Cytoskeleton and Nucleotide Signaling in Glioma C6 Cells

Kłopocka, Wanda; Korczyński, Jarosław; Pomorski, Paweł

doi:10.1007/978-3-030-30651-9_6

Cited by 8 publications

(9 citation statements)

References 132 publications

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“…PAK1 is an important downstream effector of Rac1 and Cdc42 (35). Rac1 and Cdc42 can activate LIM kinase1 (LIMK1) through PAK, which leads to the decrease of cofilin activity and enhance mobility through phosphorylation (36). The effect of PAK on cell mechanics depends on Rac1, and the formation of the Rac1-PAK pathway plays an important role in cytoskeleton reorganization during cell migration (19).…”

Section: Rac1 Regulates Cell Adhesion Morphology and Movementmentioning

confidence: 99%

Rac1, A Potential Target for Tumor Therapy

et al. 2021

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RAS-related C3 botulinum toxin substrate 1 (Rac.1) is one of the important members of Rho GTPases. It is well known that Rac1 is a cytoskeleton regulation protein that regulates cell adhesion, morphology, and movement. Rac1 is highly expressed in different types of tumors, which is related to poor prognosis. Studies have shown that Rac1 not only participates in the tumor cell cycle, apoptosis, proliferation, invasion, migration and angiogenesis, but also participates in the regulation of tumor stem cell, thus promoting the occurrence of tumors. Rac1 also plays a key role in anti-tumor therapy and participates in immune escape mediated by the tumor microenvironment. In addition, the good prospects of Rac1 inhibitors in cancer prevention and treatment are exciting. Therefore, Rac1 is considered as a potential target for the prevention and treatment of cancer. The necessity and importance of Rac1 are obvious, but it still needs further study.

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Section: Rac1 Regulates Cell Adhesion Morphology and Movementmentioning

confidence: 99%

Rac1, A Potential Target for Tumor Therapy

et al. 2021

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“…Thus, Rac/PAK and Rho/ROCK signalling triggers cofilin inactivation on the one hand and myosin II activation through the MLC pathway on the other hand, causing overall actin cytoskeleton reorganization that leads to stress fibre assembly and lamellipodium formation in the cell periphery. These alterations in cell morphology are performed in order to favour cell migration [ 34 ]. Besides this, in this study, significant differences were also found in the gene expression of some of the downstream targets of Cdc42 GTPase.…”

Section: Discussionmentioning

confidence: 99%

Acquisition of New Migratory Properties by Highly Differentiated CD4+CD28null T Lymphocytes in Rheumatoid Arthritis Disease

Rioseras

Moro-García

García-Torre

et al. 2021

JPM

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Expanded CD4+CD28null T lymphocytes are found in the tissues and peripheral blood of patients with many autoimmune diseases, such as rheumatoid arthritis (RA). These highly differentiated cells present potent inflammatory activity and capability to induce tissue destruction, which has been suggested to predispose to the development of more aggressive disease. In fact, preferential migration to inflammatory sites has been proposed to be a contributing factor in the progression of autoimmune and cardiovascular diseases frequently found in these patients. The functional activity of CD4+CD28null T lymphocytes is largely dependent on interleukin 15 (IL-15), and this cytokine may also act as a selective attractor of these cells to local inflammatory infiltrates in damaged tissues. We have analysed, in RA patients, the migratory properties and transcriptional motility profile of CD4+CD28null T lymphocytes compared to their counterparts CD28+ T lymphocytes and the enhancing role of IL-15. Identification of the pathways involved in this process will allow us to design strategies directed to block effector functions that CD4+CD28null T lymphocytes have in the target tissue, which may represent therapeutic approaches in this immune disorder.

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“…Using specific Rho kinase inhibitors targeting this pathway reduces the level of phosphorylated myosin II and cofilin, subsequently prevents tumor cell migration by inhibiting the dynamic assembly of f-actin structures. 101 P2Y2 nucleotide receptor (P2Y2R), 129 reticulon-4 isoform A (Nogo-A), 130 electroneutral Na + -K + -2Cl − -co-transporter1 (NKCC1), 131 miR-451, 132 C1q tumor necrosis factor-related peptide8 (CTRP8), 133 miR-29a/b/c 134 etc. are considered regulating phosphorylated LIMK1/2 and cofilin through targeting different members of Rho family of GTPases, including Rac1, the member A of Rho (RhoA) and CDC42, subsequently regulating glioma cell migration and invasion.…”

Section: Methodsmentioning

confidence: 99%

Cofilin Acts as a Booster for Progression of Malignant Tumors Represented by Glioma

Lv¹,

Chen²,

Mi³

et al. 2022

CMAR

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Cofilin, as a depolymerization factor of actin filaments, has been widely studied. Evidences show that cofilin has a role in actin structural reorganization and dynamic regulation. In recent years, several studies have demonstrated a regulatory role for cofilin in the migration and invasion mediated by cell dynamics and epithelial to mesenchymal transition (EMT)/EMT-like process, apoptosis, radiotherapy resistance, immune escape, and transcriptional dysregulation of malignant tumor cells, particularly glioma cells. On this basis, it is practical to evaluate cofilin as a biomarker for predicting tumor metastasis and prognosis. Targeting cofilin regulating kinases, Lin11, Isl-1 and Mec-3 kinases (LIM kinases/LIMKs) and their major upstream molecules inhibits tumor cell migration and invasion and targeting cofilin-mediated mitochondrial pathway induces apoptosis of tumor cells represent effective options for the development of novel anti-malignant tumor drug, especially anti-glioma drugs. This review explores the structure, general biological function, and regulation of cofilin, with an emphasis on the critical functions and prospects for clinical therapeutic applications of cofilin in malignant tumors represented by glioma.

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Cytoskeleton and Nucleotide Signaling in Glioma C6 Cells

Cited by 8 publications

References 132 publications

Rac1, A Potential Target for Tumor Therapy

Rac1, A Potential Target for Tumor Therapy

Acquisition of New Migratory Properties by Highly Differentiated CD4+CD28null T Lymphocytes in Rheumatoid Arthritis Disease

Cofilin Acts as a Booster for Progression of Malignant Tumors Represented by Glioma

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