Plasma membrane repair provides a new strategy for targeting metastatic cancer cells

2015 ◽  
Keyword(s):  
Plasma Membrane ◽  
Cancer Cells ◽  
Metastatic Cancer ◽  
Membrane Repair ◽  
New Strategy ◽  
Plasma Membrane Repair ◽  
Metastatic Cancer Cells

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 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 Normal cells repel WWOX-negative or -dysfunctional cancer cells via WWOX cell surface epitope 286-299

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Yu-An Chen ◽  
Yong-Da Sie ◽  
Tsung-Yun Liu ◽  
Hsiang-Ling Kuo ◽  
Pei-Yi Chou ◽  
...  
Keyword(s):  
Cell Surface ◽  
Cancer Cells ◽  
Room Temperature ◽  
Metastatic Cancer ◽  
Normal Cells ◽  
Tgfβ Receptor ◽  
Membrane Type ◽  
Cell Invasiveness ◽  
And Control ◽  
Metastatic Cancer Cells

AbstractMetastatic cancer cells are frequently deficient in WWOX protein or express dysfunctional WWOX (designated WWOXd). Here, we determined that functional WWOX-expressing (WWOXf) cells migrate collectively and expel the individually migrating WWOXd cells. For return, WWOXd cells induces apoptosis of WWOXf cells from a remote distance. Survival of WWOXd from the cell-to-cell encounter is due to activation of the survival IκBα/ERK/WWOX signaling. Mechanistically, cell surface epitope WWOX286-299 (repl) in WWOXf repels the invading WWOXd to undergo retrograde migration. However, when epitope WWOX7-21 (gre) is exposed, WWOXf greets WWOXd to migrate forward for merge. WWOX binds membrane type II TGFβ receptor (TβRII), and TβRII IgG-pretreated WWOXf greet WWOXd to migrate forward and merge with each other. In contrast, TβRII IgG-pretreated WWOXd loses recognition by WWOXf, and WWOXf mediates apoptosis of WWOXd. The observatons suggest that normal cells can be activated to attack metastatic cancer cells. WWOXd cells are less efficient in generating Ca2+ influx and undergo non-apoptotic explosion in response to UV irradiation in room temperature. WWOXf cells exhibit bubbling cell death and Ca2+ influx effectively caused by UV or apoptotic stress. Together, membrane WWOX/TβRII complex is needed for cell-to-cell recognition, maintaining the efficacy of Ca2+ influx, and control of cell invasiveness.

scholarly journals Amoebic Foraging Model of Metastatic Cancer Cells

Symmetry ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1140
Author(s):  
Daiki Andoh ◽  
Yukio-Pegio Gunji
Keyword(s):  
Bayesian Inference ◽  
Cancer Cells ◽  
Metastatic Cancer ◽  
Gait Patterns ◽  
Lévy Walk ◽  
Levy Walk ◽  
Unicellular Organisms ◽  
Living Organisms ◽  
Walk Algorithm ◽  
Metastatic Cancer Cells

The Lévy walk is a pattern that is often seen in the movement of living organisms; it has both ballistic and random features and is a behavior that has been recognized in various animals and unicellular organisms, such as amoebae, in recent years. We proposed an amoeba locomotion model that implements Bayesian and inverse Bayesian inference as a Lévy walk algorithm that balances exploration and exploitation, and through a comparison with general random walks, we confirmed its effectiveness. While Bayesian inference is expressed only by P(h) = P(h|d), we introduce inverse Bayesian inference expressed as P(d|h) = P(d) in a symmetry fashion. That symmetry contributes to balancing contracting and expanding the probability space. Additionally, the conditions of various environments were set, and experimental results were obtained that corresponded to changes in gait patterns with respect to changes in the conditions of actual metastatic cancer cells.

scholarly journals Light- and Melanin Nanoparticle-Induced Cytotoxicity in Metastatic Cancer Cells

Pharmaceutics ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 965
Author(s):  
Victoria R. Gabriele ◽  
Robabeh M. Mazhabi ◽  
Natalie Alexander ◽  
Purna Mukherjee ◽  
Thomas N. Seyfried ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Metastatic Cancer ◽  
Energy Levels ◽  
Nanoparticle Concentration ◽  
Visible Radiation ◽  
Laser Illumination ◽  
Wide Range ◽  
Low Glucose ◽  
Melanin Nanoparticles ◽  
Metastatic Cancer Cells

Melanin nanoparticles are known to be biologically benign to human cells for a wide range of concentrations in a high glucose culture nutrition. Here, we show cytotoxic behavior at high nanoparticle and low glucose concentrations, as well as at low nanoparticle concentration under exposure to (nonionizing) visible radiation. To study these effects in detail, we developed highly monodispersed melanin nanoparticles (both uncoated and glucose-coated). In order to study the effect of significant cellular uptake of these nanoparticles, we employed three cancer cell lines: VM-M3, A375 (derived from melanoma), and HeLa, all known to exhibit strong macrophagic character, i.e., strong nanoparticle uptake through phagocytic ingestion. Our main observations are: (i) metastatic VM-M3 cancer cells massively ingest melanin nanoparticles (mNPs); (ii) the observed ingestion is enhanced by coating mNPs with glucose; (iii) after a certain level of mNP ingestion, the metastatic cancer cells studied here are observed to die—glucose coating appears to slow that process; (iv) cells that accumulate mNPs are much more susceptible to killing by laser illumination than cells that do not accumulate mNPs; and (v) non-metastatic VM-NM1 cancer cells also studied in this work do not ingest the mNPs, and remain unaffected after receiving identical optical energy levels and doses. Results of this study could lead to the development of a therapy for control of metastatic stages of cancer.

scholarly journals The In Vivo Selection Method in Breast Cancer Metastasis

2021 ◽  
Vol 22 (4) ◽  
pp. 1886
Author(s):  
Jun Nakayama ◽  
Yuxuan Han ◽  
Yuka Kuroiwa ◽  
Kazushi Azuma ◽  
Yusuke Yamamoto ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Metastasis ◽  
Metastatic Cancer ◽  
Expression Patterns ◽  
Selection Method ◽  
Gene Signatures ◽  
In Vivo Selection ◽  
Metastatic Cancer Cells

Metastasis is a complex event in cancer progression and causes most deaths from cancer. Repeated transplantation of metastatic cancer cells derived from transplanted murine organs can be used to select the population of highly metastatic cancer cells; this method is called as in vivo selection. The in vivo selection method and highly metastatic cancer cell lines have contributed to reveal the molecular mechanisms of cancer metastasis. Here, we present an overview of the methodology for the in vivo selection method. Recent comparative analysis of the transplantation methods for metastasis have revealed the divergence of metastasis gene signatures. Even cancer cells that metastasize to the same organ show various metastatic cascades and gene expression patterns by changing the transplantation method for the in vivo selection. These findings suggest that the selection of metastasis models for the study of metastasis gene signatures has the potential to influence research results. The study of novel gene signatures that are identified from novel highly metastatic cell lines and patient-derived xenografts (PDXs) will be helpful for understanding the novel mechanisms of metastasis.

Experimental Study of the Survival of Metastatic Cancer Cells in Corneal Organ Culture

2006 ◽  
Vol 47 (4) ◽  
pp. 1339 ◽  
Author(s):  
Nilanjana Deb-Joardar ◽  
Gilles Thuret ◽  
Jean-Marc Dumollard ◽  
Lena Absi ◽  
Lydia Campos-Guyotat ◽  
...  
Keyword(s):  
Experimental Study ◽  
Organ Culture ◽  
Cancer Cells ◽  
Metastatic Cancer ◽  
Corneal Organ Culture ◽  
Metastatic Cancer Cells
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