Proto-Oncogene and Onco-Suppressor Gene Expression
Enrique Pimentel in Handbook of Growth Factors, 2017
The use of specific inhibitors may contribute to elucidation of the mechanisms of regulation of gene expression by growth factors and other extracellular stimuli. The application of the protein synthesis inhibitor cycloheximide in serum-stimulated human and murine cells suggests that an unstable protein is involved in modulating the expression of cell cycle-associated genes,540 including the expression of c-fos and c-myc.535 The effects of the protein kinase inhibitor, 2-aminopurine, suggest that a protein kinase may be involved in serum-stimulated c-fos and c-myc expression as well as in the induction of the IFN-β gene by viruses or synthetic double-stranded RNAs.541 The use of the protein synthesis inhibitor anisomycin indicates that the regulatory mechanisms of c-fos and c-myc gene expression induced by growth factors may be different in different types of cells.163 Thus, there are multiple levels and mechanisms through which c-fos and c-myc gene expression is regulated.
Paradoxical Sleep (ps) Factors
Shojiro Inoué in Biology of Sleep Substances, 2020
Drucker-Colín et al.24 also reported the enhancement of PS during the first 3-h period following rat GH administration (0.1 to 1 mg/kg i.p.) in rats. It was further noted that PS reduction induced by anisomycin, a protein synthesis inhibitor, was blocked by the concurrent administration of GH.
Cytotoxic Phenanthridone Alkaloid Constituents of the Amaryllidaceae
Spyridon E. Kintzios, Maria G. Barberaki, Evangelia A. Flampouri in Plants That Fight Cancer, 2019
Following sustained interest on the interaction of Amaryllidaceae alkaloids with eukaryote ribosomes, Carrasco et al. (1975) showed that narciclasine inhibited protein synthesis in rabbit reticulocytes and yeast cell-free systems by blocking peptide bond formation at the ribosome level, similar to the known inhibitors anisomycin and trichodermin. It was also reported that resistance to narciclasine by the mutant TR 1 strain of Saccharomyces cerevisiae, which is anisomycin and trichodermin resistant, is due to an alteration on the peptidyl transferase center of the 60S ribosomal unit (Jimenez et al. 1975a). Interestingly narciclasine (11) and haemanthamine (64), an α-crinane alkaloid of the Amaryllidaceae, shared a common binding site on the peptidyl transferase center of the 60S ribosomal unit that was different from the other Amaryllidaceae alkaloids lycorine (3) and pseudolycorine (65) (Figure 3.1) (Jimenez et al. 1975b). Later on evidence revealed that the alkaloids lycorine (3), haemanthamine (64), pseudolycorine (65), and dihydrolycorine (66) were able to interfere with the binding of [3H]narciclasine to yeast ribosomes suggesting that there was an overlap of their respective binding sites (Baez and Vazquez 1978). At growth inhibitory concentrations narciclasine (11) also blocked protein synthesis in S180 ascites tumors and stabilized HeLa cell polysomes in vivo, indicating that it is capable of halting protein synthesis in eukaryote cells by inhibiting peptide bond formation (Jimenez et al. 1976). Studies by Rodriguez-Fonseca et al. (1995) were directed at the ribosomal binding sites of known peptidyl transferase inhibitors including several antibiotics (such as anisomycin and chloramphenicol amongst others) as well as narciclasine (11). These compounds exhibited varying degrees of specificity for bacterial, archaeal, and eukaryotic ribosomes despite a high level of conservation in the sequence and secondary structure of the peptidyl transferase center of the 23S-like rRNAs (Rodriguez-Fonseca et al. 1995). Binding experiments revealed that these entities were capable of effecting changes to the nucleotides at the peptidyl transferase center, which ranged from one or two changes (in anthelmycin and narciclasine) to eight or nine (virginiamycin M1), from which it was inferred that they were capable of inducing and stabilizing a particular functional conformer of the peptidyl transferase center (Rodriguez-Fonseca et al. 1995).
Tanshinone IIA inhibits osteosarcoma growth through modulation of AMPK-Nrf2 signaling pathway
Published in Journal of Receptors and Signal Transduction, 2020
Zengjun Xie, Binbin He, Ziyun Jiang, Liang Zhao
There are many drugs have been investigated to regulate the viability of osteosarcoma. For example, marrubenol inhibits osteosarcoma cancer growth through inducing autophagic cell death [38,39]. Anisomycin is able to induce cycle arrest and apoptosis through regulation of mitochondrial biogenesis in osteosarcoma [40]. Icarisid II has been found to regulate cancer proliferation in human osteosarcoma [41]. In addition, osteosarcoma cell energy metabolism and invasion capacity are also under the control of gambogic acid [42]. Similar to these results, this study explored the influence of Tan IIA on osteosarcoma viability, migration, and proliferation. Our study not only observed the proapoptotic effect of Tan IIA on osteosarcoma but also confirmed the anti-invasion effect of Tan IIA. These results indicate that cancer biological features of osteosarcoma could be comprehensive regulated by Tan IIA. In fact, several previous studies have reported the antitumor actions of Tan IIA. For example, cervical cancer glucose metabolism is controlled by Tan IIA [43]. Gastric cancer proliferation and tumor growth are inhibited by Tan IIA [44]. The chemosensitivity of nonsmall-cell lung cancer could be enhanced by Tan IIA [45]. The oncogene expression of liver cancer is affected by Tan IIA [4]. Colorectal cancer viability and mitochondrial performance are modulated by Tan IIA [46]. Similar to the previous studies, our results add more information about the anticancer impacts of Tan IIA. However, more animal studies or clinical trials are required to support our finding.
Small interfering LncRNA-TUG1 (siTUG1) decreases ketamine-induced neurotoxicity in rat hippocampal neurons
Published in International Journal of Neuroscience, 2019
Chunni Cao, Yanxiang Zhang, Zuofu Zhang, Qi Chen
Hippocampal neurons-treated KET had a lower expression of Bcl-2, compared to Con group, by contrast, it had higher cleaved-caspase-3 and p-p38 levels (Figure 3A–E). siTUG1 group had the lowest ratio of p-p38 to p38 and cleaved-caspase-3 level among all groups. Besides, siTUG1 group had the highest Bcl-2 level. The levels of Bcl-2, cleaved-caspase-3 and p-p38 in siTUG1 + KET group were somewhere between those in KET group and siTUG1 group (Figure 3A–E). Anisomycin can activate the p38 [24]. In Figure 4, hippocampal neurons-treated anisomycin decreased viability. Besides, siTUG1 + Anisomycin group decreased cell viability, compared to siTUG1 group. In addition, siTUG1 + KET + Anisomycin group (siTUG1, KET and Anisomycin treated neurons) decreased cell viability, compared to siTUG1 group and KET group. Significant changes were identified between combination group and two single drug groups (p < 0.05, p < 0.01).
The Role of C-Jun N-terminal Kinase-1 in Controlling Aquaporin-1 and Choroidal Thickness during Recovery from Form-deprivation Myopia in Guinea Pigs
Published in Current Eye Research, 2021
Wei Chen, Zhiwei Li, Qimiao Wang, Yan Wang, Yue Zhang
The animals wore the face mask for 21 days to induce myopia. Then, the face masks were removed, and the guinea pigs were re-exposed to the normal visual environment. Ninety-six guinea pigs were divided into four groups: the recovery group (REC, n = 24), the REC plus SP600125 group (REC-SP, n = 24), the REC plus anisomycin group (REC-AN, n = 24) and the REC plus dimethyl sulfoxide (DMSO) group (vehicle) (REC-DM, n = 24). SP600125 (Abcam, Cambridge, MA, USA) and anisomycin (Abcam, Cambridge, MA, USA) were injected into the REC-SP group and the REC-AN group, respectively, with the same concentration and volume (0.2 nmol, 0.01 ml). SP600125, which is an inhibitor of JNK, and anisomycin, which is an agonist of JNK, were both dissolved in DMSO and diluted with PBS to their final concentrations. In the REC-DM group, the form-deprived eyes were injected with sterilized DMSO solution (0.01 ml, diluted with PBS), which is the carrier. All intravitreal injections were performed once using a microinjector (Shanghai Meter Glass Factory, Shanghai, China) with a 30-gauge needle at 1.5 mm posterior to the temporal limbus under anesthesia with 95 mg/kg pentobarbital (intraperitoneal injection) when the face masks were removed. In the REC group, the guinea pigs were raised without any injection after the face mask was removed. Moreover, the normal control group (NC) included 32 guinea pigs that were free of form deprivation and were left untreated.
Related Knowledge Centers
- Antibiotic
- DNA Replication
- Enzyme Inhibitor
- Peptidyl Transferase
- Ribosome
- Signal Transduction
- Streptomyces Halstedii
- Translation
- Mitogen-Activated Protein Kinase
- Psychiatric Medication