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gaining invasiveness and overcoming the physical barriers imposed by the extracellular matrix ( ecm ) are the first , and arguably most critical , steps of tumor metastasis . in addition to facilitating dissemination , remodeling of the ecm
invadopodia of malignant cancer cells are actin - rich , ecm - degrading membrane protrusions that are critical for tumor invasion and metastasis . in a recent study , we investigated the regulation of invadopodium formation and metastasis by ca signaling in melanoma .
we unexpectedly discovered that hyperactive ca signaling in metastatic melanoma cells is organized in the form of oscillatory waves to orchestrate invadopodia assembly and melanoma invasion . in recent years , dysregulated ca signaling has been increasingly implicated in cancer invasion and metastasis , yet the underlying mechanism remained largely unclear . to gain mechanistic insight into ca - mediated invasion and metastasis , we examined the role of ca signaling in invadopodium formation in melanoma cells and discovered that blocking store - operated calcium ( soc ) channel signaling significantly decreased invadopodium number and activity .
accompanying the assembly of invadopodia was an oscillatory ca signal mediated by the soc channel proteins stim1 and orai1 .
interestingly , disruption of the ca oscillation by either blocking store operated calcium entry ( soce ; which decreased cytosolic ca concentration ) , or by inducing constitutive calcium entry with thapsigargin or the ionophore a-23187 ( which increased cytosolic ca concentration ) similarly inhibited invadopodium assembly and melanoma invasion , signifying the importance of temporal ca signal coding during metastatic dissemination . by screening a panel of protein kinases
, we identified the non - receptor tyrosine kinase src as a downstream effector of soce . the notion that soce regulates invadopodium assembly through src
is further supported by the rescue of defective invadopodium formation in stim1 knockdown melanoma cells by constitutively active v - src , and the abrogation of stim1-mediated invadopodium assembly by the src inhibitor dasatinib .
the fact that constitutive ca influx induced by thapsigargin and a-23187 was a robust activator of src begs the question : why do melanoma cells use an oscillatory ca signal instead of a steady ca increase ?
it is estimated that hundreds of genes in the human genome contain ca binding ef - hand or c2 domains .
the specificity and versatility of ca signaling relies on the intricate spatial and temporal coding of cytosolic ca concentration . by compartmentalizing ca signals into spatial - temporal patterns ,
cells are able to activate selective downstream signaling events at a defined time and subcellular location .
it is believed that the frequency and amplitude of ca oscillations serve as digital signals that selectively activate threshold - dependent downstream events .
the tight control of cytosolic ca is critical not only for signaling specificity but also for cell survival , since a prolonged and uncontrolled global increase in cytosolic ca is toxic to the cell and eventually leads to cell death . by organizing soce signals in the form of ca oscillation
, melanoma cells are able to provide the ca signal necessary for invadopodium assembly and ecm remodeling over an extended period of time without causing cytotoxicity ( fig . 
in contrast , although constitutive ca influx induced by thapsigargin and a23187 robustly increases src activity it might also indiscriminately activate hundreds of other ca - dependent signaling pathways , which eventually reduce melanoma cell fitness and inhibit melanoma invasion ( fig . 
( a ) hyperactive store - operated calcium entry ( soce ) increases ca oscillation frequency and amplitude , which selectively activates src to promote invadopodium assembly and extracellular matrix remodeling .
( b ) disruption of ca oscillation , either by a constitutive increase in cytosolic ca or by blockage of soce , inhibits invadopodium formation and melanoma invasion . 
 
( a ) hyperactive store - operated calcium entry ( soce ) increases ca oscillation frequency and amplitude , which selectively activates src to promote invadopodium assembly and extracellular matrix remodeling .
( b ) disruption of ca oscillation , either by a constitutive increase in cytosolic ca or by blockage of soce , inhibits invadopodium formation and melanoma invasion .
it is also possible that melanoma invasion and invadopodium assembly require a coordinated cycle of ca peaks and valleys , as recently demonstrated in mast cell exocytosis by wollman and meyer .
ca oscillation in antigen - activated mast cells drives the cyclic assembly and disassembly of cortical actin .
newly assembled cortex actin serves as a carrier to capture secretory vesicles , whereas disassembly of cortical actin allows the passage of vesicles to facilitate membrane fusion .
intriguingly , we discovered that recycling of membrane type 1 matrix metalloprotease ( mt1-mmp , also known as mmp14 ) to the plasma membrane required soce , blockage of which resulted in entrapment of mt1-mmp in endosomes .
it would be interesting to determine whether soce - mediated ca oscillation coordinates the recycling of endocytosed mt1-mmp to the plasma membrane . of note
, tumor - promoting ca oscillation has also recently been observed in esophageal squamous cell carcinoma and hepatocellular carcinoma ( hcc ) .
overexpression of orai1 in esophageal carcinoma cells is responsible for hyperactive ca oscillation , which promotes cancer cell motility and proliferation in vitro and tumor growth in a xenograft model . in hcc
the voltage - gated calcium channel subunit cacna2d1 was found to be a marker for recurrent disease .
recurrent hcc cells had higher expression of 21 and hyperactive ca oscillation , which could be inhibited by a blocking antibody targeting cacna2d1 . these observations , together with our recent finding , suggest that ca oscillation might be a signaling mechanism that is commonly hijacked by malignant cells to facilitate cancer progression .
future investigation in this area will likely significantly advance our understanding of how deregulated ca signaling promotes cancer malignancy .
dysregulated calcium signaling has been increasingly implicated in tumor dissemination and progression . in a recent study , 
 we investigated the mechanism underlying calcium - mediated invasion and metastasis in melanoma and discovered that hyperactive ca2 + oscillation in melanoma cells enhanced invasion and metastasis by promoting invadopodium formation and extracellular matrix remodeling .