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Biochemical and biophysical research communication...Biochemical and biophysical research communications 14건

  1. [해외논문]   FOXP4-AS1 participates in the development and progression of osteosarcoma by downregulating LATS1 via binding to LSD1 and EZH2  

    Yang, Lei (Department of Orthopedic Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China ) , Ge, Dawei (Department of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China ) , Chen, Xi (Department of Orthopedic Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China ) , Qiu, Junjun (Department of Orthopedic Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China ) , Yin, Zhaowei (Department of Orthopedic Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China ) , Zheng, Shengnai (Department of Orthopedic Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China ) , Jiang, Chunzhi (Department of Orthopedic Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China)
    Biochemical and biophysical research communications v.502 no.4 ,pp. 493 - 500 , 2018 , 0006-291x ,

    초록

    Abstract Osteosarcoma (OS) is the most common malignant bone tumor in children and adolescents. LncRNA has been confirmed to participate in a variety of cancers. The purpose of this study was to explore the effect of FOXP4-AS1 on the development of osteosarcoma (OS) and its underlying mechanism. FOXP4-AS1 expressions in 60 OS tissues and paracancerous tissues were detected by qRT-PCR (quantitative real-time polymerase chain reaction). We confirmed that FOXP4-AS1 was overexpressed in OS tissues than that of paracancerous tissues. The disease-free survival and overall survival of OS patients were not correlated with age, gender and tumor location, but remarkably correlated with FOXP4-AS1 expression, tumor size and lung metastasis. For in vitro experiments, MG63 cells expressed a higher expression of FOXP4-AS1, whereas U2OS cells expressed a lower expression, which were selected for the following studies. Overexpressed FOXP4-AS1 led to enhanced proliferation, migration and invasion, shortened G0/G1 phase, as well as inhibited cell cycle. Knockdown of FOXP4-AS1 in MG63 cells obtained the opposite results. Furthermore, RIP assay indicated that FOXP4-AS1 could inhibit LATS1 expression by binding to LSD1 and EZH2, so as to participate in OS development. In conclusion, these results revealed that FOXP4-AS1 is overexpressed in OS, and is the independent risk factor in OS prognosis. Upregulated FOXP4-AS1 promotes the proliferation, migration and cell cycle, but inhibits apoptosis of OS cells. Furthermore, FOXP4-AS1 participates in the development and progression of OS by downregulating LATS1 via binding to LSD1 and EZH2. Highlights We first confirmed that FOXP4-AS1 is overexpressed in OS, and is the independent risk factor in OS prognosis. We further clarified that Upregulated FOXP4-AS1 promotes the proliferation, migration and cell cycle, but inhibits apoptosis of OS cells. Finally, we demonstrated that FOXP4-AS1 participates in the development and progression of OS by downregulating LATS1.

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  2. [해외논문]   Alternative translation initiation from two in-frame start codons in DHX33 gene  

    Wang, Jiuling (Department of Biology, Southern University of Science and Technology, Shenzhen, Guangdong, China ) , Yuan, Zhen (Bioimaging Core, Faculty of Health Sciences, University of Macau, Macau, China ) , Zhang, Yandong (Department of Biology, Southern University of Science and Technology, Shenzhen, Guangdong, China)
    Biochemical and biophysical research communications v.502 no.4 ,pp. 501 - 507 , 2018 , 0006-291x ,

    초록

    Abstract DHX33 has been shown to play key roles in promoting cell proliferation. We have previously found that DHX33 protein is a doublet. In this report, we discovered that DHX33 doublet is due to alternative translation initiation by two in-frame initiation codons. This is supported by studies from both cell lines and mouse models. DHX33 translation initiation from either AUG codon happens at equal efficiency. Short DHX33 protein has similar cellular location and functions with full-length DHX33. Our results suggest that leaky scanning normally occur in DHX33 mRNA translation, which may serve as a safeguard mechanism to ensure optimal DHX33 translation efficiency. This is the first report of DEAD/DEAH box proteins that can be regulated by alternative translation initiation. Highlights DHX33 can be translated via leaky scanning. The isoforms of DHX33 via leaky scanning have similar localization and functions. Leaky scanning of DHX33 is conserved in human and in mouse.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  3. [해외논문]   HIF involvement in the regulation of rat Sertoli cell proliferation by FSH  

    Gorga, Agostina (Corresponding author.) , Rindone, Gustavo , Regueira, Mariana , Riera, Marí , a Fernanda , Pellizzari, Eliana Herminia , Cigorraga, Selva Beatriz , Meroni, Silvina Beatriz , Galardo, Marí , a Noel
    Biochemical and biophysical research communications v.502 no.4 ,pp. 508 - 514 , 2018 , 0006-291x ,

    초록

    Abstract The final number of Sertoli cells reached during the proliferative periods determines sperm production capacity in adulthood. It is well known that FSH increases the rate of proliferation of Sertoli cells; however, little is known about the transcription factors that are activated by the hormone in order to regulate Sertoli cell proliferation. On the other hand, Hypoxia Inducible Factors (HIFs) are master regulators of cell growth. HIFs are dimers of HIF-β and HIF-α subunits. Considering that HIF-β is constitutively expressed, HIF transcriptional activity is regulated through the abundance of HIF-α subunits. To date, three HIF-α isoforms have been described. The association of the different HIF-α subunits with HIF-β subunit constitutes three active transcription factors —HIF-1, HIF-2 and HIF-3— which interact with consensus hypoxia-response elements in the promoter region of target genes. Hypoxia has been classically considered the main stimulus that increases HIF transcriptional activity, however, regulation by hormones under normoxic conditions was also demonstrated. The aim of this work has been to investigate whether HIFs participate in the regulation of rat Sertoli cell proliferation by FSH. Sertoli cells obtained from 8-day old rats were cultured in the absence or presence of FSH. It has been observed that FSH increases HIF transcriptional activity and HIF-2α mRNA levels without modifying either HIF-1α or HIF-3α expression. Incubations with FSH have been also performed in the absence or presence of a pharmacological agent that promotes HIF-α subunit degradation, LW6. It has been observed that LW6 inhibits the FSH effect on proliferation, CCND1 expression and c-Myc transcriptional activity. Altogether, these results suggest that HIFs might be involved in the regulation of Sertoli cell proliferation by FSH. Highlights FSH increases HIF transcriptional activity in immature Sertoli cells. FSH upregulates CCND1 expression in a HIF-dependent manner. FSH upregulates c-Myc transcriptional activity in a HIF-dependent manner. HIFs might be involved in the regulation of Sertoli cell proliferation by FSH.

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  4. [해외논문]   Exosomal miR-93 promotes proliferation and invasion in hepatocellular carcinoma by directly inhibiting TIMP2/TP53INP1/CDKN1A  

    Xue, Xiaofeng (Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China ) , Wang, Xiaona (Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China ) , Zhao, Yubin (College of Life Sciences, Shanxi Normal University, Xi'an, China ) , Hu, Rongkuan (Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, University of Science & Technology of China, Hefei, China ) , Qin, Lei (Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China)
    Biochemical and biophysical research communications v.502 no.4 ,pp. 515 - 521 , 2018 , 0006-291x ,

    초록

    Abstract Hepatocellular carcinoma (HCC) is a malignant cancer worldwide; lacking biomarkers for early prognostication contributes to its high lethality. Herein, we report a novel biomarker, exosome delivered miR-93, is up-regulated in HCC cell line media and serum samples of HCC patients. We measured the proliferation and invasion ability of HCC cell lines following exosomal miR-93 treatment. After prediction with online algorithms, we further confirmed that TP53INP1, TIMP2 and CDKN1A are direct targets of miR-93 by dual-luciferase reporter assay. In addition, the diagnostic value of exosomal miR-93 was evaluated by qPCR and ROC analysis. The significant correlation between serum exosomal miR-93 and clinical information including stage, tumor size were observed. Furthermore, the survival differences of HCC patients with high or low miR-93 were statistically significant using Kaplan-Meier analysis. In summary, our work identified exosomal miR-93 as a novel biomarker for both diagnosis and prognosis in HCC. Highlights Exosomal miR-93 is up-regulated both in HCC cell lines' media and HCC patients' serum. Exosomal miR-93 promotes HCC proliferation and invasion by regulating TIMP2/TP53INP1/CDKN1A. Exosomal miR-93 is correlated with clinical information including stage, tumor size and predict patients' survival rate.

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