Journal of Receptors and Signal Transduction最新文献

{"title":"Pulsatilla saponin E suppresses viability, migration, invasion and promotes apoptosis of NSCLC cells through negatively regulating Akt/FASN pathway <i>via</i> inhibition of flotillin-2 in lipid raft.","authors":"Minghua Zhu,&nbsp;Wei Shi,&nbsp;Ke Chen,&nbsp;Huiqun Hu,&nbsp;Xiangqing Ye,&nbsp;Yinfang Jiang","doi":"10.1080/10799893.2020.1839764","DOIUrl":"https://doi.org/10.1080/10799893.2020.1839764","url":null,"abstract":"<p><strong>Purpose: </strong>Pulsatilla saponins from <i>pulsatilla chinensis (Bunge) Regel</i> have potential anti-tumor activities to certain human cancers. However, the roles of pulsatilla saponin E separated from pulsatilla saponins in non-small cell lung cancer (NSCLC) have not been reported.</p><p><strong>Materials and methods: </strong>After treating NSCLC cells by pulsatilla saponin E at different concentrations, cell viability was measured by MTT and CCK-8 assays, and cell migration, invasion and apoptosis were detected by scratch wound-healing, transwell and flow cytometry assays. The contents of free cholesterol (FC) and total cholesterol (TC) were measured by high performance liquid chromatography (HPLC). The expression levels of flotillin-1, flotillin-2, Akt, fatty acid synthase (FASN) were detected by qRT-PCR and Western blot assays.</p><p><strong>Results: </strong>Pulsatilla saponin E suppressed viability, migration, invasion and promoted apoptosis of NSCLC cells followed by regulation of apoptosis-related proteins, reduced contents of FC and TC, and the expression levels of flotillin-1, flotillin-2, Akt, and FASN in a concentration-dependent manner. However, the inhibitory effects of pulsatilla saponin E on viability, migration, invasion of A549 cells and the expression levels of flotillin-1, flotillin-2, Akt, and FASN were reversed by flotillin-2 overexpression.</p><p><strong>Conclusions: </strong>Our study revealed that pulsatilla saponin E suppressed migration, invasion and promoted apoptosis of NSCLC cells through negatively regulating Akt/FASN signaling pathway <i>via</i> the inhibition of flotillin-2 in lipid raft (LR). The current findings could be explored for developing a novel therapeutic drug for NSCLC treatment.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"23-33"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1839764","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38647341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergistic effects of BKM120 and panobinostat on pre-B acute lymphoblastic cells: an emerging perspective for the simultaneous inhibition of PI3K and HDACs.","authors":"Mahdieh Mehrpouri,&nbsp;Majid Momeny,&nbsp;Davood Bashash","doi":"10.1080/10799893.2020.1853159","DOIUrl":"https://doi.org/10.1080/10799893.2020.1853159","url":null,"abstract":"<p><p>The reputation of conventional treatment in acute lymphoblastic leukemia (ALL) has recently been questioned due to the considerable increment in the number of relapsed patients. The remarkable role of histone deacetylase (HDAC) enzymes in induction of chemo-resistance has provided an opportunity for HDAC inhibitors to be used as a treatment strategy in ALL; however, the compensatory activation of oncogenic pathways may negatively affect their promising effects. In the present study, we found an attenuating effect for PI3K axis on the anti-leukemic effects of panobinostat in pre-B ALL-derived Nalm-6 cells, as the harnessing of this pathway using BKM120 or CAL-101 resulted in a significant reduction in the number of viable cells as well as the metabolic activity. Moreover, we found the altered expression of p21, p27, c-Myc, and CDK4 upon co-treatment of the cells with panobinostat and BKM120, which was associated with a substantial blockage of cell cycle progression at G2/M phase. The companionship of the PI3K inhibitor with HDAC inhibitor also potentiated panobinostat-induced apoptotic cell death and enhanced the mRNA of Foxo3a and Foxo4. Conclusively, this study sheds light on the adjuvantive effects of BKM120 on panobinostat efficacy and outlined that the simultaneous inhibition of PI3K and HDACs may be a promising therapeutic approach to improve the cure rates of ALL.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"100-108"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1853159","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38897361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-noncoding RNA LINC00461 promotes proliferation and invasion of nonsmall cell lung cancer cells via targeting miR-518a-3p/WDR1 pathway.","authors":"Zuopei Wang,&nbsp;Yi Lu,&nbsp;Bo Sheng,&nbsp;Yi Ding,&nbsp;Xiaoke Cheng","doi":"10.1080/10799893.2020.1850786","DOIUrl":"https://doi.org/10.1080/10799893.2020.1850786","url":null,"abstract":"<p><p>Long noncoding RNAs (lncRNAs) are a class of RNAs participating in many biological processes such as imprinting, alternative splicing and RNA decay. Recently, lncRNAs have drawn a great deal of attention for their critical role in cancer progression. LINC00461, a newly identified lncRNA, has been reported to be significantly overexpressed in breast cancer and markedly expedited breast cancer progression. However, the specific role of LINC00461 in nonsmall cell lung cancer (NSCLC) remains unknown. In this study, we for the first time showed the biological functions of LINC00461 in NSCLC. Our results demonstrated that LINC00461 was significantly up-regulated in NSCLC tissues and cell lines. Furthermore, knockdown of LINC00461 inhibited NSCLC cell proliferation and invasion <i>in vitro</i> as well as suppressed tumor growth and metastasis <i>in vivo</i>. We also performed luciferase reporter assays and found that LINC00461 functioned as a sponge for miR-518a-3p and WDR1 was a target of miR-518a-3p. Taken together, we suggested an essential role of LINC00461/miR-518a-3p/WDR1 axis in NSCLC, which could be used as a potential therapeutic target for NSCLC treatment.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"80-87"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1850786","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38648520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aloperine protects human retinal pigment epithelial cells against hydrogen peroxide-induced oxidative stress and apoptosis through activation of Nrf2/HO-1 pathway.","authors":"Junhui Zhang,&nbsp;Haitao Zhou,&nbsp;Juanli Chen,&nbsp;Xiaoyan Lv,&nbsp;Hongsong Liu","doi":"10.1080/10799893.2020.1850787","DOIUrl":"https://doi.org/10.1080/10799893.2020.1850787","url":null,"abstract":"<p><p>Age-related macular degeneration (AMD) is a complex multifactorial disease associated with the dysfunction of retinal pigment epithelium (RPE). Aloperine is a quinolizidine alkaloid that has been proven to possess broad pharmacological activities. However, the effects of aloperine on AMD remain unclear. In the present study, we used hydrogen peroxide (H₂O₂) to induce oxidative injury in human RPE cells (ARPE-19 cells). ARPE-19 cells were pretreated with different concentrations of aloperine for 2 h, followed by H₂O₂ exposure. Cell cytotoxicity was determined using lactate dehydrogenase (LDH) release assay. Cell viability was measured using Cell Counting Kit-8 (CCK-8) assay. The reactive oxygen species (ROS) generation, malondialdehyde (MDA) level, superoxide dismutase (SOD) activity and glutathione peroxidase (GSH-PX) activity were detected to reflect oxidative status. Western blot was performed to detect the expressions of bcl-2, bax, nuclear factor-erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1). The activity of caspase-3 was also assessed to indicate cell apoptosis. In addition, ARPE-19 cells were transfected with siNrf2 to knock down Nrf2. Our results showed that pretreatment with aloperine elevated the reduced cell viability of H₂O₂-induced ARPE-19 cells in a dose-dependent manner. Aloperine greatly decreased the production of ROS and MDA, and increased the activities of SOD and GSH-PX in H₂O₂-stimulated ARPE-19 cells. H₂O₂-caused a decrease in bcl-2 expression and increases in bax expression and caspase-3 activity were mitigated by aloperine. Moreover, aloperine treatment enhanced the expression levels of Nrf2 in nuclear fraction and the HO-1 expression in lysates. Knockdown of Nrf2 reversed the protective effects of aloperine on H₂O₂-induced ARPE-19 cells. In conclusion, these findings demonstrated that aloperine protected ARPE-19 cells from H₂O₂-induced oxidative stress and apoptosis in part <i>via</i> activating the Nrf2/HO-1 signaling pathway. The findings suggested a therapeutic potential of aloperine for the treatment of ADM.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"88-94"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1850787","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38657064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Safflor yellow A protects vascular endothelial cells from ox-LDL-mediated damage.","authors":"Hu Zhang,&nbsp;Li-Juan Fan,&nbsp;Jun Liu,&nbsp;Jia-Qi Zhu,&nbsp;Ting-Ting Tan,&nbsp;Ming Li,&nbsp;You-Li Zhou","doi":"10.1080/10799893.2020.1843492","DOIUrl":"https://doi.org/10.1080/10799893.2020.1843492","url":null,"abstract":"<p><p>Atherosclerosis is a chronic disease of arteries, which constitutes the pathological basis of a series of cardiovascular diseases. The inflammatory response of vascular endothelial cells mediated by oxidized low density lipoprotein (ox-LDL) is the early behavior and main signal of atherosclerosis. In this study, the damage model of vascular endothelial cells treated with ox-LDL was used to reproduce the damage process of vascular endothelial cells in the process of atherosclerosis. Cell viability was detected by CCK-8. The release levels of reactive oxygen species, nitric oxide, and superoxide dismutase (SOD) were detected by commercial kits. EdU cell proliferation assay was used to detect cell proliferation, real-time fluorescent quantitative PCR and Western blot were used to detect the expression level of related genes. The results showed we successfully constructed a vascular endothelial injury model by incubating vascular endothelial cells with gradient concentrations of ox-LDL. The incubation of safflor yellow A (SYA) partially restored the loss of viability of vascular endothelial cells mediated by ox-LDL, and SYA could promote the proliferation of injured vascular endothelial cells. In addition, SYA may transmit related signals through the AMPK pathway to protect vascular endothelial cells from ox-LDL-mediated damage. All these results provide a further understanding of the occurrence and development of atherosclerosis, provide a theoretical basis for the use of SYA-related drugs in the treatment of cardiovascular diseases, and provide a reference paradigm for studying the pharmacology, toxicology, and mechanism of action of key active substances in TCM.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"52-59"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1843492","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38590564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of Sirt1/PGC1α pathway attenuates neuroinflammation injury in Parkinson's disease.","authors":"Yang Yang,&nbsp;Zhongying Gong,&nbsp;Zhiyun Wang,&nbsp;Yi Lu","doi":"10.1080/10799893.2020.1843494","DOIUrl":"https://doi.org/10.1080/10799893.2020.1843494","url":null,"abstract":"<p><p>Parkinson's disease is a brain disorder that is featured by shaking palsy, which affect the motor system. The pathogenesis of Parkinson's disease has been ascribed to neurodegenerative disorder, neural oxidative stress, neuroinflammation, and neurotransmitter disorder. In the present study, we explored the influence of Sirt1/PGC1α pathway in regulating BV-2 cells viability under TNFα treatment. Our results demonstrated that the activity of Sirt1/PGC1α pathway was significantly downregulated in response to TNFα treatment. Reactivation of Sirt1/PGC1α pathway through supplementation of SRT1720 significantly elevated the viability of BV-2 cells under an <i>in vitro</i> neuroinflammation model. Therefore, our results report a novel signaling pathway responsible for the survival of neuron under neuroinflammation. Re-activation of Sirt1/PGC1α pathway may be a potential therapeutic approach for the treatment of Parkinson's disease through enhancing neuronal viability.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"67-70"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1843494","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38589885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liothyronine could block the programmed death-ligand 1 (PDL1) activity: an e-Pharmacophore modeling and virtual screening study.","authors":"Navid Pourzardosht,&nbsp;Zahra Sadat Hashemi,&nbsp;Maysam Mard-Soltani,&nbsp;Abolfazl Jahangiri,&nbsp;Mohammad Reza Rahbar,&nbsp;Alireza Zakeri,&nbsp;Ebrahim Mirzajani,&nbsp;Saeed Khalili","doi":"10.1080/10799893.2020.1839765","DOIUrl":"https://doi.org/10.1080/10799893.2020.1839765","url":null,"abstract":"<p><strong>Purpose: </strong>The interaction between PD-L1 on tumor cells and the programmed death 1 (PD1) on immune cells helps them to escape the immune system elimination. Therefore, developing therapeutic agents to block this interaction has garnered a lot of attention as a therapeutic approach. In the present study, we have tried to screen for an inhibitory compound to inhibit the interaction between the PD1/PD-L1 molecules.</p><p><strong>Methods: </strong>In this regard, the structure of PD-L1 and its inhibitor were prepared and employed to generate an e-Pharmacophore model. A library of approved compounds was prepared and toxicity analysis using Absorption, Distribution, Metabolism, Excretion, and Toxicity (ADMET) predictor was performed. The built e-Pharmacophore model was validated and used to screen the prepared compound library. Ligand docking and binding energy calculation were performed on the screened ligands.</p><p><strong>Results: </strong>A seven-feature e-Pharmacophore model was generated using the PD-L1 complex. All of the compounds within the library passed the ADMET criteria. Performing the virtual screening, only 79 compounds have survived the criteria to fit four pharmacophoric features. The compound with the highest binding energy was the liothyronine (T3).</p><p><strong>Conclusion: </strong>The ability of T3 in PD1/PD-L1 checkpoint blockade along with its potential in T4 reduction could be a desirable combination in cancer treatment. These abilities of T3 could be used to restore the ability of the immune system to eliminate tumor cells.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"34-42"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1839765","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38525209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Formononetin inhibits inflammation and promotes gastric mucosal angiogenesis in gastric ulcer rats through regulating NF-κB signaling pathway.","authors":"Lanjie Yi,&nbsp;Yan Lu,&nbsp;Shun Yu,&nbsp;Qian Cheng,&nbsp;Lanjuan Yi","doi":"10.1080/10799893.2020.1837873","DOIUrl":"https://doi.org/10.1080/10799893.2020.1837873","url":null,"abstract":"<p><p>To investigate the effects of formononetin on rats with gastric ulcer and further to explore its possible mechanism. Rats were randomly divided into sham operation group (Sham), model group (Model), omeprazole control group (Omeprazole) and formononetin in different dose groups (FOR-L, FOR-M, FOR-H). Rats model with gastric ulcer were established by 100% glacial acetic acid. Hematoxylin-eosin (H&E) staining was used to observe the pathological morphology of gastric mucosa. Immunohistochemistry and enzyme-linked immunosorbent assay (ELISA) were used to detect the level of inflammatory and angiogenesis related factors. The expressions of nuclear factor kappa-B (NF-κB) signaling pathway-related proteins were detected by western blot. Formononetin and omeprazole could ameliorate the pathological morphology of gastric mucosa in gastric ulcer rats. Compared with Model group, the levels of tumor necrosis factor (TNF)-α, Interleukin (IL)-1β, IL-6, myeloperoxidase (MPO), human endothelin (ET)-1 and p-P65 protein in formononetin treatment and omeprazole groups were significantly decreased (<i>p</i> < 0.05). Moreover, formononetin could increase the content of vascular endothelial growth factor (VEGF), nitric oxide (NO) and the levels of CD34, tight junction proteins (ZO-1 and occludin) and p-IκBα in a dose-dependent manner. Formononetin can ameliorate gastric ulcer in rats by inhibiting inflammation and promoting gastric mucosal angiogenesis, and its mechanism maybe related to NF-κB signaling pathway.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"16-22"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1837873","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38525586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transmembrane protein 88 inhibits transforming growth factor-β1-induced-extracellular matrix accumulation and epithelial-mesenchymal transition program in human pleural mesothelial cells through modulating TGF-β1/Smad pathway.","authors":"Zhongmin Sun,&nbsp;Qian Ning,&nbsp;Hong Li,&nbsp;Tinghua Hu,&nbsp;Ling Tang,&nbsp;Qing Wen,&nbsp;Liangrong Shen","doi":"10.1080/10799893.2020.1843493","DOIUrl":"https://doi.org/10.1080/10799893.2020.1843493","url":null,"abstract":"<p><p>Pleural fibrosis is an irreversible pathological process occurred in the development of several lung diseases. TMEM88 is a member of transmembrane (TMEM) family and has been found to be involved in the regulation of fibrogenesis. However, the role of TMEM88 in pleural fibrosis remains unknown. In this study, we aimed to explore the role of TMEM88 in pleural fibrosis <i>in vitro</i> using transforming growth factor-β1 (TGF-β1)-induced human pleural mesothelial cell line MeT-5A cells. Our results showed that the expression levels of TMEM88 were downregulated in pleural fibrosis tissues and TGF-β1-treated Met-5A cells. Overexpression of TMEM88 inhibited the proliferation of Met-5A cells under TGF-β1 stimulation. In addition, TMEM88 overexpression prevented TGF-β1-induced extracellular matrix (ECM) accumulation and epithelial-mesenchymal transition (EMT) in Met-5A cells with decreased expression levels of Col I and fibronectin, increased levels of cytokeratin-8 and E-cadherin, as well as decreased levels of vimentin and α-SMA. Furthermore, overexpression of TMEM88 inhibited the expression of TGF-β receptor I (TβRI) and TβRII and suppressed the phosphorylation of Smad2 and Smad3 in Met-5A cells. In conclusion, these results indicated that TMEM88 exhibited an anti-fibrotic activity in pleural fibrosis <i>via</i> inhibiting the activation of TGF-β1/Smad signaling pathway.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"60-66"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1843493","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38678584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The stimulative function of long noncoding RNA CDKN2B-AS1 in osteosarcoma by targeting the microRNA-122/CCNG1 axis.","authors":"Abulaiti Abula,&nbsp;Guliayixiamu Saimaiti,&nbsp;Xayimardan Maimaiti,&nbsp;Wumitijiang Wuqikun,&nbsp;Alimujiang Abulaiti,&nbsp;Peng Ren,&nbsp;Aihemaitijiang Yusufu","doi":"10.1080/10799893.2020.1850784","DOIUrl":"https://doi.org/10.1080/10799893.2020.1850784","url":null,"abstract":"<p><p>Osteosarcoma (OS), a prevalent aggressive malignancy in the bone, has limited therapeutic targets and diagnostic biomarkers. In the current investigation, RT-qPCR showed that CDKN2B-AS1 was enhanced in OS samples and cells. This research was set to examine the modulation of CDKN2B-AS1 in OS. The expression of CDKN2B-AS1 and downstream molecules was analyzed by RT-qPCR method. CCK8, EdU staining along with Transwell assays were applied to evaluate cell proliferation and invasion. Those <i>in vitro</i> investigations specified that silencing of CDKN2B-AS1 with shRNAs obviously impeded the proliferation and invasion of MG63 cells. To authenticate the relationships between CDKN2B-AS1 and microRNA-122-5p (miR-122-5p) or cyclin G1 (CCNG1) and miR-122-5p, we next employed luciferase reporter assay. We displayed that CDKN2B-AS1 repressed miR-122-5p to restore CCNG1 expression. All in all, our findings substantiated the indispensable function of CDKN2B-AS1 in OS progression and the possible molecular mechanism.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"71-79"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1850784","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38341969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}