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Cell cycle
Landes Bioscience
Cell cycle

Landes Bioscience

1538-4101

Cell cycle/Journal Cell cycleSCIISTP
正式出版
收录年代

    From Alpha to Beta - a co-translational way to fold?

    Komar, Anton A.
    4页
    查看更多>>摘要：Protein folding in the cell is largely a co-translational process occurring during protein synthesis on the ribosome. It has become evident that co-translational folding is characteristic to almost every protein in the cell of pro- and eukaryotic origin that are single and multidomain, single and multisubunit, cytosolic, secretory and membrane. Co-translational protein folding begins very early during the process of polypeptide chain synthesis on the ribosome, with some secondary structure elements forming inside the ribosomal tunnel and some tertiary structures forming inside the vestibule (lower/wider) region of the ribosomal exit tunnel. However, many details of co-translational folding remains incompletely understood. New data show that folding of a beta-barrel protein begins with formation of an alpha-helix inside the ribosome that rearranges into a beta-hairpin structure as the growing peptide reaches the wider/vestibule region of the exit tunnel. While it was previously suggested that such scenario can take place on the ribosome, the new data provide the first experimental evidence in support of this notion.
      原文链接:
    • NSTL
    • Taylor & Francis

    A long non-coding RNA H19/microRNA-138/TLR3 network is involved in high phosphorus-mediated vascular calcification and chronic kidney disease

    Liu, QiangQi, HuimengYao, Li
    17页
    查看更多>>摘要：Vascular calcification, characterized by the accumulation of calcium-phosphate crystals in blood vessels, is a major cause of cardiovascular complications and chronic kidney disease (CKD)-related death. This work focuses on the molecules involved in high-phosphorus-mediated vascular calcification in CKD. A rat model of CKD was established by 5/6 nephrectomy, and the rats were given normal phosphorus diet (NPD) or high phosphorus diet (HPD). HPD decreased kidney function, increased the concentration of calcium ion and damaged vascular structure in the thoracic aorta of diseased rats. A high phosphorus condition enhanced calcium deposition in vascular smooth muscle cells (VSMCs). High phosphorus also increased the expression of RUNX2 whereas reduced the expression of alpha-SM actin in the aortic tissues and VSMCs. Long non-coding RNA (lncRNA) H19 was upregulated in the aortic tissues after HPD treatment. H19 bound to microRNA (miR)-138 to block its inhibitory effect on TLR3 mRNA and activated the NF-kappa B signaling pathway. Downregulation of H19 or TLR3 alleviated, whereas downregulation of miR-138 aggravated the calcification and vascular damage in model rats and VSMCs. In conclusion, this study demonstrates that the H19/miR-138/TLR3 axis is involved in high phosphorus-mediated vascular calcification in rats with CKD.
      原文链接:
    • NSTL
    • Taylor & Francis

    Expression status and prognostic value of autophagy-related lncRNAs in prostate cancer

    Chen, GuoQin, XiaopingWang, YuGao, Biyun...
    13页
    查看更多>>摘要：LncRNAs involve in the autophagy to regulate prostate cancer (PCA) initiation and progression. Therefore, it urges to explore more significant AR-lncRNAs in PCa. mRNA data and clinical information of PCa were achieved from TCGA database, and ARGs were obtained from the HADb. AR-lncRNAs were identified by correlation analysis of DE ARGs and lncRNAs. Univariate Cox regression, LASSO regression, and multivariate Cox regression were used to identify the prognostic AR-lncRNA signature and constructed a risk model. GESA was used to biological function analysis between high- and low-risk score group. A nomogram was constructed and used to predicate the survival of PCa patients. A calibration curve was used to determine the accuracy of the predication model. AR-related ceRNA network was constructed by correlation analysis. Expression of six AR-related lncRNAs were detected by qRT-PCR. 222 ARGs and 385 AR-lncRNAs were screened from PCa and normal tissues, and 17 AR-lncRNAs were identified as prognostic signature for PCa. Based on the expression of prognostic signature, a risk score was calculated, and PCa samples were distributed into high- and low-risk score groups. The biological function and predicated value of the prognostic signature were also examined. Finally, based on the correlation between each ARG and its prognostic signature, three modules of AR-lncRNA-miRNA-mRNA regulatory networks were constructed based on 6 AR-lncRNAs, 17 miRNAs, and 12 ARGs. And we found that AC012085.2, UBXN10-AS1, LINC00261 downregulated, whereas AP004608.1, AC104667.2, AC008610.1 upregulated in PCa compared with BPH tissues. Our finding supplied the potential AR-lncRNAs prognostic signature for PCa.
      原文链接:
    • NSTL
    • Taylor & Francis

    Suppression of CX3CL1 by miR-497-5p inhibits cell growth and invasion through inactivating the ERK/AKT pathway in NSCLC cells

    Tang, WenJia, PingZuo, LinZhao, Jia...
    13页
    查看更多>>摘要：Non-small cell lung cancer (NSCLC) is the most common lung cancer with a highest mortality rate. MiR-497-5p has been reported as tumor suppressor in many cancers, but the role and mechanism of miR-497-5p in regulating NSCLC progression are still largely unknown in vitro and in vivo. Here, miR-497-5p was significantly downregulated in human NSCLC tissues and cell lines, compared with matched adjacent tissues and normal lung epithelial cell line. Then, miR-497-5p mimic and inhibitor were, respectively, transfected into human NSCLC cells A549 and H460, CCK-8 assay, transwell assay, and flow cytometry were used to detect the capacities of cell proliferation, invasion and apoptosis. MiR-497-5p negatively regulated proliferation and invasion of NSCLC cancer cells. MiR-497-5p was demonstrated to directly bound to 3'-UTR of CX3CL1 mRNA and post-transcriptionally suppressed its expression thus inactivating its downstream oncogenic pathway ERK/AKT. Moreover, transfection with short hairpin RNA (shRNA) against CX3CL1 decreased capacity of cell proliferation and invasion and promoted cell apoptosis in NSCLC cells. In addition, ERK inhibitor U0126 attenuated the promotion effect of miR-497-5p inhibitor on activation of ERK/AKT and cell proliferation and migration. Finally, overexpression of miR-497-5p substantially suppressed activation of the ERK/AKT pathway and tumor growth in tumor-bearing mice in vivo. Taken together, our findings showed that miR-497-5p is downregulated in human NSCLC tissues and cell lines, and it inhibited tumor growth and cell invasion by targeting CX3CL1 gene to inactivate the ERK/AKT pathway in NSCLC cells.
      原文链接:
    • NSTL
    • Taylor & Francis

    ADAMTS9-AS2 regulates PPP1R12B by adsorbing miR-196b-5p and affects cell cycle-related signaling pathways inhibiting the malignant process of esophageal cancer

    Chen, ZhaoTang, WeijianYe, WeiwenSong, Lijiang...
    16页
    查看更多>>摘要：This study explored the mechanism that ADAMTS9-AS2/miR-196b-5p/PPP1R12B/cell cycle pathway axis in inhibiting the malignant progression of esophageal cancer (EC), providing a new idea for targeted molecular therapy of EC. The expression data of EC tissue were acquired from TCGA database. The target lncRNA, downstream miRNA and its target gene were determined by bioinformatics analysis. ADAMTS9-AS2, miR-196b-5p and PPP1R12B levels in EC tissue and cells were assayed through qRT-PCR. Western blot was applied to assess protein level of PPP1R12B in cells and tissues, as well as protein expression of CDK1, cyclin A2, cyclin B1 and Plk1 in EC cells. Cell proliferation was assayed via CCK-8 assay. Cell cycle distribution was analyzed by flow cytometry. Cell migratory and invasive abilities were measured through scratch healing and transwell assays. Pearson correlation analysis was utilized to analyze relationship among ADAMTS9-AS2, miR-196b-5p and PPP1R12B. RIP was introduced to assess binding among the three. Dual-luciferase assay was utilized to verify targeted binding sites. The tumor formation in nude mice assay was utilized to detect tumorigenesis of EC cells in vivo. ADAMTS9-AS2 was significantly lowly expressed while miR-196b-5p was increased in EC tissue and cells. ADAMTS9-AS2 bound to miR-196b-5p and constrained its expression. Overexpressed ADAMTS9-AS2 inhibited EC cell malignant progression via downregulating miR-196b-5p, while overexpressed miR-196b-5p reversed this inhibitory effect. ADAMTS9-AS2 modulated PPP1R12B level by competitively inhibiting miR-196b-5p. PPP1R12B played a modulatory role in EC by inhibiting cell cycle pathway. Overexpressed ADAMTS9-AS2 regulated the tumor-forming ability of EC cells in vivo through miR-196b-5p/PPP1R12B/cell cycle signaling pathway axis. ADAMTS9-AS2 downregulated PPP1R12B by adsorbing miR-196b-5p, so as to regulate the cell cycle signaling pathway to inhibit EC malignant progression.
      原文链接:
    • NSTL
    • Taylor & Francis

    Beta-carotene regulates the biological activity of EGF in IEC6 cells by alleviating the inflammatory process

    Wang GuoxiaYang YuZhang, ShuaiLan Hainan...
    14页
    查看更多>>摘要：Epidermal growth factor (EGF) has many important biological functions. It plays an important role in regulating the growth, survival, migration, apoptosis, proliferation, and differentiation of intestinal tissues and cells. However, until now, the effect of inflammation on the biological activity of EGF in intestinal cells or tissues is still unclear. For this reason, in the current research, we have conducted a detailed study on this issue. Using the rat small intestinal crypt epithelial cell line (IEC6) was used as an in vitro model, and Confocal laser scanning microscope (CLSM), Flow cytometry (FCM), Indirect immunofluorescence assay (IFA), Western-blotting (WB), and Quantitative real-time RT-PCR (QRT-PCR) methods were used to explore the effects of inflammation on EGF/EGFR biological activity and signal transduction profiles. We found that the EGF/EGFR nuclear signal almost disappeared in the inflammatory state, and the phosphorylation levels of EGFR, AKT, and STAT3 were all significantly down-regulated. In addition, we also studied the effect of beta-carotene on the biological activity of EGF, and found that when cells were pretreated with beta-carotene, the cellular behavior, biological activity, and nuclear signal of EGF/EGFR under inflammation stimulation were partially restored. In summary, the current study shows that inflammation can disrupt EGF/EGFR-mediated signaling in IEC6 cells, suggesting that inflammation negatively regulates the biological activity of EGF/EGFR. Furthermore, we found that beta-carotene not only attenuated lipopolysaccharide (LPS)-induced inflammation but also partially restored the biological activity of EGF in IEC6 cells, laying a solid foundation for studying the biological functions of EGF and beta-carotene.
      原文链接:
    • NSTL
    • Taylor & Francis

    CBX3 regulated by miR-139 promotes the development of HCC by regulating cell cycle progression

    Zhang, PanYang, XiaoyanZha, ZhongmingZhu, Yumeng...
    13页
    查看更多>>摘要：Hepatocellular carcinoma (HCC), a major primary liver cancer, is one of the most lethal malignancies worldwide. Increasing evidence has demonstrated that chromobox protein homolog 3 (CBX3) functions as an oncogene in different cancers. However, its expression profiles and biological functions in HCC remain unknown. Data on CBX3 expression in HCC acquired from the GEO and TCGA databases were analyzed. The biological functions of CBX3 in HCC were examined by in vitro experiments. Bioinformatics analysis, qRT-PCR and western blotting were performed to explore the mechanism of CBX3 in HCC. CBX3 mRNA was upregulated in HCC tissues, and overexpression of CBX3 mRNA was negatively correlated with malignancies and poor prognosis in HCC patients. CBX3 knockdown decreased growth, migration and invasion of HCC cells in vitro. Moreover, bioinformatics analysis and experimental observation indicated that CBX3 expression was correlated with cell cycle regulatory proteins in HCC cells. Finally, starBase predicted that miR-139 could directly target CBX3 in HCC. Confirmatory experiments verified that miR-139 overexpression attenuated HCC cell proliferation and migration, and these effects could be reversed by overexpressing CBX3. Our results showed that the miR-139/CBX3 axis may be involved in HCC development by regulating cell cycle progression and may be a promising target in the treatment of HCC.
      原文链接:
    • NSTL
    • Taylor & Francis

    An innovative systematic approach introduced the involved lncRNA-miR-mRNA network in cell cycle and proliferation after conventional treatments in breast cancer patients

    Mohsenikia, MaryamKhalighfard, SolmazAlizadeh, Ali MohammadKhori, Vahid...
    22页
    查看更多>>摘要：The present study aimed to explore the involved lncRNA-miRNA-mRNA network in the cell cycle and proliferation after conventional treatments in Luminal A breast cancer patients.The candidate miRNAs (miRs), lncRNAs, and mRNAs were first taken from the Gene Expression Omnibus and TCGA databases. The lncRNA-miR-mRNA network was then constructed using the high-throughput sequencing data. The expression levels of selected targets were measured in the breast cancer and healthy samples by the Real-Time PCR technique and compared with the clinical outcomes by the Kaplan-Meier method.Our analysis revealed a group of differentially expressed 3 lncRNAs, 9 miRs, and 14 mRNAs in breast cancer patients. A significant expression decrease of the selected tumor suppressor lncRNAs, miRs, and genes and a substantial expression increase of the selected onco-lncRNAs, oncomiRs, and oncogenes were obtained in the patients compared to the healthy group. The plasma levels of the lncRNAs, miRs, and mRNAs were more significant after the operation, chemotherapy, and radiotherapy than the pre-treatment. The Kaplan-Meier analysis indicated that the patients with a high expression of miR-21, miR-20b, IGF1R, and E2F2 and a low expression of miR-125a, PDCD4, and PTEN had exhibited a shorter overall survival rate.Our results suggested that the underlying mechanisms of the lncRNA, miRs, and mRNAs and relevant signaling pathways may be considered predictive and therapeutic targets for breast cancer.
      原文链接:
    • NSTL
    • Taylor & Francis

    In vitro experimental study on the formation of microRNA-34a loaded exosomes and their inhibitory effect in oral squamous cell carcinoma

    Deng, WeiMeng, YingWang, BinWang, Chen-Xing...
    9页
    查看更多>>摘要：Studies have shown the inhibitory effect of microRNA-34a on proliferation, migration, and invasion of oral squamous cell carcinoma. However, the lack of a safe and effective delivery system limits the clinical application of microRNA-34a in oral cancer treatment. An exosome is a small extracellular vesicle that mediates intercellular communication by delivering proteins, nucleic acids, and other contents, and functions as a natural drug delivery carrier. Here, we aimed to explore whether exosomes could be used to load microRNA-34a via co-incubation and further used to treat OSCC. Ultracentrifugation was used to obtain exosomes derived from HEK293T cells and the extracted exosomes were analyzed via transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and Western blotting. Subsequently, we loaded cholesterol-modified microRNA-34a into HEK293T cell exosomes by co-incubation. Then, PKH67 and Cy3 co-labeled exo-microRNA-34a were co-incubated with HN6 cells and exosome entry into the HN6 cells was observed using a confocal laser scanning microscope. The cell proliferation, migration, and invasion were assessed by CCK-8 and Transwell assay analysis. SATB2 expression in HN6 cells was analyzed via western blotting. In this study, cholesterol-modified microRNA-34a was loaded into exosomes of HEK293T cells by co-incubation. The microRNA-34a-loaded exosomes were secreted from HEK293T cells and were absorbed by HN6 oral squamous carcinoma cells. Further, microRNA-34a-loaded exosomes led to a significant inhibition of HN6 cell proliferation, migration, and invasion by down regulating SATB2 expression. These results report a new delivery method for microRNA-34a, providing a new approach for the treatment of oral cancer.
      原文链接:
    • NSTL
    • Taylor & Francis