The function of miR-543 was abolished by Numb, as shown in rescue experiments. Moreover, miR-543 was verified to promote CSC properties, whereas Numb elicited the opposite effects. MiR-543 also influenced the expression of several stem-like factors, including Dll4, NF-κB, c-myc, and Oct-4, and the Numb/p53 signaling pathway. Taken together, these results demonstrate that miR-543 plays an oncogenic role by negatively controlling Numb, revealing the existence of an miR-543/Numb/p53 regulatory pathway in PCa tumorigenesis and development.Oxaliplatin (OXA), as a third-generation platinum anticancer drug, is a treatment drug for gastric cancer (GC). However, OXA resistance has become the main reason for OXA treatment failure. Serine beta-lactamase-like protein (LACTB), acts as a mitochondrial protein, can affect multiple cancer processes. Here, we aimed to investigate the function and mechanism of LACTB in OXA-resistant GC. After LACTB overexpression or autophagy activator (RAPA) treatment, cell proliferation, reactive oxygen species (ROS), apoptosis, mitochondrial dysfunction were evaluated through CCK-8 assay, Edu staining, flow cytometry and immunofluorescence assay. Moreover, DNA double-stranded damage and autophagy-related proteins were examined via western blot. We revealed that LACTB was downregulated in OXA-resistant MGC-803 cells, and overexpression of LACTB reduced the resistance of GC cells to OXA. Besides, our results uncovered that overexpression of LACTB induced apoptosis, reduced the mitochondrial membrane potential (MMP) and accelerated ROS accumulation in OXA-resistant MGC-803 (MGC-803/OXA) cells. Meanwhile, we verified that overexpression of LACTB decreased glucose uptake and ATP synthesis, induced mitochondria and DNA damages, and inhibited autophagy of MGC-803/OXA cells. Furthermore, our results certified that RAPA could weaken the function of LACTB on apoptosis and mitochondrial morphology and function in OXA-resistant MGC-803 cells with OXA treatment. Therefore, we demonstrated that LACTB could attenuate the resistance of MGC-803/OXA cells to OXA through autophagy-mediated mitochondrial morphological changes, mitochondrial dysfunction, and apoptosis, suggesting that LACTB, functions as a suppressor, is conducive to the therapy of OXA-resistant GC.Increasing evidence suggests that the long non-coding RNAs (lncRNAs) participate in the development and progression of breast cancer. The lncRNA small nucleolar RNA host gene 3 (SNHG3) reportedly acts as an oncogene in hepatocellular carcinoma and colorectal cancer; however, little is known about the biological function and oncogenic mechanisms of SNHG3 in breast cancer. We demonstrated that the expression of SNHG3 was abnormally high in breast cancer tissues and cells, and transgenic expression of SNHG3 promoted the proliferation, migration, and invasion of breast cancer cell lines (MCF-7 and MDA-MB-231). The mean volume of the xenografts from the SNHG3-knockdown MCF-7 cells was lower than that of the control tumor cells. Moreover, the expression of zinc finger E-box binding homeobox 1 (ZEB1) increased after SNHG3 overexpression and vice versa. Overexpression of ZEB1 triggered cellular migration and invasion behaviors. Analysis of the mechanism underlying these effects suggested that SNHG3 is an effective sink for miR-186-5p and modulates ZEB1 repression, conferring an additional level to its post-transcriptional regulation. In conclusion, SNHG3 promotes the migration and invasion of breast cancer cells through miR-186-5p/ZEB1 regulation and the induction of the epithelial to mesenchymal transition, indicating that SNHG3 is a potential treatment target for breast cancer.Post-surgery arthrofibrosis is one of the most restrictive factors in the development of intra-articular surgery and has presented tremendous obstacles for most orthopaedic surgeons. Tanshinone IIA (Tan IIA), a key active ingredient of Den-shen, has been used to treat fibrosis-related diseases, such as pulmonary, hepatic and myocardial fibrosis. https://www.selleckchem.com/CDK.html In the present study, we aimed to investigate the effects of Tan IIA on post-surgery arthrofibrosis in vivo and in vitro. Histological analysis indicated that topical application of Tan IIA (10 mg/mL) could significantly alleviate postsurgery arthrofibrosis in rabbits. Immunohistochemistry results showed that proliferating cell nuclear antigen (PCNA) and tubulin protein expression was inhibited, whereas LC3 was activated in vivo. In vitro, EdU and flow cytometry assays demonstrated that Tan IIA could inhibit fibroblast proliferation by arresting cells in G2 phase. Scratch, Transwell and cytoskeleton protein immunofluorescence assays revealed that fibroblast migration was attenuated. Interestingly, LC3 immunofluorescence staining and transmission electron microscopy indicated that autophagy flux could be induced in fibroblasts by Tan IIA. However, the inhibitory effects of Tan IIA against fibroblast proliferation and migration were partially restored when fibroblast autophagy was suppressed after combined treatment with the autophagy inhibitor 3-methyladenine (3-MA). Finally, the expression of p-mTOR was suppressed in a dose-dependent manner after Tan IIA treatment but partially restored when Tan IIA treatment was combined with 3-MA intervention. The inhibitory effect of Tan IIA against fibroblast proliferation and migration may be related to autophagy induction mediated by the PI3K and AMPK-mTOR signaling pathway.This study was designed to investigate the effects of the aging process on peripheral and central auditory functions in adults with normal hearing. In this study, 149 participants with normal hearing were divided into four groups aged 20-29, 30-39, 40-49 and 50-59 years for statistical purposes. Electrocochleography (EcochG), transient evoked otoacoustic emissions (TEOAE), Mandarin Hearing in Noise Test (MHINT) and the Gap Detection Test (GDT) were used. Our study found (1) MHINT is significantly associated with aging (left ear R2=0.29, right ear R2=0.35). (2) TEOAE amplitude, TEOAE contralateral acoustic stimulation (CS) amplitude, EcochG action potential (AP), EcochG AP latency, EcochG summating potential (SP) and GDT progressively declined with age. (3) The EcochG SP/AP has no statistically significant difference among different age groups. (4) The peripheral auditory function of the right ear declines more slowly than that of the left ear. (5) Hypofunction of the central auditory system accelerates after age 40.