L1 increases adhesion-mediated proliferation and chemoresistance of retinoblastoma

Jo, Dong Hyun; Lee, Kyung-Min; Kim, Jin Hyoung; Jun, Hyoung Oh; Kim, Young-Hoon; Cho, Young Lai; Yu, Young Suk; Min, Jeong Ki; Kim, Jeong Hun

doi:10.18632/oncotarget.14487

Cited by 25 publications

(39 citation statements)

References 53 publications

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“…Further along this line, a combination of anti-L1CAM antibody and cisplatin was found to improve the therapeutic response in cholangiocarcinoma by enhancing tumor growth inhibition compared to treatment with the drug alone ( 27 ). Recently, Jo et al showed that L1CAM increased the adhesion-mediated proliferation and resistance of Y-79 and SNUOT-Rb1 RB cells to carboplatin, vincristine and etoposide ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

Characterization of etoposide- and cisplatin-chemoresistant retinoblastoma cell lines

et al. 2017

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Abstract. Retinoblastoma (RB) is the most common malignant intraocular tumor in early childhood. Imminent chemotherapy resistance diminishes the clinical-therapeutic options and emphasizes the necessity for new therapeutic approaches. The present study aimed at characterizing and comparing etoposide and cisplatin-resistant human RB cell lines with regard to changes in proliferation and apoptosis levels, anchorage independent growth behavior in vitro as well as tumor formation capacity in vivo. The proliferation rates were significantly increased in the etoposide-resistant RB cell lines Y-79, WERI-Rb1 and RB-355 reflecting significantly higher growth kinetics compared to the parental controls. In line with these findings in in vivo chicken chorioallantoic (CAM) assays, etoposide-resistant cell lines generated significantly increased numbers of tumors with higher tumor weights compared to their parental counterparts. In contrast to etoposide, the cisplatin-resistant RB cell lines Y-79, WERIRb1 and RB-355 displayed significantly increased apoptosis rates and reduced proliferation rates resulting in significantly decreased growth kinetics. Tumor formation capacity of cisplatin-resistant cell lines did not significantly change, and in comparison with parental controls cisplatin-resistant Y-79 cells displayed significantly reduced tumor weight. Soft agarose assays indicated that anchorage-independent growth of all chemotherapy-resistant cell lines analyzed was significantly decreased. Summarizing, one can state that etoposide-resistant RB cells behave more aggressively than the tumor cells of origin and potentially represent a risk factor for local relapse, while cisplatin-resistant cells show a significantly decreased tumorigenic potential.

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Section: Discussionmentioning

confidence: 99%

Characterization of etoposide- and cisplatin-chemoresistant retinoblastoma cell lines

et al. 2017

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“…Beginning at 2 weeks after injection, eyeballs were examined daily to monitor tumor formation. A visual grading system was employed to grade the degree of tumor formation from 0–5: grade 0 (no tumor formation), grade 1 (streak-like tumor), grade 2 (plaque-like tumor), grade 3 (definite mass formation), grade 4 (vitreous-filling tumor), and grade 5 (accompanying globe enlargement or eyeball rupture), according to the standard photographs in a previous publication 18 . Two independent observers (D.H. Jo and C.S.…”

Section: Methodsmentioning

confidence: 99%

Development of a patient-derived xenograft model of glioblastoma via intravitreal injection in mice

Lee

Kim

et al. 2019

Exp Mol Med

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Currently, the two primary patient-derived xenograft (PDX) models of glioblastoma are established through intracranial or subcutaneous injection. In this study, a novel PDX model of glioblastoma was developed via intravitreal injection to facilitate tumor formation in a brain-mimicking microenvironment with improved visibility and fast development. Glioblastoma cells were prepared from the primary and recurrent tumor tissues of a 39-year-old female patient. To demonstrate the feasibility of intracranial tumor formation, U-87 MG and patient-derived glioblastoma cells were injected into the brain parenchyma of Balb/c nude mice. Unlike the U-87 MG cells, the patient-derived glioblastoma cells failed to form intracranial tumors until 6 weeks after tumor cell injection. In contrast, the patient-derived cells effectively formed intraocular tumors, progressing from plaques at 2 weeks to masses at 4 weeks after intravitreal injection. The in vivo tumors exhibited the same immunopositivity for human mitochondria, GFAP, vimentin, and nestin as the original tumors in the patient. Furthermore, cells isolated from the in vivo tumors also demonstrated morphology similar to that of their parental cells and immunopositivity for the same markers. Overall, a novel PDX model of glioblastoma was established via the intravitreal injection of tumor cells. This model will be an essential tool to investigate and develop novel therapeutic alternatives for the treatment of glioblastoma.

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“…Chemotherapy resistance to antineoplastic agents, including carboplatin, etoposide and vincristine, is a major problem in the treatment of high-risk advanced RB [5,8,9]. Etoposide is well known for its use in the treatment of many malignancies, such as Hodgkin's disease, lung cancer, ovarian cancer, myeloma, gastric cancer and breast cancer [10][11][12][13]; the drug is a DNA topoisomerase-II inhibitor that can directly bind to DNA and cause DNA damage [14].…”

Section: Introductionmentioning

confidence: 99%

Different transcriptome profiles between human retinoblastoma Y79 cells and an etoposide-resistant subline reveal a chemoresistance mechanism

et al. 2020

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Background: Retinoblastoma (RB) is the most frequent pediatric retinal tumor. In the present study, to elucidate chemoresistance mechanisms and identify potential biomarkers in RB, we utilized RNA sequencing (RNAseq) technological platforms to reveal transcriptome profiles and identify any differentially expressed genes (DEGs) between an etoposide drugresistant subline (Y79/EDR) and parental Y79 cells. Methods: To test whether Y79/EDR cells showed resistance to antineoplastic agents for RB, we treated the cells with etoposide, carboplatin and vincristine and analyzed them with a Cell Counting Kit-8 (CCK-8). Y79/EDR and parental Y79 cells were used for RNAseq and bioinformatics analysis to enable a genome-wide review of DEGs between the two lines using the DESeq R package (1.10.1). Then, DEG enrichment in Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways was analyzed with KOBAS software. Next, real-time quantitative reverse transcription polymerase chain reaction (real time QRT-PCR) and cytotoxicity assays were performed to experimentally and functionally validate the identified candidate biomarkers. Results: Y79/EDR cells showed resistance to etoposide, carboplatin and vincristine at different concentrations. In total, 524 transcripts were differentially expressed in Y79/EDR cells based on analysis of fragments per kilobase of transcript per million fragments mapped (FPKM); among these, 57 genes were downregulated and 467 genes were upregulated in Y79/EDR cells compared to parental Y79 cells. We selected candidate DEGs, including ARHGAP9, HIST1H4H, RELN, DDIT4, HK2, STC1 and PFKFB4, for mRNA expression validation with real time QRT-PCR assays and found that the expression levels determined by real time QRT-PCR were consistent with the RNAseq data. Further studies involving downregulation of ARHGAP9 with a specific siRNA showed that ARHGAP9 altered the cellular sensitivity of Y79 cells to etoposide and carboplatin.

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L1 increases adhesion-mediated proliferation and chemoresistance of retinoblastoma

Cited by 25 publications

References 53 publications

Characterization of etoposide- and cisplatin-chemoresistant retinoblastoma cell lines

Characterization of etoposide- and cisplatin-chemoresistant retinoblastoma cell lines

Development of a patient-derived xenograft model of glioblastoma via intravitreal injection in mice

Different transcriptome profiles between human retinoblastoma Y79 cells and an etoposide-resistant subline reveal a chemoresistance mechanism

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