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Endogenous Bioelectric Phenomena and Interfaces for Exogenous Effects
Published in Ben Greenebaum, Frank Barnes, Bioengineering and Biophysical Aspects of Electromagnetic Fields, 2018
Complex voltage-sensitive receptors, like the voltage-sensitive phosphatase (VSP) were found as direct EF sensors. This is again a special case of coupling by changing of conformation in channel proteins. Here, e.g., a molecular lever is moved by the charges leading to changes of topography), which leads to an ion flux and hence produces new currents and fields by this ion flux. Furthermore, voltage-sensitive phosphatases (VSP) were found to be direct EF sensors and links to relevant signaling cascades (171). VSP is a phosphoinositide phosphatase that converts PtdIns (3,4,5)P3 to PtdIns (4,5) P2, under regulation of a voltage sensor domain (172). Levin (22) reports that the lipid phosphatase PTEN was found to be a component of an intrinsic voltage sensor (171). PTEN negatively regulates the PI3K and Akt pathway by reducing the available amount of PtdIns (3,4,5) P3. Furthermore, genetic abrogation of PTEN enhanced ERK and Akt phosphorylation, and potentiated field-induced keratinocyte migration (22, 67).
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Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
Eun-Kyung Lim, Taekhoon Kim, Soonmyung Paik, Seungjoo Haam, Yong-Min Huh, Kwangyeol Lee
PI3K and PIP3 levels are barely detectable in mammalian cells under unstimulated growth conditions and tightly controlled, owing to the combined effects of stringent PI3K regulation and the action of several PIP3 phosphatases (phosphatase and tensin homologue [PTEN], SH2-containing inositol phosphatase, SH2-containing inositol phosphatase 2) [172, 176, 177]. Among them, PTEN acts as a tumor suppressor gene through the action of its phosphatase protein product and has subsequently been implicated more broadly in various human cancers [173, 174]. PIP3 in turn contributes to the recruitment and activation of a wide range of downstream targets, including the serine-threonin protein kinase Akt, which can indirectly promote cell survival [176, 177].
Brain cancer
Published in Ruijiang Li, Lei Xing, Sandy Napel, Daniel L. Rubin, Radiomics and Radiogenomics, 2019
William D. Dunn, Rivka R. Colen
Other markers include interleukins (ILs) and phosphatase and tensin homolog (PTEN). ILs play significant roles in a variety of cancers by activating proliferation or signaling pathways that involve cell migration and invasion, ultimately leading to resistance to chemotherapy.62 The expression of specific ILs such as IL-6 have been associated with lower survival in glioblastoma patients.63PTEN is a tumor suppressor found mutated or silenced in approximately 40% of glioblastomas and causes disruption in cell cycle, apoptosis, and cell migration pathways.64 Heterogeneous PTEN expression was found to lead to poorer prognosis in glioblastoma patients.42
Transcriptome alterations in zebrafish gill after exposure to different sizes of microplastics
Published in Journal of Environmental Science and Health, Part A, 2022
Ying-Hao Xue, Tao Jia, Ning Yang, Zhan-Xiang Sun, Zhi-Yu Xu, Xin-Li Wen, Liang-Shan Feng
As one of the most frequently mutated tumor suppressor gene, PTEN antagonizes the activity of PI3K (phosphoinositide-3-kinase). The balance between them finally affect proliferation, cell migration, apoptosis, cell survival, angiogenesis, and metabolism.[52] In zebrafish, lack of PTEN function arrested proliferation of embryo cells and enhanced the apoptosis.[53] In the present study, both pten and pi3k were upregulated in response to MPs exposure. However, their downstream gene TSC1/2 (tuberous sclerosis complex 1/2) was upregulated, which has been reported to protect stress-induced apoptosis in HeLa cells.[54] Therefore, the upregulation of pten and TSC1/2 might inhibit cell apoptosis in response to the physical damage caused by MPs.
Two mixed-ligand Cd(II)-coordination polymers: structural diversity and antitumor activity against human osteogenic sarcoma cells
Published in Inorganic and Nano-Metal Chemistry, 2020
Feng Han, Shun Cao, Hongwei Ding, Ziwei Chen, Qiang Zhang, Shi-Dong Xu
After confirming the induction activity of the compounds in the MG-63 cell apoptosis, we further aimed to explore the detail mechanism. As reported, the PTEN-AKT signaling pathway has a significant function in the cancer cell proliferation and apoptosis. Therefore, in this experiment, the western blot was finished to detect PTEN–AKT activation level after indicated treatment. As results shown in Figure 6, after treated with compound 1, the PTEN relative expression was increased, which is significantly different from the control group. The p-AKT is a common downstream target of PTEN, which is negatively regulated by PTEN, was decreased remarkably. However, the ligands H2opda, H2ppda, and metal cadmium ions have no effect on the activation level of PTEN–AKT signal pathway. This result indicated compound 1 has stronger induction effect on the PTEN-AKT signal pathway activation than compound 2.