Dataset Information

OIP5 Promotes Growth, Metastasis and Chemoresistance to Cisplatin in Bladder Cancer Cells.

ABSTRACT: Opa interacting protein 5 (OIP5) has previously been identified as a tumorigenesis gene. The purpose of this study is to explore the role of OIP5 in the progression of bladder cancer (BC). The OIP5 expression and clinical behaviors in bladder cancer were collected from lager database. Our study showed that OIP5 was highly expressed in bladder cancer tissues and cells. Overexpression of OIP5 in tumor patients predicted worse overall survival (OS) and higher histological grade. Vitro and vivo experiments demonstrated that knockdown of OIP5 significantly inhibited cell growth of BC. Scratch assay and transwell assay suggested that migration capacity of BC cells was decreased after knockdown of OIP5. Cisplatin sensitivity assay indicated that depletion of OIP5 increased the sensitivity of BC cells to cisplatin. Finally, we identified 38 overlapping differentially expressed genes (DEGs) between RNA-seq and TCGA analyses which were closely linked to OIP5. Bioinformatics analysis showed that these DEGs enriched in oocyte meiosis, fanconi anemia pathway, cell cycle, and microRNAs regulation. TOP2A, SPAG5, SKA1, EXO1, TK1 were confirmed to associated with bladder cancer development. Our study suggests that OIP5 may be a potential biomarker for growth, metastasis and drug-resistance in bladder cancer.

SUBMITTER: Wang D

PROVIDER: S-EPMC6299379 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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OIP5 Promotes Growth, Metastasis and Chemoresistance to Cisplatin in Bladder Cancer Cells.

Wang Dailian D Chen Zhicong Z Lin Fan F Wang Ziqiang Z Gao Qunjun Q Xie Haibiao H Xiao Huizhong H Zhou Yifan Y Zhang Fuyou F Ma Yingfei Y Mei Hongbin H Cai Zhiming Z Liu Yuchen Y Huang Weiren W

Journal of Cancer 20181124 24

Opa interacting protein 5 (OIP5) has previously been identified as a tumorigenesis gene. The purpose of this study is to explore the role of OIP5 in the progression of bladder cancer (BC). The OIP5 expression and clinical behaviors in bladder cancer were collected from lager database. Our study showed that OIP5 was highly expressed in bladder cancer tissues and cells. Overexpression of OIP5 in tumor patients predicted worse overall survival (OS) and higher histological grade. Vitro and vivo expe ...[more]

PMID: 30588253

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Project description:The Cancer associated Sm-like (CaSm) oncogene is overexpressed in 87% of human pancreatic tumor samples and CaSm knockdown has demonstrated therapeutic efficacy in murine models of pancreatic cancer. Evidence indicates that CaSm modulates mRNA degradation; however, its target genes and the mechanisms by which CaSm promotes pancreatic cancer remain largely unknown. Here, we demonstrate that the CaSm overexpression alters several hallmarks of cancer â including transformation, proliferation, chemoresistance, and metastasis. Doxycycline-induced CaSm expression enhanced proliferation and both anchorage-dependent and -independent growth of the human Panc-1 cells in vitro. CaSm induction decreased gemcitabine-induced cytotoxicity and altered the expression of apoptotic regulation genes, including Bad, E2F1, and Bcl-XL. CaSm-overexpressing Panc-1 cells were 2-fold more migratory and 4-fold more invasive than the driver controls and demonstrated characteristics of epithelial-to-mesenchymal transition such as morphological changes and decreased E-cadherin expression. CaSm induction resulted in changes in RNA expression of metastasis-associated genes such as MMP1, SerpinB5, uPAR, and Slug. Using a murine model of metastatic pancreatic cancer, injection of CaSm-induced Panc-1 cells resulted in a higher abundance of hepatic metastatic lesions. Overall, CaSm overexpression contributed to a more aggressive cancer phenotype in Panc-1 cells, further supporting the use of CaSm as a therapeutic target against pancreatic cancer. Tet-on driver and tet-on CaSm Panc-1 cells were grown with and without doxycycline (1 Î¼g/mL) for 4 weeks. Levels of CaSm expression were confirmed using RT-PCR (Supplementary Figure 2a). RNA isolation was performed using RNeasy Plus kit (Qiagen, Valencia, CA) following the manufacturerâs protocols. The Hollings Cancer Center Tissue Biorepository core facility confirmed RNA quality using the 18S/28S Ratio Integrity Number using Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA); RNA with a RIN of 10 was used for further analysis (Supplementary Figure 2b). Complement DNA synthesis was performed using RT2 First Strand kit and RT2 SYBR Green qPCR master mix was used for the microarray master mix reagent according to the manufacturerâs manual (SABiosciences). The Cancer PathwayFinder PCR array (SABiosciences) was run on the Roche 480 Lightcycler (Roche, Indianapolis, IN) with 2 plates run for each tet-on driver + doxycycline, tet-on CaSm, and tet-on CaSm + doxycycline. The plates included controls for genomic DNA contamination, reverse transcription, and positive controls. Analysis was performed using SABioscienceâs Free PCR Array Data Analysis Software (ÎÎCt method) with B2M, HPRT1, and GAPDH as pooled housekeeping genes.

Dataset Information

OIP5 Promotes Growth, Metastasis and Chemoresistance to Cisplatin in Bladder Cancer Cells.

Publications

OIP5 Promotes Growth, Metastasis and Chemoresistance to Cisplatin in Bladder Cancer Cells.

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