Breast cancer already taken the first place of incidence in Chinese female cancer patients. TRPM8 is found to be over-expressed in breast cancer, but whether it promotes breast cancer aggressiveness remains unknown. In our study, TRPM8 was identified highly expressing in all the tested breast cancer cell lines including MCF-7, T47D, MDA-MB-231, BT549, SKBR3 and ZR-75-30, while it just could be detected in MCF-10A, the normal breast epithelial cell. Then four pairs of clinical samples were analyzed using Western blotting and the result showed that TRPM8 expression is higher in tumor tissues than in adjacent nontumor tissues. Subsequently, we established TRPM8 high-expressing MCF-7 cell line and TRPM8 knockout MDA-MB-231 cell line to explore expression status of cancer-related proteins. The Western blotting and immunofluorescence analysis outcomes demonstrated that TRPM8 might influence cancer cell metastasis by regulating the EMT phenotype via activating AKT/GSK-3β pathway, and the hypothesis had been supported by cell function tests. All the results demonstrated that TRPM8 significantly up-expressed in breast cancer cells and promoted their metastasis by regulating EMT via activating AKT/GSK-3β pathway, indicating TRPM8 gets the prospects of to be developed as medication or diagnostic indicator to be applied in clinical work.
We investigate the effect of inertial particles on the stability and decay of a prototypical vortex tube, represented by a two-dimensional Lamb–Oseen vortex. In the absence of particles, the strong stability of this flow makes it resilient to perturbations, whereby vorticity and enstrophy decay at a slow rate controlled by viscosity. Using Eulerian–Lagrangian simulations, we show that the dispersion of semidilute inertial particles accelerates the decay of the vortex tube by orders of magnitude. In this work, mass loading is unity, ensuring that the fluid and particle phases are tightly coupled. Particle inertia and vortex strength are varied to yield Stokes numbers 0.1–0.4 and circulation Reynolds numbers 800–5000. Preferential concentration causes these inertial particles to be ejected from the vortex core forming a ring-shaped cluster and a void fraction bubble that expand outwards. The outward migration of the particles causes a flattening of the vorticity distribution, which enhances the decay of the vortex. The latter is further accelerated by small-scale clustering that causes enstrophy to grow, in contrast with the monotonic decay of enstrophy in single-phase two-dimensional vortices. These dynamics unfold on a time scale that is set by preferential concentration and is two orders of magnitude lower than the viscous time scale. Increasing particle inertia causes a faster decay of the vortex. This work shows that the injection of inertial particles could provide an effective strategy for the control and suppression of resilient vortex tubes.
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