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Cancer Cells

Cancer cells have greater elasticity and deformability than normal cells, allowing them to more easily penetrate tissues during metastasis. Oncologists diagnose cancer by detecting changes in tissue stiffness. A stiffer extracellular matrix can promote tumor formation by making cells stiffer. When cultured on stiff substrates, mammary epithelial cells do not display normal attachment and proliferation behaviors, but on softer matrices, integrins activate signaling to influence cell behavior. The extracellular matrix receptors and focal adhesions form a feedback loop between the cytoskeleton and extracellular environment to modulate processes like proliferation.

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Shubhendu Kumar Tripathi
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31 views2 pages

Cancer Cells

Cancer cells have greater elasticity and deformability than normal cells, allowing them to more easily penetrate tissues during metastasis. Oncologists diagnose cancer by detecting changes in tissue stiffness. A stiffer extracellular matrix can promote tumor formation by making cells stiffer. When cultured on stiff substrates, mammary epithelial cells do not display normal attachment and proliferation behaviors, but on softer matrices, integrins activate signaling to influence cell behavior. The extracellular matrix receptors and focal adhesions form a feedback loop between the cytoskeleton and extracellular environment to modulate processes like proliferation.

Uploaded by

Shubhendu Kumar Tripathi
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd
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Cancer cells have more elasticity and deformability then normal cells as an important step in cancer

metastasis involves the penetration of epithelial cells through the endothelial layer, which critically
depends on cell elasticity and deformability.

The onset and advance of cancer leads to distinct changes in the stiffness of the surrounding tissue.
Oncologists usually diagnose cancer by sensing the change in elasticity of tissue. It has long been known
that the mechanical response of the ECM itself can play a critical role in tumor formation; a stiffer ECM
can result in a stiffer solid tumor.

Healthy cells attach to a stiffer substrate to spread, stretch and proliferate. However, malignant cells do
not display such characteristics. When mammary epithelial cells are cultured on ECM gels, integrins are
activated in order to modulate the epidermal growth factor receptor (EGF receptor, or EGFR) and to
influence cell differentiation and transformation.

The ECM receptors and the focal adhesions link the integrins to the cytoskeleton and align them
appropriately for proper cell signaling. However, if the epithelial cells are cultured on flat, rigid
substrates instead, these signaling processes are suppressed.

ECM receptor and focal adhesion sites on the cell exterior also sense the traction forces of the actin
microfilaments inside the cell, thereby forming a feedback loop between the cytoskeleton and the ECM
through integrins and focal adhesions. Such feedback can also modulate traction by activating the small
G protein Rho and its target Rho-associated kinase (ROCK). These processes influence cell proliferation.

Persistence length is the length till which tangent at end points are same(mainly for
molecules). If less then persistence length then is more rigid. If more then it then is more
flexible (like noodle).
Bending stiffness is the tendency to not allow bending.(more stiffness more don’t allow)
Elasticity is tendency to get back at same position.
More young’s modulus, less tendency.
Focal adhesion is a type of adhesive contact between the cell and extracellular matrix through
the interaction of the transmembrane proteins integrins with their extracellular ligands, and
intracellular multiprotein assemblies connected to the actin cytoskeleton.
Comparing viscoelasticity of filaments of cytoskeleton

• Among the different cytoskeletal filaments, F-actin provides the highest resistance to
deformation until a certain critical value of local strain. This characteristic offers a rationale for
the existence of actin networks at the cell cortex where the networks can easily “fluidize” under
high shear stresses to facilitate cell locomotion.

• Intermediate filaments are sufficiently compliant to generate moderate deformation, and yet
they maintain their resistance to shear deformation at large local strains to provide structural
integrity to the cell. They also strain harden to bear the mechanical stress at strain levels where
actin networks do not retain their structural integrity.

• Microtubules do not have sufficient tensile or shear stiffness to impart significant mechanical
integrity to the cytoskeleton. However, they act in concert with the other filamental
biopolymers to stabilize the cytoskeleton. Individual intracellular microtubules have been
considered resistant to large-scale compression from physiological processes because of lateral
reinforcement from the cytoskeleton.

• The vastly different relative responses of each of these three types of biopolymers also indicate
the manner in which the cell is able to engineer its internal composite properties by
continuously modulating the components’ relative concentrations and architectures in response
to the local biochemical environment and extracellular matrix.

F-actin is filamentous

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