these results underline that along the cell
cycle cells have different abilities to dynamically remodel their
actin cytoskeleton and induce nuclear shape changes, which determines
their pore penetration efficiency. Thus, our results support a mechanism
in which cell proliferation and pore penetration are functionally
linked to favor the interstitial dissemination of metastatic cells
A Nanoprinted Model of Interstitial Cancer Migration Reveals a Link between Cell Deformability and Proliferation
Metastatic
progression of tumors requires the coordinated dissemination
of cancerous cells through interstitial tissues and their replication
in distant body locations. Despite their importance in cancer treatment
decisions, key factors, such as cell shape adaptation and the role
it plays in dense tissue invasion by cancerous cells, are not well
understood. Here, we employ a 3D electrohydrodynamic nanoprinting
technology to generate vertical arrays of topographical pores that
mimic interstitial tissue resistance to the mesenchymal migration
of cancerous cells, in order to determine the effect of nuclear size,
cell deformability, and cell-to-substrate adhesion on tissue invasion
efficiency. The high spatial and temporal resolution of our analysis
demonstrates that the ability of cells to deform depends on the cell
cycle phase, peaks immediately after mitosis, and is key to the invasion
process. Increased pore penetration efficiency by cells in early G1
phase also coincided with their lower nuclear volume and higher cell
deformability, compared with the later cell cycle stages. Furthermore,
artificial decondensation of chromatin induced an increase in cell
and nuclear deformability and improved pore penetration efficiency
of cells in G1. Together, these results underline that along the cell
cycle cells have different abilities to dynamically remodel their
actin cytoskeleton and induce nuclear shape changes, which determines
their pore penetration efficiency. Thus, our results support a mechanism
in which cell proliferation and pore penetration are functionally
linked to favor the interstitial dissemination of metastatic cells
A Nanoprinted Model of Interstitial Cancer Migration Reveals a Link between Cell Deformability and Proliferation
Metastatic
progression of tumors requires the coordinated dissemination
of cancerous cells through interstitial tissues and their replication
in distant body locations. Despite their importance in cancer treatment
decisions, key factors, such as cell shape adaptation and the role
it plays in dense tissue invasion by cancerous cells, are not well
understood. Here, we employ a 3D electrohydrodynamic nanoprinting
technology to generate vertical arrays of topographical pores that
mimic interstitial tissue resistance to the mesenchymal migration
of cancerous cells, in order to determine the effect of nuclear size,
cell deformability, and cell-to-substrate adhesion on tissue invasion
efficiency. The high spatial and temporal resolution of our analysis
demonstrates that the ability of cells to deform depends on the cell
cycle phase, peaks immediately after mitosis, and is key to the invasion
process. Increased pore penetration efficiency by cells in early G1
phase also coincided with their lower nuclear volume and higher cell
deformability, compared with the later cell cycle stages. Furthermore,
artificial decondensation of chromatin induced an increase in cell
and nuclear deformability and improved pore penetration efficiency
of cells in G1. Together, these results underline that along the cell
cycle cells have different abilities to dynamically remodel their
actin cytoskeleton and induce nuclear shape changes, which determines
their pore penetration efficiency. Thus, our results support a mechanism
in which cell proliferation and pore penetration are functionally
linked to favor the interstitial dissemination of metastatic cells
A Nanoprinted Model of Interstitial Cancer Migration Reveals a Link between Cell Deformability and Proliferation
Metastatic
progression of tumors requires the coordinated dissemination
of cancerous cells through interstitial tissues and their replication
in distant body locations. Despite their importance in cancer treatment
decisions, key factors, such as cell shape adaptation and the role
it plays in dense tissue invasion by cancerous cells, are not well
understood. Here, we employ a 3D electrohydrodynamic nanoprinting
technology to generate vertical arrays of topographical pores that
mimic interstitial tissue resistance to the mesenchymal migration
of cancerous cells, in order to determine the effect of nuclear size,
cell deformability, and cell-to-substrate adhesion on tissue invasion
efficiency. The high spatial and temporal resolution of our analysis
demonstrates that the ability of cells to deform depends on the cell
cycle phase, peaks immediately after mitosis, and is key to the invasion
process. Increased pore penetration efficiency by cells in early G1
phase also coincided with their lower nuclear volume and higher cell
deformability, compared with the later cell cycle stages. Furthermore,
artificial decondensation of chromatin induced an increase in cell
and nuclear deformability and improved pore penetration efficiency
of cells in G1. Together, these results underline that along the cell
cycle cells have different abilities to dynamically remodel their
actin cytoskeleton and induce nuclear shape changes, which determines
their pore penetration efficiency. Thus, our results support a mechanism
in which cell proliferation and pore penetration are functionally
linked to favor the interstitial dissemination of metastatic cells
A Nanoprinted Model of Interstitial Cancer Migration Reveals a Link between Cell Deformability and Proliferation
Metastatic
progression of tumors requires the coordinated dissemination
of cancerous cells through interstitial tissues and their replication
in distant body locations. Despite their importance in cancer treatment
decisions, key factors, such as cell shape adaptation and the role
it plays in dense tissue invasion by cancerous cells, are not well
understood. Here, we employ a 3D electrohydrodynamic nanoprinting
technology to generate vertical arrays of topographical pores that
mimic interstitial tissue resistance to the mesenchymal migration
of cancerous cells, in order to determine the effect of nuclear size,
cell deformability, and cell-to-substrate adhesion on tissue invasion
efficiency. The high spatial and temporal resolution of our analysis
demonstrates that the ability of cells to deform depends on the cell
cycle phase, peaks immediately after mitosis, and is key to the invasion
process. Increased pore penetration efficiency by cells in early G1
phase also coincided with their lower nuclear volume and higher cell
deformability, compared with the later cell cycle stages. Furthermore,
artificial decondensation of chromatin induced an increase in cell
and nuclear deformability and improved pore penetration efficiency
of cells in G1. Together, these results underline that along the cell
cycle cells have different abilities to dynamically remodel their
actin cytoskeleton and induce nuclear shape changes, which determines
their pore penetration efficiency. Thus, our results support a mechanism
in which cell proliferation and pore penetration are functionally
linked to favor the interstitial dissemination of metastatic cells
A Nanoprinted Model of Interstitial Cancer Migration Reveals a Link between Cell Deformability and Proliferation
Metastatic
progression of tumors requires the coordinated dissemination
of cancerous cells through interstitial tissues and their replication
in distant body locations. Despite their importance in cancer treatment
decisions, key factors, such as cell shape adaptation and the role
it plays in dense tissue invasion by cancerous cells, are not well
understood. Here, we employ a 3D electrohydrodynamic nanoprinting
technology to generate vertical arrays of topographical pores that
mimic interstitial tissue resistance to the mesenchymal migration
of cancerous cells, in order to determine the effect of nuclear size,
cell deformability, and cell-to-substrate adhesion on tissue invasion
efficiency. The high spatial and temporal resolution of our analysis
demonstrates that the ability of cells to deform depends on the cell
cycle phase, peaks immediately after mitosis, and is key to the invasion
process. Increased pore penetration efficiency by cells in early G1
phase also coincided with their lower nuclear volume and higher cell
deformability, compared with the later cell cycle stages. Furthermore,
artificial decondensation of chromatin induced an increase in cell
and nuclear deformability and improved pore penetration efficiency
of cells in G1. Together, these results underline that along the cell
cycle cells have different abilities to dynamically remodel their
actin cytoskeleton and induce nuclear shape changes, which determines
their pore penetration efficiency. Thus, our results support a mechanism
in which cell proliferation and pore penetration are functionally
linked to favor the interstitial dissemination of metastatic cells
A Nanoprinted Model of Interstitial Cancer Migration Reveals a Link between Cell Deformability and Proliferation
Metastatic
progression of tumors requires the coordinated dissemination
of cancerous cells through interstitial tissues and their replication
in distant body locations. Despite their importance in cancer treatment
decisions, key factors, such as cell shape adaptation and the role
it plays in dense tissue invasion by cancerous cells, are not well
understood. Here, we employ a 3D electrohydrodynamic nanoprinting
technology to generate vertical arrays of topographical pores that
mimic interstitial tissue resistance to the mesenchymal migration
of cancerous cells, in order to determine the effect of nuclear size,
cell deformability, and cell-to-substrate adhesion on tissue invasion
efficiency. The high spatial and temporal resolution of our analysis
demonstrates that the ability of cells to deform depends on the cell
cycle phase, peaks immediately after mitosis, and is key to the invasion
process. Increased pore penetration efficiency by cells in early G1
phase also coincided with their lower nuclear volume and higher cell
deformability, compared with the later cell cycle stages. Furthermore,
artificial decondensation of chromatin induced an increase in cell
and nuclear deformability and improved pore penetration efficiency
of cells in G1. Together, these results underline that along the cell
cycle cells have different abilities to dynamically remodel their
actin cytoskeleton and induce nuclear shape changes, which determines
their pore penetration efficiency. Thus, our results support a mechanism
in which cell proliferation and pore penetration are functionally
linked to favor the interstitial dissemination of metastatic cells
Pore Shape Defines Paths of Metastatic Cell Migration
Invasion
of dense tissues by cancer cells involves the interplay
between the penetration resistance offered by interstitial pores and
the deformability of cells. Metastatic cancer cells find optimal paths
of minimal resistance through an adaptive path-finding process, which
leads to successful dissemination. The physical limit of nuclear deformation
is related to the minimal cross section of pores that can be successfully
penetrated. However, this single biophysical parameter does not fully
describe the architectural complexity of tissues featuring pores of
variable area and shape. Here, employing laser nanolithography, we
fabricate pore microenvironment models with well-controlled pore shapes,
through which human breast cells (MCF10A) and their metastatic offspring
(MCF10CA1a.cl1) could pervade. In these experimental settings, we
demonstrate that the actual pore shape, and not only the cross section,
is a major and independent determinant of cancer penetration efficiency.
In complex architectures containing pores demanding large deformations
from invading cells, tall and narrow rectangular openings facilitate
cancer migration. In addition, we highlight the characteristic traits
of the explorative behavior enabling metastatic cells to identify
and select such pore shapes in a complex multishape pore environment,
pinpointing paths of least resistance to invasion