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Glioblastoma is one of the most frequent malignant tumors derived from the brain in adults with very poor prognosis. Ferroptosis is implicated in the initiation and progression of various tumors, including the glioblastoma. The present study aims to investigate the function of microRNA (miR)-670-3p in glioblastoma, and tries to demonstrate whether ferroptosis is involved in this process. Human glioblastoma cell lines, U87MG and A172, were transfected with the inhibitor, mimic and matched negative controls of miR-670-3p to manipulate intracellular miR-670-3p level. To validate the involvement of ferroptosis in miR-670-3p inhibitor-mediated tumor suppressive effects, ferrostain-1 and liproxstatin-1 were used to inhibit ferroptosis in the presence of miR-670-3p inhibitor. In addition, the small interfering RNA against acyl-CoA synthase long chain family member 4 (ACSL4) was used to knock down endogenous ACSL4 expression. To validate the combined effects between miR-670-3p inhibitor and temozolomide (TMZ), cells were pretreated with TMZ and then transfected with or without miR-670-3p inhibitor. miR-670-3p level was elevated in human glioblastoma, but decreased upon ferroptotic stimulation. miR-670-3p inhibitor suppressed, while miR-670-3p mimic promoted glioblastoma cell growth through modulating ferroptosis. Mechanistically, ACSL4 was required for the regulation on ferroptosis and growth of glioblastoma cells by miR-670-3p. Moreover, U87MG and A172 cells treated with miR-670-3p inhibitor showed an increased chemosensitivity to TMZ. We prove that miR-670-3p suppresses ferroptosis of human glioblastoma cells through targeting ACSL4, and that inhibiting miR-670-3p can be an alternative, at least adjuvant strategy to treat glioblastoma. [ABSTRACT FROM AUTHOR]

A digital image correlation (DIC) method was used to obtain the full-field strain and crack propagation path for a rock-like specimen with a single prefabricated crack under uniaxial compression. Additionally, scanning electron microscopy (SEM) was used to scan the fracture surface of the specimen after compression. The macro-mechanical response of the loading process was found to be in accordance with the micro-mechanism obtained by SEM, which demonstrates that the DIC system is accurate and that the full-field strain is accordant with crack propagation. Thereafter, a strain criterion was proposed and was applied to the extending discrete element method to simulate crack propagation. The strain criterion was found to be appropriate for simulating the crack initiation stress, peak strength and crack growth morphology of the specimen. Moreover, both the numerical simulation and experimental results show that the specimen failure process had four typical stages - initiation, unstable propagation, stable propagation and failure. [ABSTRACT FROM AUTHOR]