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Understanding the migration of cancer cells
June 23, 2008Activity of regulatory proteins for the growth of filopodia and lamelopodia clarified
Lamellipodia are veil-shaped protrusions of the plasma membrane, that can turn into upward-curled ruffles if they fail to adhere to the substrate. A dendritic meshwork of short and highly branched actin filaments might constitute their main structural component. The other type of protrusion, the filopodia, are finger-like and consist of parallel, long and unbranched actin filaments. Interestingly, fast-crawling cells mainly form lamellipodia/ruffles while poorly migrating or non-motile cells often show the coexistence of both lamellipodial and filopodial protrusions. These observations suggest that the lamellipodia-to-filopodia selection might regulate cell migration. Moreover, the pivotal contribution of lamellipodial and filopodial protrusions to important developmental and homeostatic processes certainly requires tight regulatory mechanisms.
Unfortunately, while the microscopic morphology, dynamic development and protein signature of both lamellipodia/ruffles and filopodia have been investigated, little is known about the mechanisms whereby cells co-ordinate these actin-based extensions. Therefore, we urgently need to better understand this basic process to ultimately increase our therapeutic intervention arsenal against the metastatic progression of cancers.
It is known that the activity of regulatory proteins for the growth of the actin cytoskeleton Arp2/3 complex along with WAVE and mDia2 produce a burst of actin polymerization required for the formation of lamellipodia/ruffles and filopodia, respectively. In the forthcoming issue of Nature Cell Biology Metello Innocenti and coworkers report that, starting from the unexpected observation that mDia2, WAVE and Arp2/3 form a complex, they discovered how filopodia extensions are generated and integrated with lamellipodia/ruffles in human cancer cells. At the molecular level, WAVE and Arp2/3 jointly promote lamellipodia/ruffles outgrowth and cell migration and at the same time inhibit mDia2-dependent filopodia formation. Moreover, emission of filopodia occurs only after the disassembly of the mDia2-WAVE-Arp2/3 complex. Thus, it is likely that suppression of filopodia by the ruffling-making machinery is needed for cancer cells to move efficiently.
Their results pave the way to a cogent molecular analysis of the interplay between lamellipodia/ruffles and filopodia in regulating both the migratory and invasive abilities of cancer cells. The researchers anticipate that new and more specific therapies to counteract cancer will be developed exploiting these exciting findings.
Goethe University Frankfurt
It is known that the activity of regulatory proteins for the growth of the actin cytoskeleton Arp2/3 complex along with WAVE and mDia2 produce a burst of actin polymerization required for the formation of lamellipodia/ruffles and filopodia, respectively. In the forthcoming issue of Nature Cell Biology Metello Innocenti and coworkers report that, starting from the unexpected observation that mDia2, WAVE and Arp2/3 form a complex, they discovered how filopodia extensions are generated and integrated with lamellipodia/ruffles in human cancer cells. At the molecular level, WAVE and Arp2/3 jointly promote lamellipodia/ruffles outgrowth and cell migration and at the same time inhibit mDia2-dependent filopodia formation. Moreover, emission of filopodia occurs only after the disassembly of the mDia2-WAVE-Arp2/3 complex. Thus, it is likely that suppression of filopodia by the ruffling-making machinery is needed for cancer cells to move efficiently.
Their results pave the way to a cogent molecular analysis of the interplay between lamellipodia/ruffles and filopodia in regulating both the migratory and invasive abilities of cancer cells. The researchers anticipate that new and more specific therapies to counteract cancer will be developed exploiting these exciting findings.
Goethe University Frankfurt
Cancer Cells Current Events and Cancer Cells News RSSResearchers Identify Role of Gene in Tumor Development, Growth and Progression
Virginia Commonwealth University Massey Cancer Center and VCU Institute of Molecular Medicine researchers have identified a gene that may play a pivotal role in two processes that are essential for tumor development, growth and progression to metastasis.
Cancer metabolism discovery uncovers new role of IDH1 gene mutation in brain cancer
Agios Pharmaceuticals today announced that its scientists have established, for the first time, that the mutated IDH1 gene has a novel enzyme activity consistent with a cancer-causing gene, or oncogene.
New cancer target for non-Hodgkin's lymphoma
Physician-scientists from Weill Cornell Medical College have discovered a molecular mechanism that may prove to be a powerful target for the treatment of non-Hodgkin's lymphoma, a type of cancer that affects lymphocytes, or white blood cells.
Common pain relief medication may encourage cancer growth
Although morphine has been the gold-standard treatment for postoperative and chronic cancer pain for two centuries, a growing body of evidence is showing that opiate-based painkillers can stimulate the growth and spread of cancer cells.
Cancers' Sweet Tooth May Be Weakness
The pedal-to-the-metal signals driving the growth of several types of cancer cells lead to a common switch governing the use of glucose, researchers at Winship Cancer Institute of Emory University have discovered.
UCLA researchers create 'fly paper' to capture circulating cancer cells
Just as fly paper captures insects, an innovative new device with nano-sized features developed by researchers at UCLA is able to grab cancer cells in the blood that have broken off from a tumor.
Paradoxical protein might prevent cancer
One difficulty with fighting cancer cells is that they are similar in many respects to the body's stem cells. By focusing on the differences, researchers at Karolinska Institutet have found a new way of tackling colon cancer. The study is presented in the prestigious journal Cell.
Cornell researchers identify a weak link in cancer cell armor
The seeming invincibility of cancerous tumors may be crumbling, thanks to a promising new gene therapy that eliminates the ability of certain cells to repair themselves.
Aileron collaborates study in Nature: Stapled peptides inhibit Notch1 transcription factor
This research validates the potential for Stapled Peptides to modulate key intracellular biological targets, such as transcription factors, that have not been addressable with current small molecule or biologic drug modalities.
Researchers 'notch' a victory toward new kind of cancer drug
Scientists have devised an innovative way to disarm a key protein considered to be "undruggable," meaning that all previous efforts to develop a drug against it have failed.
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