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Expression data from human cell lines before and after treated with drugs.

ABSTRACT: Analysis of HER2-amplified NCI-N87 gastric cancer cell line exposed to 0.1 µg/mL T-DM1 and subsequently cultured in the presence of gradually increasing doses, up to a maximum of 4 µg/mL. The resultant cell lines that grew exponentially in the presence of T-DM1 were designated as drug resistant gastric cancer cell lines, and named N87-TDMR. We used microarrays to detail the gene expression in N87-TDMR and N87-parent cells to screen for transcripts correlated with T-DM1 resistance.

ORGANISM(S): Homo sapiens

PROVIDER: GSE95414 | GEO | 2017/10/01

SECONDARY ACCESSION(S): PRJNA377092

REPOSITORIES: GEO

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Project description:Background: Zinc finger and scan domain containing 18 (ZSCAN18) belongs to zinc finger transcription factor superfamily, which consists of the hundreds of members that play critical roles in all steps of tumorigenesis. Although hypermethylation of ZSCAN18 promoter and its consequent deficiency in a variety of malignancies has been reported recently, its functions and mechanisms in the initiation and progression of gastric cancer (GC) are not clear. This study aims to investigate the roles of ZSCAN18 in gastric carcinogenesis. Methods: Methylation of ZSCAN18 promoter in GC cell lines were analyzed via MassARRAY and treatment of 5-Aza-2'-deoxycytidine. Bioinformatics analysis, qRT-PCR, western blot, immunohistochemistry, CCK-8, colony formation, and in vivo xenograft tumor model were used to examine the expression and function of ZSCAN18. Survival analysis was performed to determine the correlation between ZSCAN18 expression and prognosis of patients with GC. Genes modulated by ZSCAN18 in NCI-N87 cells were identified through RNA next generation sequence screening and further verified by qRT-PCR in AGS and NCI-N87 cells. Results: ZSCAN18 expression was markedly reduced in GC tissues as compared with that in adjacent normal tissues due to hypermethylation in GC. Likewise, ZSCAN18 expression was also significantly reduced in a panel of GC cell lines as the result of densely methylated ZSCAN18 promoter. Forced expression of ZSCAN18 inhibited proliferation in AGS and NCI-N87 cells in vitro. Additionally, ZSCAN18 impaired growth of NCI-N87 cells in immunodeficient mice. Survival analysis showed that ZSCAN18 expression was positively associated with favorable outcome in patients with GC. RNA next generation sequence screening showed three representative genes (FGF20, CEACAM5 and TP53INP2) involved in downstream signaling pathways modulated by ZSCAN18. Conclusions: Collectively, this study unveils the anti-cancer role of ZSCAN18 in GC, providing a promising diagnostic and therapeutic target.

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Expression data from human cell lines before and after treated with drugs.

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