Cell structure and function最新文献_第9页

Implication of a novel function of Sar1 in the nucleus. Sar1在细胞核中的新功能。

IF 1.5 4区生物学

Cell structure and function Pub Date : 2019-08-09 DOI: 10.1247/csf.19019

K. Horikawa, Tomohiro Yorimitsu, C. Kodera, Ken Sato

引用次数: 3

A Peptide Derived from Phosphoinositide 3-kinase Inhibits Endocytosis and Influenza Virus Infection. 磷酸肌肽3-激酶衍生肽抑制内吞作用和流感病毒感染。

IF 1.5 4区生物学

Cell structure and function Pub Date : 2019-04-25 Epub Date: 2019-03-21 DOI: 10.1247/csf.19001

Yoichiro Fujioka, Aya O Satoh, Kosui Horiuchi, Mari Fujioka, Kaori Tsutsumi, Junko Sasaki, Prabha Nepal, Sayaka Kashiwagi, Sarad Paudel, Shinya Nishide, Asuka Nanbo, Takehiko Sasaki, Yusuke Ohba

{"title":"A Peptide Derived from Phosphoinositide 3-kinase Inhibits Endocytosis and Influenza Virus Infection.","authors":"Yoichiro Fujioka, Aya O Satoh, Kosui Horiuchi, Mari Fujioka, Kaori Tsutsumi, Junko Sasaki, Prabha Nepal, Sayaka Kashiwagi, Sarad Paudel, Shinya Nishide, Asuka Nanbo, Takehiko Sasaki, Yusuke Ohba","doi":"10.1247/csf.19001","DOIUrl":"https://doi.org/10.1247/csf.19001","url":null,"abstract":"Endocytosis mediates the internalization and ingestion of a variety of endogenous or exogenous substances, including virus particles, under the control of intracellular signaling pathways. We have previously reported that the complex formed between the small GTPase Ras and phosphoinositide 3-kinase (PI3K) translocates from the plasma membrane to endosomes, signaling from which thereby regulates clathrin-independent endocytosis, endosome maturation, influenza virus internalization, and infection. However, the molecular mechanism by which the Ras-PI3K complex is recruited to endosomes remains unclear. Here, we have identified the amino acid sequence responsible for endosomal localization of the Ras-PI3K complex. PI3K lacking this sequence failed to translocate to endosomes, and expression of the peptide comprising this PI3K-derived sequence inhibited clathrin-independent endocytosis, influenza virus internalization, and infection. Moreover, treatment of cells with this peptide in an arginine-rich, cell-penetrating form successfully suppressed influenza virus infection in vitro and ex vivo, making this peptide a potential therapeutic agent against influenza virus infection.Key words: signal transduction, endocytosis, endosome, imaging, influenza virus.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":"44 1","pages":"61-74"},"PeriodicalIF":1.5,"publicationDate":"2019-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1247/csf.19001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37085971","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}

引用次数: 6

MiR-187-3p Enhances Propranolol Sensitivity of Hemangioma Stem Cells. MiR-187-3p增强血管瘤干细胞对心得安的敏感性。

IF 1.5 4区生物学

Cell structure and function Pub Date : 2019-03-20 Epub Date: 2019-02-02 DOI: 10.1247/csf.18041

Chao Liu, Zeliang Zhao, Zhidong Ji, Yanyan Jiang, Jiawei Zheng

{"title":"MiR-187-3p Enhances Propranolol Sensitivity of Hemangioma Stem Cells.","authors":"Chao Liu, Zeliang Zhao, Zhidong Ji, Yanyan Jiang, Jiawei Zheng","doi":"10.1247/csf.18041","DOIUrl":"https://doi.org/10.1247/csf.18041","url":null,"abstract":"Infantile hemangioma is the most common soft tissue tumors in childhood. In clinic, propranolol is widely used for infantile hemangioma therapy. However, some of the infantile hemangioma patients display resistance to propranolol treatment. Previous studies show that miR-187-3p is inhibited in hepatocellular carcinoma and lung cancer, while the role of miR-187-3p in infantile hemangioma remains unclear. In the present study, we explore the biological role of miR-187-3p in infantile hemangioma. The mRNA and protein levels of related genes were detected by real-time PCR and Western blotting. CCK8 assay was used to detect cell viability and IC50 values of propranolol. Cell apoptosis was detected by Caspase-3 Activity assay. Luciferase reporter assay and biotin RNA pull down assay were used to detect the interaction between miR-187-3p and the targeted gene. MiR-187-3p was down-regulated in infantile hemangioma tissues and promoted propranolol sensitivity of HemSCs. Mechanically, NIPBL was the direct target of miR-187-3p in HemSCs. NIPBL downregulation inhibited propranolol resistance of HemSCs. Re-introduction of NIPBL reversed miR-187-3p-meidated higher propranolol sensitivity of HemSCs. MiR-187-3p enhanced propranolol sensitivity of hemangioma stem cells via targeting NIPBL. MiR-187-3p may serve as a novel prognostic indicator and potential target for infantile hemangioma therapy.Key words: MiR-187-3p, infantile hemangioma, propranolol, resistance, NIPBL.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":"44 1","pages":"41-50"},"PeriodicalIF":1.5,"publicationDate":"2019-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1247/csf.18041","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36923509","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}

引用次数: 12

PGSE Is a Novel Enhancer Regulating the Proteoglycan Pathway of the Mammalian Golgi Stress Response. PGSE是调节哺乳动物高尔基应激反应蛋白聚糖途径的新型增强子。

IF 1.5 4区生物学

Cell structure and function Pub Date : 2019-01-11 Epub Date: 2018-11-28 DOI: 10.1247/csf.18031

Kanae Sasaki, Ryota Komori, Mai Taniguchi, Akie Shimaoka, Sachiko Midori, Mayu Yamamoto, Chiho Okuda, Ryuya Tanaka, Miyu Sakamoto, Sadao Wakabayashi, Hiderou Yoshida

{"title":"PGSE Is a Novel Enhancer Regulating the Proteoglycan Pathway of the Mammalian Golgi Stress Response.","authors":"Kanae Sasaki, Ryota Komori, Mai Taniguchi, Akie Shimaoka, Sachiko Midori, Mayu Yamamoto, Chiho Okuda, Ryuya Tanaka, Miyu Sakamoto, Sadao Wakabayashi, Hiderou Yoshida","doi":"10.1247/csf.18031","DOIUrl":"https://doi.org/10.1247/csf.18031","url":null,"abstract":"The Golgi stress response is a homeostatic mechanism that augments the functional capacity of the Golgi apparatus when Golgi function becomes insufficient (Golgi stress). Three response pathways of the Golgi stress response have been identified in mammalian cells, the TFE3, HSP47 and CREB3 pathways, which augment the capacity of specific Golgi functions such as N-glycosylation, anti-apoptotic activity and pro-apoptotic activity, respectively. On the contrary, glycosylation of proteoglycans (PGs) is another important function of the Golgi, although the response pathway upregulating expression of glycosylation enzymes for PGs in response to Golgi stress remains unknown. Here, we found that expression of glycosylation enzymes for PGs was induced upon insufficiency of PG glycosylation capacity in the Golgi (PG-Golgi stress), and that transcriptional induction of genes encoding glycosylation enzymes for PGs was independent of the known Golgi stress response pathways and ER stress response. Promoter analyses of genes encoding these glycosylation enzymes revealed the novel enhancer elements PGSE-A and PGSE-B (the consensus sequences are CCGGGGCGGGGCG and TTTTACAATTGGTC, respectively), which regulate their transcriptional induction upon PG-Golgi stress. From these observations, the response pathway we discovered is a novel Golgi stress response pathway, which we have named the PG pathway.Key words: Golgi stress, proteoglycan, ER stress, organelle zone, organelle autoregulation.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":"44 1","pages":"1-19"},"PeriodicalIF":1.5,"publicationDate":"2019-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1247/csf.18031","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36726626","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}

引用次数: 13

Organelle Zones. 细胞器区。

IF 1.5 4区生物学

Cell structure and function Pub Date : 2019-01-01 DOI: 10.1247/csf.19010

Kanae Sasaki, Hiderou Yoshida

引用次数: 6

CCL20 Promotes Ovarian Cancer Chemotherapy Resistance by Regulating ABCB1 Expression. CCL20通过调控ABCB1表达促进卵巢癌化疗耐药

IF 1.5 4区生物学

Cell structure and function Pub Date : 2019-01-01 DOI: 10.1247/csf.18029

Shan Su, Xueqin Sun, Qinghua Zhang, Zhe Zhang, Ju Chen

{"title":"CCL20 Promotes Ovarian Cancer Chemotherapy Resistance by Regulating ABCB1 Expression.","authors":"Shan Su, Xueqin Sun, Qinghua Zhang, Zhe Zhang, Ju Chen","doi":"10.1247/csf.18029","DOIUrl":"https://doi.org/10.1247/csf.18029","url":null,"abstract":"Ovarian cancer (OC) is one of prevalent tumors and this study aimed to explore CCL20's effects on doxorubicin resistance of OC and related mechanisms. Doxorubicin-resistant SKOV3 DR cells were established from SKOV3 cells via 6-month continuous exposure to gradient concentrations of doxorubicin. Quantitative PCR and Western blot assay showed that SKOV3 DR cells had higher level of CCL20 than SKOV3 cells, and doxorubicin upregulated CCL20 expression in SKOV3 cells. MTT and cell count assay found that CCL20 overexpression plasmid enhanced doxorubicin resistance of SKOV3 and OVCA433 cells compared to empty vector, as shown by the increase in cell viability. In contrast, CCL20 shRNA enhanced doxorubicin sensitivity of SKOV3 DR cells compared to control. CCL20 overexpression plasmid promoted NF-kB activation and positively regulated ABCB1 expression. Besides, ABCB1 overexpression plasmid enhanced the viability of SKOV3 and OVCA433 cells compared to empty vector under treatment with the same concentration of doxorubicin, whereas ABCB1 shRNA inhibited doxorubicin resistance of SKOV3 DR cells compared to control. In conclusion, CCL20 enhanced doxorubicin resistance of OC cells by regulating ABCB1 expression.Key words: CCL20, ovarian cancer, doxorubicin resistance, tumor-promoting, ABCB1.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":"44 1","pages":"21-28"},"PeriodicalIF":1.5,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1247/csf.18029","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36950841","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}

引用次数: 13

Long Noncoding RNA LINC00202 Promotes Tumor Progression by Sponging miR-3619-5p in Retinoblastoma. 长链非编码RNA LINC00202通过海绵miR-3619-5p在视网膜母细胞瘤中促进肿瘤进展。

IF 1.5 4区生物学

Cell structure and function Pub Date : 2019-01-01 DOI: 10.1247/csf.18033

Guigang Yan, Yi Su, Zhao Ma, Lianzhi Yu, Ning Chen

{"title":"Long Noncoding RNA LINC00202 Promotes Tumor Progression by Sponging miR-3619-5p in Retinoblastoma.","authors":"Guigang Yan, Yi Su, Zhao Ma, Lianzhi Yu, Ning Chen","doi":"10.1247/csf.18033","DOIUrl":"https://doi.org/10.1247/csf.18033","url":null,"abstract":"Retinoblastoma (RB) is the most common intraocular malignancy in childhood, and the prognosis in the advanced RB is poor. It is urgent to find novel therapeutic targets. Long noncoding RNAs (lncRNAs) have critical functions in cancer progression, and lncRNA LINC00202 is found associated with poor prognosis in RB. However, the functions of LINC00202 in RB remain unclear. We employed qRT-PCR and immunoblot to detect the expression levels of mRNAs and proteins, respectively. Cell proliferation was determined by CCK-8 assay and colony formation assay. Transwell assays were applied to evaluate the cell abilities of migration and invasion. Luciferase reporter assay was applied to examine RNA stability, and RNA pulldown assays were used to detect interaction between lncRNA and microRNA (miRNA). LINC00202 expression in RB tissues is higher than that in the paired adjacent normal tissues, which has correlation with poor prognosis in RB. RB cell proliferation, migration and invasion were weakened by LINC00202 depletion, but enhanced by LINC00202 overexpression. MiR-3619-5p was identified to directly bind and mediate LINC00202-promoted RB progression, meanwhile, miR-3619-5p directly regulated expression of an oncongene, RIN1. Moreover, RIN1 knockdown completely blocked miR-3619-5p-enhanced RB progression. In summary, high LINC00202 levels are correlated with poor prognosis in RB, and it promotes RB progression by sponging miR-3619-5p and therefore up-regulating RIN1 expression.Key words: LINC00202, miR-3619-5p, retinoblastoma, progression, RIN1.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":"44 1","pages":"51-60"},"PeriodicalIF":1.5,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1247/csf.18033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37085578","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}

引用次数: 28

Erratum: Takeda A., Saitoh S., Ohkura H., Sawin K.E., Goshima G. (2019) Identification of 15 New Bypassable Essential Genes of Fission Yeast. 更正:Takeda A.， saito S.， Ohkura H.， Sawin K.E.， Goshima G.(2019)裂变酵母15个新的可跳过必需基因的鉴定。

IF 1.5 4区生物学

Cell structure and function Pub Date : 2019-01-01 DOI: 10.1247/csf.19025e

引用次数: 0

PUM2 Promotes Glioblastoma Cell Proliferation and Migration via Repressing BTG1 Expression. PUM2通过抑制BTG1表达促进胶质母细胞瘤细胞增殖和迁移。

IF 1.5 4区生物学

Cell structure and function Pub Date : 2019-01-01 DOI: 10.1247/csf.18030

Yuanyu Wang, Weili Sun, Jiankai Yang, Liang Yang, Chen Li, Hongjiang Liu, Xiaopeng Liu, Baohua Jiao

{"title":"PUM2 Promotes Glioblastoma Cell Proliferation and Migration via Repressing BTG1 Expression.","authors":"Yuanyu Wang, Weili Sun, Jiankai Yang, Liang Yang, Chen Li, Hongjiang Liu, Xiaopeng Liu, Baohua Jiao","doi":"10.1247/csf.18030","DOIUrl":"https://doi.org/10.1247/csf.18030","url":null,"abstract":"PUM2, an RNA binding protein, is known to promote stem cell proliferation via repressing expressions of cell cycle genes. Similar with stem cells, malignant cells are characterized by unlimited proliferation and remote migration. However, roles of PUM2 in cancer development are controversial. Here, we investigated PUM2's role in glioblastoma development and its relationship with the cell cycle regulator BTG1. Immunoblotting and RT-qPCR were used to evaluate protein expression level and transcript level, respectively. ShRNAs were designed to knock down PUM2 and BTG1 expression. CCK-8 assay was used to evaluate cell viability. Cell migration assay and evasion assay were used to evaluate metastatic capability of glioblastoma cell. RNA pull-down assay and RNA immunoprecipitation assay were used to test the interaction between PUM2 and BTG1 3'UTR. PUM2 expression is elevated in glioblastoma tumor tissues as well as glioblastoma cell lines. PUM2 knockdown remarkably suppresses glioblastoma cell proliferation and migration. In addition, PUM2 knockdown increases BTG1 expression. RNA pull-down assay and RNA immunoprecipitation assay show PUM2 binds to BTG1 3'UTR directly. Furthermore, knockdown of BTG1 reverses the effect of PUM2 knockdown on glioblastoma cell proliferation and migration. Our results suggest that PUM2 promote glioblastoma development via repressing BTG1 expression.Key words: PUM2, BTG1, glioblastoma, cell proliferation, metastasis.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":"44 1","pages":"29-39"},"PeriodicalIF":1.5,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1247/csf.18030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36984516","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}

引用次数: 15

[Towards Enhancing Therapeutic Glycoprotein Bioproduction: Interventions in the PI3K/AKT/mTOR Pathway]. [促进治疗性糖蛋白生物生成:干预PI3K/AKT/mTOR通路]。

IF 1.5 4区生物学

Cell structure and function Pub Date : 2019-01-01 DOI: 10.1247/csf.19013

Mohamed Mahameed, Afnan Sulieman, Duah Alkam, B. Tirosh

引用次数: 4