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Search Results (4)

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Keywords = mechanopathologies

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12 pages, 1324 KiB  
Review
Mechanisms of PIEZO Channel Inactivation
by Zijing Zhou and Boris Martinac
Int. J. Mol. Sci. 2023, 24(18), 14113; https://doi.org/10.3390/ijms241814113 - 14 Sep 2023
Cited by 9 | Viewed by 4228
Abstract
PIEZO channels PIEZO1 and PIEZO2 are the newly identified mechanosensitive, non-selective cation channels permeable to Ca2+. In higher vertebrates, PIEZO1 is expressed ubiquitously in most tissues and cells while PIEZO2 is expressed more specifically in the peripheral sensory neurons. PIEZO channels [...] Read more.
PIEZO channels PIEZO1 and PIEZO2 are the newly identified mechanosensitive, non-selective cation channels permeable to Ca2+. In higher vertebrates, PIEZO1 is expressed ubiquitously in most tissues and cells while PIEZO2 is expressed more specifically in the peripheral sensory neurons. PIEZO channels contribute to a wide range of biological behaviors and developmental processes, therefore driving significant attention in the effort to understand their molecular properties. One prominent property of PIEZO channels is their rapid inactivation, which manifests itself as a decrease in channel open probability in the presence of a sustained mechanical stimulus. The lack of the PIEZO channel inactivation is linked to various mechanopathologies emphasizing the significance of studying this PIEZO channel property and the factors affecting it. In the present review, we discuss the mechanisms underlying the PIEZO channel inactivation, its modulation by the interaction of the channels with lipids and/or proteins, and how the changes in PIEZO inactivation by the channel mutations can cause a variety of diseases in animals and humans. Full article
(This article belongs to the Special Issue Membrane Channels: Mechanistic Insights)
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13 pages, 2384 KiB  
Review
Atomic Force Microscopy Methods to Measure Tumor Mechanical Properties
by Julian Najera, Matthew R. Rosenberger and Meenal Datta
Cancers 2023, 15(13), 3285; https://doi.org/10.3390/cancers15133285 - 22 Jun 2023
Cited by 16 | Viewed by 4120
Abstract
Atomic force microscopy (AFM) is a popular tool for evaluating the mechanical properties of biological materials (cells and tissues) at high resolution. This technique has become particularly attractive to cancer researchers seeking to bridge the gap between mechanobiology and cancer initiation, progression, and [...] Read more.
Atomic force microscopy (AFM) is a popular tool for evaluating the mechanical properties of biological materials (cells and tissues) at high resolution. This technique has become particularly attractive to cancer researchers seeking to bridge the gap between mechanobiology and cancer initiation, progression, and treatment resistance. The majority of AFM studies thus far have been extensively focused on the nanomechanical characterization of cells. However, these approaches fail to capture the complex and heterogeneous nature of a tumor and its host organ. Over the past decade, efforts have been made to characterize the mechanical properties of tumors and tumor-bearing tissues using AFM. This has led to novel insights regarding cancer mechanopathology at the tissue scale. In this Review, we first explain the principles of AFM nanoindentation for the general study of tissue mechanics. We next discuss key considerations when using this technique and preparing tissue samples for analysis. We then examine AFM application in characterizing the mechanical properties of cancer tissues. Finally, we provide an outlook on AFM in the field of cancer mechanobiology and its application in the clinic. Full article
(This article belongs to the Topic Biomarker Development and Application)
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10 pages, 630 KiB  
Perspective
Do Tumor Mechanical Stresses Promote Cancer Immune Escape?
by Killian Onwudiwe, Julian Najera, Saeed Siri and Meenal Datta
Cells 2022, 11(23), 3840; https://doi.org/10.3390/cells11233840 - 30 Nov 2022
Cited by 8 | Viewed by 3365
Abstract
Immune evasion—a well-established cancer hallmark—is a major barrier to immunotherapy efficacy. While the molecular mechanisms and biological consequences underpinning immune evasion are largely known, the role of tissue mechanical stresses in these processes warrants further investigation. The tumor microenvironment (TME) features physical abnormalities [...] Read more.
Immune evasion—a well-established cancer hallmark—is a major barrier to immunotherapy efficacy. While the molecular mechanisms and biological consequences underpinning immune evasion are largely known, the role of tissue mechanical stresses in these processes warrants further investigation. The tumor microenvironment (TME) features physical abnormalities (notably, increased fluid and solid pressures applied both inside and outside the TME) that drive cancer mechanopathologies. Strikingly, in response to these mechanical stresses, cancer cells upregulate canonical immune evasion mechanisms, including epithelial–mesenchymal transition (EMT) and autophagy. Consideration and characterization of the origins and consequences of tumor mechanical stresses in the TME may yield novel strategies to combat immunotherapy resistance. In this Perspective, we posit that tumor mechanical stresses—namely fluid shear and solid stresses—induce immune evasion by upregulating EMT and autophagy. In addition to exploring the basis for our hypothesis, we also identify explicit gaps in the field that need to be addressed in order to directly demonstrate the existence and importance of this biophysical relationship. Finally, we propose that reducing or neutralizing fluid shear stress and solid stress-induced cancer immune escape may improve immunotherapy outcomes. Full article
(This article belongs to the Special Issue Cellular Integrity under Mechanical Stress)
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18 pages, 3338 KiB  
Article
Unusual Association of NF-κB Components in Tumor-Associated Macrophages (TAMs) Promotes HSPG2-Mediated Immune-Escaping Mechanism in Breast Cancer
by Veronica De Paolis, Fabio Maiullari, Maila Chirivì, Marika Milan, Chiara Cordiglieri, Francesca Pagano, Alessandra Rita La Manna, Elena De Falco, Claudia Bearzi, Roberto Rizzi and Chiara Parisi
Int. J. Mol. Sci. 2022, 23(14), 7902; https://doi.org/10.3390/ijms23147902 - 18 Jul 2022
Cited by 9 | Viewed by 2854
Abstract
The cellular heterogeneity of the tumor environment of breast cancer (BC) is extremely complex and includes different actors such as neoplastic, stromal, and immunosuppressive cells, which contribute to the chemical and mechanical modification of the environment surrounding the tumor-exasperating immune-escaping mechanisms. In addition [...] Read more.
The cellular heterogeneity of the tumor environment of breast cancer (BC) is extremely complex and includes different actors such as neoplastic, stromal, and immunosuppressive cells, which contribute to the chemical and mechanical modification of the environment surrounding the tumor-exasperating immune-escaping mechanisms. In addition to molecular signals that make the tumor microenvironment (TME) unacceptable for the penetrance of the immune system, the physical properties of tumoral extracellular matrix (tECM) also have carved out a fundamental role in the processes of the protection of the tumor niche. Tumor-associated macrophages (TAMs), with an M2 immunosuppressive phenotype, are important determinants for the establishment of a tumor phenotype excluded from T cells. NF-κB transcription factors orchestrate innate immunity and represent the common thread between inflammation and cancer. Many studies have focused on canonical activation of NF-κB; however, activation of non-canonical signaling predicts poor survival and resistance to therapy. In this scenario, we demonstrated the existence of an unusual association of NF-κB components in TAMs that determines the deposition of HSPG2 that affects the stiffness of tECM. These results highlight a new mechanism counterbalanced between physical factors and a new perspective of mechano-pathology to be targeted to counteract immune evasion in BC. Full article
(This article belongs to the Special Issue Extracellular Matrix and Cancer: An Intricate Affair)
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