BMC Molecular and Cell Biology最新文献

{"title":"Hyperoxia exposure upregulates Dvl-1 and activates Wnt/β-catenin signaling pathway in newborn rat lung.","authors":"Yuting Zhu,&nbsp;Yawen Li,&nbsp;Weilai Jin,&nbsp;Zhengying Li,&nbsp;Le Zhang,&nbsp;Yuanyuan Fang,&nbsp;Yanyu Zhang","doi":"10.1186/s12860-023-00465-6","DOIUrl":"https://doi.org/10.1186/s12860-023-00465-6","url":null,"abstract":"<p><strong>Background: </strong>Bronchopulmonary dysplasia is a serious and lifelong pulmonary disease in premature neonates that influences around one-quarter of premature newborns. The wingless-related integration site /β-catenin signaling pathway, which is abnormally activated in the lungs with pulmonary fibrosis, affects cell differentiation and lung development.</p><p><strong>Methods: </strong>Newborn rats were subjected to hyperoxia exposure. Histopathological changes to the lungs were evaluated through immunohistochemistry, and the activation of disheveled and Wnt /β-catenin signaling pathway components was assessed by Western blotting and real-time PCR. The abilities of proliferation, apoptosis and migration were detected by Cell Counting Kit-8, flow cytometry and scratch wound assay, respectively.</p><p><strong>Results: </strong>Contrasting with normoxic lungs, hyperoxia-exposed lungs demonstrated larger alveoli, fewer alveoli and thicker alveolar septa. Superoxide dismutase activity was significantly decreased (7th day: P < 0.05; 14th day: P < 0.01) and malondialdehyde significantly increased (7th day: P < 0.05; 14th day: P < 0.01) after hyperoxia exposure. Protein and mRNA expression levels of β-catenin, Dvl-1, CTNNBL1 and cyclin D1 were significantly upregulated by hyperoxia exposure on 7th day (P < 0.01) and 14th day (P < 0.01). In hyperoxic conditions, Dvl-l downregulation and Dvl-l downregulation + MSAB treatment significantly increased the proliferation rates, decreased the apoptosis rates and improved the ability of cell migration. In hyperoxic conditions, Dvl-l downregulation could decrease the mRNA expression levels of GSK3β, β-catenin, CTNNBL1 and cyclin D1 and decrease the protein relative expression levels of GSK3β, p-GSK3β, β-catenin, CTNNBL1 and cyclin D1.</p><p><strong>Conclusions: </strong>We confirmed the positive role of Dvl-1 and the Wnt/β-catenin signaling pathway in promoting BPD in hyperoxia conditions and provided a promising therapeutic target.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"4"},"PeriodicalIF":2.8,"publicationDate":"2023-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9893620/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10665522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ-ATL1 silencing reverses the activation effects of SIRT5 on smooth muscle cellular proliferation, migration and contractility in intracranial aneurysm by adsorbing miR-455.","authors":"Jichong Xu,&nbsp;Chun Fang","doi":"10.1186/s12860-022-00461-2","DOIUrl":"https://doi.org/10.1186/s12860-022-00461-2","url":null,"abstract":"<p><strong>Background: </strong>Alterations in vascular smooth muscle cells (VSMCs) contribute to the pathogenesis of intracranial aneurysms (IAs). However, molecular mechanisms underlying these changes remain unknown. The present study aimed to characterize the molecular mechanisms underlying VSMC-mediated IAs.</p><p><strong>Methods: </strong>Expression of the circular RNA circ-ATL1 and microRNA miR-455 was detected in IAs by RT-qPCR. Interactions between circ-ATL1, miR-455 and SIRT5 were examined by luciferase reporter analysis and RT-qPCR. The regulatory roles of circ-ATL1, miR-455 and SIRT5 in VSMC migration, proliferation and phenotypic modulation were also examined by CCK8, Transwell® migration and western blot assays.</p><p><strong>Results: </strong>Biochemical and bioinformatic techniques were used to demonstrate that circ-ATL1 and miR-455 participated in disparate biological processes relevant to aneurysm formation. Clinically, increased expression of circ-ATL1 and downregulated miR-455 expression were observed in IA patients compared with healthy subjects. Silencing of circ-ATL1 led to suppression of VSMC migration, proliferation and phenotypic modulation. Both SIRT5 and miR-455 were found to be downstream targets of circ-ATL1. SIRT5 upregulation or miR-455 inhibition reversed the inhibitory effects induced by circ-ATL1 silencing on VSMC proliferation, migration and phenotypic modulation. We found that VSMC phenotypic modulation by circ-ATL1 upregulation and miR-455 downregulation had a critical role in the development and formation of AIs. Specifically, circ-ATL1 downregulation reversed IA formation.</p><p><strong>Conclusion: </strong>Our data provide the theoretical basis for future studies on potential clinical treatment and prevention of IAs.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"3"},"PeriodicalIF":2.8,"publicationDate":"2023-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9887762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10639022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HMGB1 mediates lipopolysaccharide-induced macrophage autophagy and pyroptosis.","authors":"Jiawei Shang,&nbsp;Feng Zhao,&nbsp;Yongmei Cao,&nbsp;Feng Ping,&nbsp;Wei Wang,&nbsp;Yingchuan Li","doi":"10.1186/s12860-023-00464-7","DOIUrl":"https://doi.org/10.1186/s12860-023-00464-7","url":null,"abstract":"<p><p>Autophagy and pyroptosis of macrophages play important protective or detrimental roles in sepsis. However, the underlying mechanisms remain unclear. High mobility group box protein 1 (HMGB1) is associated with both pyroptosis and autophagy. lipopolysaccharide (LPS) is an important pathogenic factor involved in sepsis. Lentivirus-mediated HMGB1 shRNA was used to inhibit the expression of HMGB1. Macrophages were treated with acetylation inhibitor (AA) to suppress the translocation of HMGB1 from the nucleus to the cytosol. Autophagy and pyroptosis-related protein expressions were detected by Western blot. The levels of caspase-1 activity were detected and the rate of pyroptotic cells was detected by flow cytometry. LPS induced autophagy and pyroptosis of macrophages at different stages, and HMGB1 downregulation decreased LPS-induced autophagy and pyroptosis. Treatment with acetylation inhibitor (anacardic acid) significantly suppressed LPS-induced autophagy, an effect that was not reversed by exogenous HMGB1, suggesting that cytoplasmic HMGB1 mediates LPS-induced autophagy of macrophages. Anacardic acid or an anti-HMGB1 antibody inhibited LPS-induced pyroptosis of macrophages. HMGB1 alone induced pyroptosis of macrophages and this effect was inhibited by anti-HMGB1 antibody, suggesting that extracellular HMGB1 induces macrophage pyroptosis and mediates LPS-induced pyroptosis. In summary, HMGB1 plays different roles in mediating LPS-induced autophagy and triggering pyroptosis according to subcellular localization.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"2"},"PeriodicalIF":2.8,"publicationDate":"2023-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9854035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10573964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"N-Acetyl-L-cysteine facilitates tendon repair and promotes the tenogenic differentiation of tendon stem/progenitor cells by enhancing the integrin α5/β1/PI3K/AKT signaling.","authors":"Kang Lu,&nbsp;Mei Zhou,&nbsp;Liyuan Wang,&nbsp;Yang Wang,&nbsp;Hong Tang,&nbsp;Gang He,&nbsp;Huan Wang,&nbsp;Chuyue Tang,&nbsp;Jie He,&nbsp;Wei Wang,&nbsp;Kanglai Tang,&nbsp;Yunjiao Wang,&nbsp;Zhongliang Deng","doi":"10.1186/s12860-022-00463-0","DOIUrl":"https://doi.org/10.1186/s12860-022-00463-0","url":null,"abstract":"<p><strong>Background: </strong>Tendon injury is associated with oxidative stress, leading to reactive oxygen species (ROS) production and inflammation. N-acetyl-L-cysteine (NAC) is a potent antioxidant. However, how NAC affects the biological functions of tendon stem/progenitor cells (TSPCs) and tendon repair has not been clarified.  METHOD: The impacts of NAC on the viability, ROS production, and differentiation of TSPCs were determined with the cell counting kit-8, fluorescence staining, Western blotting, and immunofluorescence. The effect of NAC on gene transcription in TSPCs was analyzed by transcriptomes and bioinformatics and validated by Western blotting. The potential therapeutic effect of NAC on tendon repair was tested in a rat model of Achilles tendon injury.</p><p><strong>Results: </strong>Compared with the untreated control, treatment with 500 µM NAC greatly promoted the proliferation of TSPCs and significantly mitigated hydrogen peroxide-induced ROS production and cytotoxicity in vitro. NAC treatment significantly increased the relative protein expression of collagen type 1 alpha 1 (COL1A1), tenascin C (TNC), scleraxis (SCX), and tenomodulin (TNMD) in TPSCs. Bioinformatics analyses revealed that NAC modulated transcriptomes, particularly in the integrin-related phosphoinositide 3-kinase (PI3K)/AKT signaling, and Western blotting revealed that NAC enhanced integrin α5β1 expression and PI3K/AKT activation in TSPCs. Finally, NAC treatment mitigated the tendon injury, but enhanced the protein expression of SCX, TNC, TNMD, and COLIA1 in the injured tissue regions of the rats.</p><p><strong>Conclusion: </strong>NAC treatment promoted the survival and differentiation of TSPCs to facilitate tendon repair after tendon injury in rats. Thus, NAC may be valuable for the treatment of tendon injury.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"1"},"PeriodicalIF":2.8,"publicationDate":"2023-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10503606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The 3-O sulfation of heparan sulfate proteoglycans contributes to the cellular internalization of tau aggregates.","authors":"Andreia Ferreira,&nbsp;Ines Royaux,&nbsp;Jian Liu,&nbsp;Zhangjie Wang,&nbsp;Guowei Su,&nbsp;Diederik Moechars,&nbsp;Nico Callewaert,&nbsp;Louis De Muynck","doi":"10.1186/s12860-022-00462-1","DOIUrl":"10.1186/s12860-022-00462-1","url":null,"abstract":"<p><strong>Background: </strong>Considering the high correlation between the functional decline in Alzheimer's disease (AD) and the propagation of aggregated tau protein, many research efforts are focused on determining the underlying molecular mechanisms of tau spreading. Heparan sulfate proteoglycans (HSPGs) were reported to mediate cellular uptake of tau aggregates. Specifically, the heparan sulfates (HS) sulfation plays a critical role in the interaction of HSPGs with aggregated tau. HS can be N-/2-O/6-O- or 3-O-sulfated, some of which have been reported to take part in the interaction with tau aggregates. However, the role of the 3-O sulfation remains enigmatic.</p><p><strong>Results: </strong>Here, we studied the contribution of HS 3-O sulfation in the binding and cellular uptake of tau aggregates. We observed reduced tau aggregates uptake in absence of 3-O sulfation or when outcompeting available cellular 3-O sulfated HS (3S-HS) with antithrombin III. The lack of HS3ST1-generated HS products in the HS3ST1^-/- cells was further corroborated with an LC-MS/MS using ¹³C-labeled HS calibrants. Here, we showed that these functional changes can be explained by a higher affinity of aggregated tau to 3S-HS. When targeting tau aggregates with 3-O sulfation-containing HS, we observed an increase in inhibition of tau aggregates uptake.</p><p><strong>Conclusions: </strong>These data indicate that HS 3-O sulfation plays a role in the binding of tau aggregates and, thus, contributes to their cellular uptake, highlighting a potential target value to modulate tau pathogenesis.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"23 1","pages":"61"},"PeriodicalIF":2.8,"publicationDate":"2022-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9789671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9402802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"microRNA-338-3p suppresses lipopolysaccharide-induced inflammatory response in HK-2 cells.","authors":"Jing Wang,&nbsp;Guokai Li,&nbsp;Min Lin,&nbsp;Sheng Lin,&nbsp;Ling Wu","doi":"10.1186/s12860-022-00455-0","DOIUrl":"https://doi.org/10.1186/s12860-022-00455-0","url":null,"abstract":"<p><strong>Background: </strong>Inflammation is the most common cause of kidney damage, and inflammatory responses in a number of diseases are mediated by microRNA-338-3p (miR-338-3p). However, there are only a few reports which described the regulation of miR-338-3p in human proximal tubular cells. The goal of this study was to see how miR-338-3p affected lipopolysaccharide (LPS)-caused inflammatory response in HK-2 cells.</p><p><strong>Methods: </strong>LPS was used to construct an inflammatory model in HK-2 cells. miR-338-3p mimic was used to increase the levels of miR-338-3p in HK-2 cells. MTT, JC-1 staining, and apoptosis assays were used to detect cell viability, mitochondrial membrane potential (MMP), and apoptosis, respectively. The production of inflammatory factors and the levels of p38, p65, phospho-p65, phospho-p38, Bax, Bcl-2, cleaved caspase-9, and cleaved caspase-3 were investigated using real-time polymerase chain reaction, western blotting, or enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>The levels of miR-338-3p were significantly lower in serum from patients with sepsis-induced kidney injury compared to the serum from healthy volunteers (P < 0.05). LPS reduced the level of miR-338-3p in HK-2 cells (P < 0.05). HK-2 cell viability, mitochondrial membrane potential, and Bcl-2 mRNA and protein levels were decreased by LPS (all P < 0.05). Apoptosis, the mRNA and protein levels of inflammatory cytokines (IL-1β, IL-6, IL-8, and TNF-α) and Bax, and the levels of cleaved caspase-9 and caspase-3 were increased by LPS (all P < 0.05). Raising the level of miR-338-3p mitigated these effects of LPS (all P < 0.05).</p><p><strong>Conclusion: </strong>LPS-induced inflammation in HK-2 cells is reduced by miR-338-3p.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"23 1","pages":"60"},"PeriodicalIF":2.8,"publicationDate":"2022-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9789656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10495046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpression of lncRNA HOXA-AS2 promotes the progression of oral squamous cell carcinoma by mediating SNX5 expression.","authors":"Zhangyi Li","doi":"10.1186/s12860-022-00457-y","DOIUrl":"https://doi.org/10.1186/s12860-022-00457-y","url":null,"abstract":"<p><strong>Background: </strong>Oral squamous cell carcinoma (OSCC) is one of the most common head and neck cancers. Long non-coding RNA HOXA-AS2 (lncRNA HOXA-AS2) have been extensively studied in various cancers. However, the expression and function of HOXA-AS2 in OSCC still remain unknown. The aim of this study is to investigate the roles of HOXA-AS2 in OSCC.</p><p><strong>Methods: </strong>OSCC tissues and adjacent normal tissues were obtained from OSCC patients. RT-qPCR and Western blot assays were used to detect the expression of target genes in OSCC tissues or cells. Cells proliferation, migration and invasion were detected by CCK-8 and transwell assays, respectively. The target gene of HOXA-AS2 was confirmed by dual-luciferase reporter gene assay.</p><p><strong>Results: </strong>We found that HOXA-AS2 expression was remarkably upregulated in OSCC tissues and cell lines. The downregulation of HOXA-AS2 inhibited cells proliferation, migration and invasion. Our bioinformatics analysis found that HOXA-AS2 can target miR-520c-3p, which was confirmed by dual-luciferase reporter gene assay. The expression of HOXA-AS2 was found to be negatively associated with miR-520c-3p in OSCC tissues. Moreover, sorting nexin 5 (SNX5), a downstream target of miR-520c-3p, was inhibited by miR-520c-3p overexpression. SNX5 was also increased in OSCC tissues and cell lines. Additionally, we found that the higher expression of SNX5 was strongly associated with the tumor grade of OSCC patients in Oncomine database. Most importantly, the knockdown of HOXA-AS2 induced cells apoptosis by promoting autophagy by regulating SNX5.</p><p><strong>Conclusion: </strong>HOXA-AS2 served an oncogene and promoted OSCC progression via the miR-520c-3p/SNX5 axis. Thus, HOXA-AS2 may be a new biomarker for diagnosis and treatment of OSCC.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"23 1","pages":"59"},"PeriodicalIF":2.8,"publicationDate":"2022-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9759889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10484483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpressed cold inducible RNA-binding protein improves cell viability and EGF expression in glial cells.","authors":"Aijun Liu,&nbsp;Shouchun Li,&nbsp;Yongcheng Jiao,&nbsp;Haibo Kong,&nbsp;Zhiwen Zhang","doi":"10.1186/s12860-022-00460-3","DOIUrl":"https://doi.org/10.1186/s12860-022-00460-3","url":null,"abstract":"<p><strong>Background: </strong>Cold inducible RNA-binding protein (CIRP) is a key protein in the hypothermic therapy. Highly expressed CIRP exerts a neuroprotective effect on neurons. The aim of this study is to provide the evidence of the protective effects of CIRP on the glial cells and explore the downstream pathway of CIRP.</p><p><strong>Results: </strong>The results of this study demonstrated that the cell viability of the glial cells with CIRP overexpression was increased significantly compared to the control. With CIRP overexpression, the epidermal growth factor (EGF) mRNA expression was found increasing significantly and the mRNA expressions of derived neurotrophic factor (BDNF), bcl-2, vascular endothelial growth factor (VEGF) and nerve growth factor (NGF) were not upregulated compared to the control. EGF and CIRP co-expression was demonstrated on the glial cells. With CIRP expression, EGF expression on the glial cells was increased statistically compared to the control.</p><p><strong>Conclusion: </strong>CIRP overexpression increases the cell viability of the glial cells, exerting a neuroprotective effect. EGF expression is activated on the glial cells with CIRP overexpression, implying a pathway of CIRP neuroprotection via EGF activation.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"23 1","pages":"58"},"PeriodicalIF":2.8,"publicationDate":"2022-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9756664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10399672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CREB1 regulates KPNA2 by inhibiting mir-495-3p transcription to control melanoma progression : The role of the CREB1/miR-495-3p/KPNA2 axis in melanoma progression.","authors":"Xuerui Geng,&nbsp;Xiujuan Qiu,&nbsp;Jun Gao,&nbsp;Zhifan Gong,&nbsp;Xiaogang Zhou,&nbsp;Chunlei Liu,&nbsp;Haichao Luo","doi":"10.1186/s12860-022-00446-1","DOIUrl":"https://doi.org/10.1186/s12860-022-00446-1","url":null,"abstract":"<p><strong>Background: </strong>Melanoma is a common type of skin cancer, and its incidence is increasing gradually. Exploring melanoma pathogenesis helps to find new treatments.</p><p><strong>Objective: </strong>We aimed to explore the potential molecular mechanisms by which CREB1 regulates melanoma.</p><p><strong>Methods: </strong>TransmiR and ALGGEN were used to predict targets of CREB1 in the promoter of miR-495-3p or miR-495-3p and KPNA2, and a dual-luciferase reporter assay was performed to detect binding of CREB1 to these promoters. In addition, binding of CREB1 to the miR-495-3p promoter was confirmed by a ChIP assay. qRT‒PCR was carried out to detect mRNA levels of miR-495-3p, CREB1 and KPNA2. An EdU assay was conducted to detect cell viability. Transwell assays and flow cytometry were performed to assess cell migration and invasion and apoptosis, respectively. Moreover, factors associated with overall survival were analysed by using the Cox proportional hazards model.</p><p><strong>Results: </strong>Our results show miR-495-3p to be significantly decreased in melanoma. Additionally, miR-495-3p overexpression inhibited melanoma cell viability. CREB1 targeted miR-495-3p, and CREB1 overexpression enhanced melanoma cell viability by inhibiting miR-495-3p transcription. Moreover, miR-495-3p targeted KPNA2, and CREB1 regulated KPNA2 by inhibiting miR-495-3p transcription to enhance melanoma cell viability.</p><p><strong>Conclusion: </strong>CREB1 regulates KPNA2 by inhibiting miR-495-3p transcription to control melanoma progression. Our results indicate the molecular mechanism by which the CREB1/miR-495-3p/KPNA2 axis regulates melanoma progression.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"23 1","pages":"57"},"PeriodicalIF":2.8,"publicationDate":"2022-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9756468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10386979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic analysis of the regulatory mechanism of sugars on secondary flowering in Magnolia.","authors":"Lingjuan Xuan,&nbsp;Qianqian Wang,&nbsp;Zhigao Liu,&nbsp;Bin Xu,&nbsp;Shaoyu Cheng,&nbsp;Yingjia Zhang,&nbsp;Danying Lu,&nbsp;Bin Dong,&nbsp;Dongmei Zhang,&nbsp;Lang Zhang,&nbsp;Jingjing Ma,&nbsp;Yamei Shen","doi":"10.1186/s12860-022-00458-x","DOIUrl":"https://doi.org/10.1186/s12860-022-00458-x","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Magnolia, a traditional and important ornamental plant in urban greening, has been cultivated for about 2000 years in China for its elegant flower shape and gorgeous flower color. Most varieties of Magnolia bloom once a year in spring, whereas a few others, such as Magnolia liliiflora Desr. 'Hongyuanbao', also bloom for the second time in summer or early autumn. Such a twice flowering trait is desirable for its high ornamental value, while its underlying mechanism remains unclear.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Paraffin section was used to show the flowering time and phenotypic changes of M. liliiflora 'Hongyuanbao' during the twice flowering periods from March 28 to August 25, 2018. Gas chromatography-mass spectrometry (GC-MS) was then performed to explore the chemical metabolites through the twice flower bud differentiation process in 'Hongyuanbao', and the metabolites were screened and identified by orthogonal projection to latent structures discriminant analysis (OPLS-DA). Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis (KEGG) was used to reveal the relationship between the sugar metabolites and twice-flowering characteristic. To further investigate the potential role of sucrose and trehalose on flowering regulation of 'Hongyuanbao', the plants once finished the spring flowering were regularly sprayed with sucrose and trehalose solutions at 30 mM, 60 mM, and 90 mM concentrations from April 22, 2019. The flower bud differentiation processes of sprayed plants were observed and the expression patterns of the genes involved in sucrose and trehalose metabolic pathways were studied by quantitative reverse transcription PCR (qRT-PCR).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;It showed that 'Hongyuanbao' could complete flower bud differentiation twice in a year and flowered in both spring and summer. The metabolites of flower bud differentiation had a significant variation between the first and second flower buds. Compared to the first flower bud differentiation process, the metabolites in the sucrose and trehalose metabolic pathways were significantly up-regulated during the second flower bud differentiation process. Besides that, the expression levels of a number of trehalose-6-phosphate synthase (TPS) genes including MlTPS1, MlTPS5, MlTPS6, MlTPS7 and MlTPS9 were substantially increased in the second flower differentiation process compared with the first process. Exogenous treatments indicated that compared to the control plants (sprayed with water, CK), all three concentrations of trehalose could accelerate flowering and the effect of 60 mM concentration was the most significant. For the sucrose foliar spray, only the 60 mM concentration accelerated flowering compared with CK. It suggested that different concentration of trehalose and sucrose might have different effects. Expression analysis showed that sucrose treatment increased the transcription levels of MlTPS5 and MlTPS6, whereas trehalose treatmen","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"23 1","pages":"56"},"PeriodicalIF":2.8,"publicationDate":"2022-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9753265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10353914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}