The nonlinear free vibration of an axially translating viscoelastic beam with an arbitrarily varying length and axial velocity is investigated. Based on the linear viscoelastic differential constitutive law, the extended Hamilton’s principle is utilized to derive the generalized third-order equations of motion for the axially translating viscoelastic Bernoulli–Euler beam. The coupling effects between the axial motion and transverse vibration are assessed under various prescribed time-varying velocity fields. The inertia force arising from the longitudinal acceleration emerges, rendering the coupling terms between the axial beam acceleration and the beam flexure. Semi-analytical solutions for the governing PDE are obtained through the separation of variables and the assumed modes method. The modified Galerkin’s method and the fourth-order Runge–Kutta method are employed to numerically analyze the resulting equations. Further, dynamic stabilization is examined from the system energy standpoint for beam extension and retraction. Extensive numerical simulations are presented to illustrate the influences of varying translating velocities and viscoelastic parameters on the underlying dynamic responses. The material viscosity always dissipates energy and helps stabilize the transverse vibration.

Current anti-epidermal growth factor receptor (EGFR) therapy for oral cancer does not provide satisfactory efficacy due to drug resistance or reduced EGFR level. As an alternative candidate target for therapy, here we identified an oncogene, ROS1, as an important driver for oral squamous cell carcinoma (OSCC) metastasis. Among tumors from 188 oral cancer patients, upregulated ROS1 expression strongly correlated with metastasis to lung and lymph nodes. Mechanistic studies uncover that the activated ROS1 results from highly expressed ROS1 gene instead of gene rearrangement, a phenomenon distinct from other cancers. Our data further reveal a novel mechanism that reduced histone methyltransferase EZH2 leads to a lower trimethylation of histone H3 lysine 27 suppressive modification, relaxes chromatin, and promotes the accessibility of the transcription factor STAT1 to the enhancer and the intron regions of ROS1 target genes, CXCL1 and GLI1, for upregulating their expressions. Down-regulation of ROS1 in highly invasive OSCC cells, nevertheless, reduces cell proliferation and inhibits metastasis to lung in the tail-vein injection and the oral cavity xenograft models. Our findings highlight ROS1 as a candidate biomarker and therapeutic target for OSCC. Finally, we demonstrate that co-targeting of ROS1 and EGFR could potentially offer an effective oral cancer therapy.