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Propofol Inhibits HeLa Cells by Impairing Autophagic Flux via AMP-Activated Protein Kinase (AMPK) Activation and Endoplasmic Reticulum Stress Regulated by Calcium.

BACKGROUND Propofol has antitumor effects against various cancers. However, the mechanism of action of propofol in HeLa human cervical cancer cells has not been elucidated. MATERIAL AND METHODS We treated HeLa human cervical cancer cells with different concentrations of propofol. Cell viability was evaluated with Cell Counting Kit-8 and apoptosis was analyzed by annexin V-fluorescein isothiocyanate and propidium iodide staining and flow cytometry. Autophagosome formation was evaluated based on microtubule-associated protein light chain (LC)3 conversion and light chain 3 puncta formation. Autophagosome clearance was assessed according to p62 protein level and autolysosome generation. RESULTS We found that propofol decreased cell viability and increased autophagosome generation in HeLa cells. Autophagosome formation was evaluated based on LC3 conversion and LC3 puncta formation. Autophagosome clearance was assessed according to p62 protein level. The AMPK/mTOR signaling pathway was found to be activated in propofol-induced autophagosome accumulation. Fluorescence analysis using LysoTracker dye revealed that propofol blocked autophagosome-lysosome fusion. Administration of rapamycin increased autophagosome clearance in propofol-treated HeLa cells. Additionally, propofol induced endoplasmic reticulum (ER) stress and disrupted intracellular Ca2+ balance, thereby enhancing autophagosome accumulation. Suppressing ER stress by treatment with tauroursodeoxycholic acid (TUDCA) enhanced these effects, suggesting that the cytotoxicity of propofol is related to induction of ER stress. CONCLUSIONS This study is the first to provide evidence that propofol-mediated autophagy regulation is an underlying part of the mechanism by which propofol regulates HeLa cells progression.

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Chrysin suppresses proliferation, migration, and invasion in glioblastoma cell lines via mediating the ERK/Nrf2 signaling pathway.

Chrysin, an active natural bioflavonoid, has been proven to protect against carcinogenesis. However, the role of chrysin in glioblastoma and the potential molecular mechanisms remain to be elucidated. In our previous study, we found that nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) is highly expressed in a variety of glioblastoma cell lines associated with the mitogen-activated protein kinase (MAPK) pathway. The aim of this study was to evaluate the antitumor effects of chrysin in glioblastoma cells and how chrysin is related to the MAPK/Nrf2 signaling pathway.

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High glucose downregulates the effects of autophagy on osteoclastogenesis via the AMPK/mTOR/ULK1 pathway.

Diabetes is a chronic disease that disrupts the balance between bone formation and bone desorption, which can lead to osteoporosis, increasing the risk of fracture. However, compared with osteoblasts, the biological effects of hyperglycemia on osteoclastogenesis remain to be elucidated. Therefore, we investigated the impact of glucose at different concentrations (5.5, 10.5, 15.5, 20.5, 25.5, and 30.5 mM) on osteoclastogenesis using RAW264.7 cells. Cell proliferation was measured with the cell counting kit-8 assay, and osteoclastogenesis was detected with tartrate-resistant acid phosphatase staining and bone resorption assays, as well as protein cathepsin K expression. Compound C, the AMP-activated protein kinase (AMPK) pathway inhibitor, was used to examine the relationship between the AMPK/mTOR/ULK1 signaling pathway and autophagy in osteoclasts. Autophagy was evaluated with transmission electron microscopy and immunofluorescence microscopy and associated proteins were detected with western blotting. The pharmacological autophagic reagents bafilomycin A1, 3-methyladenine, and rapamycin were used to determine the effect of autophagy on osteoclastogenesis. Our results showed that glucose negatively affected osteoclast formation and function but did not affect the proliferation of RAW264.7 cells. Suppression of the AMPK/mTOR/ULK1 signaling axis decreased autophagy in glucose-mediated osteoclast. Furthmore, High levels of glucose decreased autophagy level in osteoclasts. Additionally, interfering with autophagy affected osteoclast formation and function. These findings clarify the mechanisms underlying the effects of glucose-mediated osteoclastogenesis and will help identify novel therapeutic strategies for the protection of skeletal health in diabetic osteoporosis.

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Comprehensive molecular screening by next generation sequencing reveals a distinctive mutational profile of / genes and novel genomic alterations: results from a 20-year cohort of patients with GIST from north-western Greece.

Gastrointestinal stromal tumours (GIST) are mesenchymal neoplasms that usually carry an activating mutation in or platelet-derived growth factor receptor alpha () genes with predictive and prognostic significance. We investigated the extended mutational status of GIST in a patient population of north-western Greece in order to look at geopraphic/genotypic distinctive traits.

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MicroRNA-30b promotes lipopolysaccharide-induced inflammatory injury and alleviates autophagy through JNK and NF-κB pathways in HK-2 cells.

Acute kidney injury (AKI) is an abrupt loss of kidney function. MicroRNA-30b (miR-30b) has been reported to be involved in the inflammatory reaction of a variety of diseases. However, the role of miR-30b in AKI remains unknown. In this research, we aimed to investigate the role of miR-30b in lipopolysaccharide (LPS)-induced kindey inflammatory injury in vitro and in vivo.

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Expression profiling of c-kit and its impact after esiRNA silencing during gonadal development in catfish.

C-kit receptor is a member of a family of growth factor receptors that have tyrosine kinase activity, and are involved in the transduction of growth regulatory signals across plasma membrane by activation of its ligand, kitl/scf. The present study analysed mRNA and protein expression profiles of c-kit in the gonads of catfish, Clarias gariepinus, using real time PCR, in situ hybridization and immunohistochemistry. Tissue distribution analysis revealed higher expression mainly in the catfish gonads. Ontogeny studies showed minimal expression during early developmental stages and highest during 50-75 days post hatch, and the dimorphic expression in gonads decreased gradually till adulthood, which might suggest an important role for this gene around later stages of sex differentiation and gonadal development. Expression of C-kit was analysed at various phases of gonadal cycle in both male and female, which showed minimal expression during the resting phase, and higher expression in male compared to females during the pre-spawning phase. In vitro and in vivo induction using human chorionic gonadotropin elevated the expression of c-kit indicating the regulatory influence of hypothalamo-hypophyseal axis. In vivo transient gene silencing using c-kit-esiRNA in adult catfish during gonadal recrudescence showed a decrease in c-kit expression, which affected the expression level of germ cell meiotic marker sycp3, as well as several factors and steroidogenic enzyme genes involved in germ cell development. Decrease in the levels of serum 11-KT and T were also observed after esiRNA silencing. The findings of this study suggest that c-kit has an important role in the process of germ cell proliferation, development and maturation during gonadal development and recrudescence in catfish.

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Acetyl-11-keto-β-boswellic acid extracted from promotes Schwann cell proliferation and sciatic nerve function recovery.

Frankincense can promote blood circulation. Acetyl-11-keto-β-boswellic acid (AKBA) is a small molecule with anti-inflammatory properties that is derived from Boswellia serrata. Here, we hypothesized that it may promote regeneration of injured sciatic nerve. To address this hypothesis, we established a rat model of sciatic nerve injury using a nerve clamping method. Rats were administered AKBA once every 2 days at doses of 1.5, 3, and 6 mg/kg by intraperitoneal injection for 30 days from the 1 day after injury. Sciatic nerve function was evaluated using the sciatic functional index. Degree of muscle atrophy was measured using the triceps surae muscle Cuadros index. Neuropathological changes were observed by hematoxylin-eosin staining. Western blot analysis was used to detect expression of phospho-extracellular signal-regulated kinase 1 and 2 (p-ERK1/2) in injured nerve. S100 immunoreactivity in injured nerve was detected by immunohistochemistry. In vivo experiments showed that 3 and 6 mg/kg AKBA significantly increased sciatic nerve index, Cuadros index of triceps muscle, p-ERK1/2 expression, and S100 immunoreactivity in injured sciatic nerve of sciatic nerve injury model rats. Furthermore, for in vitro experiments, Schwann cells were treated with AKBA at 0-20 μg/mL. Proliferation of Schwann cells was detected by Cell Counting Kit-8 colorimetry assay. The results showed that 2 μg/mL AKBA is the optimal therapeutic concentration. In addition, ERK phosphorylation levels increased following 2 μg/mL AKBA treatment. In the presence of the ERK1/2 inhibitor, PD98059 (2.5 μL/mL), the AKBA-induced increase in p-ERK1/2 protein expression was partially abrogated. In conclusion, our study shows that AKBA promotes peripheral nerve regeneration with ERK protein phosphorylation playing a key role in this process.

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Comparison of plasma ctDNA and tissue/cytology-based techniques for the detection of EGFR mutation status in advanced NSCLC: Spanish data subset from ASSESS.

The analysis of epidermal growth factor receptor (EGFR) mutations in many patients with advanced non-small-cell lung cancer (aNSCLC) has provided the opportunity for successful treatment with specific, targeted EGFR tyrosine kinase inhibitors. However, this therapeutic decision may be challenging when insufficient tumor tissue is available for EGFR mutation testing. Therefore, blood surrogate samples for EGFR mutation analysis have been suggested.

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TPX2 silencing mediated by joint action of microvesicles and ultrasonic radiation inhibits the migration and invasion of SKOV3 cells.

Ovarian cancer, with its high morbidity, has one of the highest mortality rates among gynecological malignant tumors. Overexpression of targeting protein for Xklp2 (TPX2) has been identified in numerous malignant tumors. The present study sought to determine whether TPX2 silencing inhibited the growth and metastasis of ovarian cancer cells, and whether microvesicles‑ and ultrasonic radiation‑mediated small interfering (si)RNA‑TPX2 transfection may improve the therapeutic effect. The SKOV3 cell line, derived from papillary serous cytadenocarcinoma of the human ovary, was selected as a cell model. Cells were divided into five groups: Control, siRNA‑TPX2, siRNA‑TPX2 + microvesicle (M), siRNA‑TPX2 + ultrasonic irradiation (UI), and siRNA‑TPX2 + M + UI. Cell viability was evaluated under the aforementioned conditions via the Cell Counting kit 8 (CCK8) assay. Cell migration and invasion were detected using Transwell assays. The expression levels of associated genes, including epithelial cadherin (E‑cadherin), metalloproteinase inhibitor 2 (TIMP‑2), metastasis associated 1 (MTA1) and matrix metallopeptidase 2 (MMP2), were analyzed using reverse transcription‑quantitative polymerase chain reaction analysis and western blotting. MMP2 activity was determined using a gelatin zymography assay. The results suggested that TPX2 serves an important role in the development of SKOV3 cells; it is additionally able to inhibit cell migration and invasion by upregulating E‑cadherin and TIMP2, downregulating MMP2 and MTA1, and inhibiting the phosphorylation of p38 and c‑Jun N‑terminal kinase. The inhibitory effect of siRNA‑TPX2 on SKOV3 cellular metastasis in the presence of microvesicles and ultrasonic radiation was observed to be improved compared with the control. It is proposed that the combination of microvesicles and ultrasonic radiation with TPX2 silencing has the potential to be an effective gene therapy against ovarian cancer.

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The mTOR Kinase Inhibitor CZ415 Inhibits Human Papillary Thyroid Carcinoma Cell Growth.

Mammalian target of rapamycin (mTOR) plays an important role in papillary thyroid carcinoma (PTC) cell progression. CZ415 is a novel, highly-efficient and specific mTOR kinase inhibitor. The current study tested the potential anti-tumor activity of CZ415 in human PTC cells.

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