Calcium gradients underlying cell migration

Reciprocal regulation of actin cytoskeleton remodelling and cell migration by Ca2+ and Zn2+: role of TRPM2 channels

“…These cycles are driven by spatio-temporal remodelling of the actin cytoskeleton and focal adhesions (Gardel et al, 2010;Lamalice et al, 2007;Mattila and Lappalainen, 2008;Ridley et al, 2003;Small et al, 2002;Tojkander et al, 2012). Ca 2+ is widely regarded as an important coordinator of these events (Prevarskaya et al, 2011;Tsai et al, 2014;Wei et al, 2009Wei et al, , 2012. Accordingly, multiple Ca 2+ channels and pumps have been implicated in the cell migration (Prevarskaya et al, 2011).…”

“…The mechanism by which H 2 O 2 induces cell migration, however, is not fully understood, although H 2 O 2 is known to affect a number of signalling pathways associated with cell migration, including Ca 2+ signalling (Prevarskaya et al, 2011;Tsai et al, 2014;Wei et al, 2012) and Lyn activation (Yoo et al, 2011). Multiple studies have shown that Ca 2+ plays a key role in the spatial and temporal regulation of the actin cytoskeleton and focal adhesions (Brundage et al, 1991;Gilbert et al, 1994;Prevarskaya et al, 2011;Tsai et al, 2014;Wei et al, 2012).…”

Mechanosensitive ATP release from hemichannels and Ca2+ influx through TRPC6 accelerate wound closure in keratinocytes

“…8B) (Martin, 1997;Coulombe, 2003;Gurtner et al, 2008;Li and Wang, 2010). The generation of these forces or the locomotion and directional cell movement are regulated by local intracellular Ca 2+ increases (Brundage et al, 1991;Lee et al, 1999;Wei et al, 2012). It is plausible that these endogenous mechanical forces induce ATP-Ca 2+ signaling in the cells to regulate wound closure.…”

Remodelling of Ca2+transport in cancer: how it contributes to cancer hallmarks?

“…The following Ca 2þ permeable channels have been implicated in the enhanced migration of various types of cancer cells (figure 3): TRPC1 [64], TRPM7 [65 -71], TRPM8 [43,72,73], TRPV1 [74], TRPV2 [75], TRPV6 [40], STIM1 and ORAI1 SOC constituents [13,[76][77][78][79], some types of VGCCs [35,80]. Owing to the presence of mechanical stimulusdependent and Mg-ATP-dependent modes of activation TRPM7 was especially implicated in providing spatially restricted Ca 2þ entry in response to local membrane stretch in front of migrating cells [66,69] as well as promoting m-calpain-mediated disassembly of peripheral adhesions under decreased intracellular Mg-ATP levels [65] typically found in hypoxic tumour conditions. Moreover, high levels of TRPM7 expression per se was established as a prognostic marker for breast cancer [70] and pancreatic ductal adenocarcinoma (PDAC) [71] progression.…”

“…For instance, localized [Ca 2þ ] C flickers at the front of migrating fibroblasts occurred because of interaction of TRPM7-mediated Ca 2þ influx and Ca 2þ release via type 2 IP 3 R (IP 3 R2) [66,69], whereas global [Ca 2þ ] C increase associated with enhanced migration of nasopharyngeal carcinoma cells depended on activation of TRPM7 and CICR involving RyRs [67] ( figure 3).…”