MYC, TP53, and chromosome 17 copy-number alterations in multiple gastric cancer cell lines and in their parental primary tumors

Abstract

We evaluated whether MYC, TP53, and chromosome 17 copy-number alterations occur in ACP02, ACP03, and AGP01 gastric cancer cell lines and in their tumor counterpart. Fluorescence in situ hybridization for MYC and TP53 genes and for chromosome 17 was applied in the 6th, 12th, 60th, and 85th passages of the cell lines and in their parental primary tumors. We observed that three and four MYC signals were the most common alterations in gastric cell lines and tumors. ACP02 presented cells with two copies of chr17 and loss of one copy of TP53 more frequently than ACP03 and AGP01. Only ACP03 and AGP01 presented clonal chr17 trisomy with three or two TP53 copies. The frequency of MYC gain, TP53 loss, and chromosome 17 trisomy seems to increase in gastric cell lines compared to their parental tumors. Our findings reveal that these cell lines retain, in vitro, the genetic alterations presented in their parental primary tumors.

Figure 1

Fluorescence in situ hybridization assay. (a) Interphase nuclei presenting two MYC signals from normal gastric mucosa; (b) interphase nuclei presenting 2–5 MYC signals from ACP02 parental primary tumor; (c) interphase nuclei presenting MYC signal number alterations, including high amplification, from the 85th passage of AGP01 cell line; (d) interphase and metaphase cells presenting two copies of chr17/TP53 from lymphocytes control, with the green spots representing the 17 centromere probe and the red representing the TP53 gene probe; (e) interphase nuclei presenting two signals of chr17 and two or one TP53 signal(s) from ACP02 parental primary tumor; (f) interphase nuclei presenting three signals for chr17 and two TP53 signals from the 85th passage of ACP03 cell line.

Figure 2

Distribution of cells according to (a) MYC signals in AGP01 parental tumor and cell line passages; (b) MYC signals in ACP02 parental tumor and cell line passages; (c) MYC signals in ACP03 parental tumor and cell line passages; (d) mean of MYC signals of AGP01, ACP02, and ACP03 parental tumor and cell line passages; (e) TP53/chr17 signals in AGP01 parental tumor and cell line passages; (f) TP53/chr17 signals in ACP02 parental tumor and cell line passages; (g) TP53/chr17 signals in ACP03 parental tumor and cell line passages; (h) mean of TP53/chr17 signals of AGP01, ACP02, and ACP03 parental tumor and cell line passages.

Figure 2

Distribution of cells according to (a) MYC signals in AGP01 parental tumor and cell line passages; (b) MYC signals in ACP02 parental tumor and cell line passages; (c) MYC signals in ACP03 parental tumor and cell line passages; (d) mean of MYC signals of AGP01, ACP02, and ACP03 parental tumor and cell line passages; (e) TP53/chr17 signals in AGP01 parental tumor and cell line passages; (f) TP53/chr17 signals in ACP02 parental tumor and cell line passages; (g) TP53/chr17 signals in ACP03 parental tumor and cell line passages; (h) mean of TP53/chr17 signals of AGP01, ACP02, and ACP03 parental tumor and cell line passages.