Manual Cell Adhesion and Cytoskeletal Molecules in Metastasis

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Cdc42 promotes the formation of filopodia and induces cell migration and metastasis [ 90 ]. Phosphoinositide dependent kinase 1 activates ROCK1 by opposing the inhibition of RhoE and then promotes cell motility [ 92 ].


ROCK1 plays a key role in the formation of stress fibers, and this isoform is mainly responsible for rigidity-dependent invadopodia activity through actomyosin contractility [ 96 , 97 ]. ROCK2 is important for phagocytosis, cell contraction and stabilizing the cytoskeleton [ 78 , 97 , 98 ]. Cdc42 activates the formin protein mDia2 to regulate actin nucleation and elongation of microfilaments [ , ]. The straight parallel alignment of microfilaments form filopodia [ 99 ]. RhoA and RacC play important roles during the formation of invadopodia.

RhoA activates mDia2 and further induces the formation of linear actin bundles to result in the elongation of invadopodia [ ]. In addition to regulating the formation of invadopodia, Cdc42 plays an important role in the trafficking of MMPs to the invadopodia. Eventually, MMPs promote extracellular matrix remodeling to enable invasive growth [ 94 ] Fig.

Zhang et al. Wang et al. Vinculin is another motility-associated protein that is synthesized in migrating cells, and vinculin-deficient cells extend unstable lamellipodia and filopodia. Understanding these relationships may provide insights into human lncRNA regulation, cytoskeletal structure, cell migration, and cancer metastasis. We present various lncRNAs in Fig. MEG3 downregulates Rac1 expression and is linked to primary thyroid cancer with lymph node metastasis.

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From a physics viewpoint, the development of a tumor is a biological process driven by mechanics, which is regulated by the biochemical signaling pathways of tumor cells. For example, changes in cellular mechanical properties can activate signal transduction pathways. External factors stimulate the transition of normal cells to tumor cells.

The activity of the intracellular Rho signal increases, the arrangement of cytoskeleton fibers changes, and then cell morphology is affected. Some questions need to be addressed.

For example, do lncRNAs regulate other signaling pathways that are associated with the cytoskeleton? How can the cytoskeleton be targeted via lncRNAs for clinical cancer treatment? With the development of lncRNA research and technologies for measuring cell movements, the relationship between lncRNAs and cell migration and invasion in tumor metastasis can be uncovered.

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LncRNAs regulate the cytoskeleton and related Rho/ROCK signaling in cancer metastasis

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Actin cortex architecture regulates cell surface tension. Nat Cell Biol. Random versus directionally persistent cell migration.