scholarly journals S100A11 is required for efficient plasma membrane repair and survival of invasive cancer cells

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Jyoti K. Jaiswal ◽  
Stine P. Lauritzen ◽  
Luana Scheffer ◽  
Masakiyo Sakaguchi ◽  
Jakob Bunkenborg ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Cancer Cells ◽  
Invasive Cancer ◽  
Membrane Repair ◽  
Plasma Membrane Repair

scholarly journals Defective membrane repair machinery impairs survival of invasive cancer cells

2020 ◽  
Author(s):  
F. Bouvet ◽  
M. Ros ◽  
E. Bonedeau ◽  
C. Croissant ◽  
L. Frelin ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Cancer Cells ◽  
Cancer Metastasis ◽  
Invasive Cancer ◽  
Migration And Invasion ◽  
High Survival ◽  
Membrane Repair ◽  
Membrane Injury ◽  
Promising Avenue

AbstractCancer cells are able to reach distant tissues by migration and invasion processes. Enhanced ability to cope with physical stresses leading to cell membrane damages may offer to cancer cells high survival rate during metastasis. Consequently, down-regulation of the membrane repair machinery may be a therapeutic avenue for inhibiting metastasis. We show that migration of MDA-MB-231 cells on collagen I fibrils induces disruptions of plasma membrane and pullout of membrane fragments in the wake of cells. These cells are able to reseal membrane damages thanks to annexins (Anx) that are highly expressed in invasive cancer cells. In vitro membrane repair assays reveal that MDA-MB-231 cells respond heterogeneously to membrane injury and some of them possess very efficient repair machinery. Finally, we show that silencing of AnxA5 and AnxA6 leads to major defect of the membrane repair machinery responsible for the death of migrating MDA-MB-231 cells. Inhibition of membrane repair machinery may therefore represent a promising avenue for annihilating cancer metastasis.SummaryCancer cells are able to reach distant tissues by migration and invasion processes. This study shows that inhibition of the plasma membrane repair machinery may represent a promising avenue for annihilating cancer metastasis.

Annexins Bend Wound Edges during Plasma Membrane Repair

2020 ◽  
Vol 27 (22) ◽  
pp. 3600-3610 ◽  
Author(s):  
Adam Cohen Simonsen ◽  
Theresa Louise Boye ◽  
Jesper Nylandsted
Keyword(s):  
Plasma Membrane ◽  
Cancer Cells ◽  
Membrane Curvature ◽  
Eukaryotic Cells ◽  
Repair System ◽  
Membrane Repair ◽  
Membrane Injury ◽  
Anionic Phospholipids ◽  
Annexin A4 ◽  
Plasma Membrane Repair

The plasma membrane of eukaryotic cells defines the boundary to the extracellular environment and, thus provides essential protection from the surroundings. Consequently, disruptions to the cell membrane triggered by excessive mechanical or biochemical stresses pose fatal threats to cells, which they need to cope with to survive. Eukaryotic cells cope with these threats by activating their plasma membrane repair system, which is shared by other cellular functions, and includes mechanisms to remove damaged membrane by internalization (endocytosis), shedding, reorganization of cytoskeleton and membrane fusion events to reseal the membrane. Members of the annexin protein family, which are characterized by their Ca2+-dependent binding to anionic phospholipids, are important regulators of plasma membrane repair. Recent studies based on cellular and biophysical membrane models show that they have more distinct functions in the repair response than previously assumed by regulating membrane curvature and excision of damaged membrane. In cells, plasma membrane injury and flux of Ca2+ ions into the cytoplasm trigger recruitment of annexins including annexin A4 and A6 to the membrane wound edges. Here, they induce curvature and constriction force, which help pull the wound edges together for eventual fusion. Cancer cells are dependent on efficient plasma membrane repair to counteract frequent stress-induced membrane injuries, which opens novel avenues to target cancer cells through their membrane repair system. Here, we discuss mechanisms of single cell wound healing implicating annexin proteins and membrane curvature.

Annexins are instrumental for efficient plasma membrane repair in cancer cells

2015 ◽  
Vol 45 ◽  
pp. 32-38 ◽  
Author(s):  
Stine Prehn Lauritzen ◽  
Theresa Louise Boye ◽  
Jesper Nylandsted
Keyword(s):  
Plasma Membrane ◽  
Cancer Cells ◽  
Membrane Repair ◽  
Plasma Membrane Repair

scholarly journals Plasma membrane repairs by small GTPase Rab3a

2016 ◽  
Vol 213 (6) ◽  
pp. 613-615 ◽  
Author(s):  
Camilla Raiborg ◽  
Harald Stenmark
Keyword(s):  
Plasma Membrane ◽  
Small Gtpase ◽  
Membrane Repair ◽  
Cell Biol ◽  
Plasma Membrane Repair

Lysosomes fuse with the plasma membrane to help repair membrane lesions, but how they are positioned close to these lesions is not fully understood. Now, Encarnação et al. (2016. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201511093) demonstrate that the lysosomal GTPase Rab3a and its effectors orchestrate lysosome positioning and plasma membrane repair.

scholarly journals Mitochondrial fragmentation enables localized signaling required for cell repair

2020 ◽  
Vol 219 (5) ◽  
Author(s):  
Adam Horn ◽  
Shreya Raavicharla ◽  
Sonna Shah ◽  
Dan Cox ◽  
Jyoti K. Jaiswal
Keyword(s):  
Plasma Membrane ◽  
Calcium Influx ◽  
Cell Damage ◽  
Mitochondrial Fission ◽  
Adaptor Protein ◽  
Mitochondrial Fragmentation ◽  
Membrane Repair ◽  
Membrane Injury ◽  
Mitochondrial Signaling ◽  
Plasma Membrane Repair

Plasma membrane injury can cause lethal influx of calcium, but cells survive by mounting a polarized repair response targeted to the wound site. Mitochondrial signaling within seconds after injury enables this response. However, as mitochondria are distributed throughout the cell in an interconnected network, it is unclear how they generate a spatially restricted signal to repair the plasma membrane wound. Here we show that calcium influx and Drp1-mediated, rapid mitochondrial fission at the injury site help polarize the repair response. Fission of injury-proximal mitochondria allows for greater amplitude and duration of calcium increase in these mitochondria, allowing them to generate local redox signaling required for plasma membrane repair. Drp1 knockout cells and patient cells lacking the Drp1 adaptor protein MiD49 fail to undergo injury-triggered mitochondrial fission, preventing polarized mitochondrial calcium increase and plasma membrane repair. Although mitochondrial fission is considered to be an indicator of cell damage and death, our findings identify that mitochondrial fission generates localized signaling required for cell survival.

scholarly journals Annexin A7 is required for ESCRT III-mediated plasma membrane repair

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Stine Lauritzen Sønder ◽  
Theresa Louise Boye ◽  
Regine Tölle ◽  
Jörn Dengjel ◽  
Kenji Maeda ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Membrane Repair ◽  
Plasma Membrane Repair ◽  
Annexin A7

Plasma membrane repair and cellular damage control: The annexin survival kit

2011 ◽  
Vol 81 (6) ◽  
pp. 703-712 ◽  
Author(s):  
Annette Draeger ◽  
Katia Monastyrskaya ◽  
Eduard B. Babiychuk
Keyword(s):  
Plasma Membrane ◽  
Damage Control ◽  
Cellular Damage ◽  
Membrane Repair ◽  
Plasma Membrane Repair
Sign in / Sign up

Export Citation Format

Share Document