Expression of MAT1/PEA-15 mRNA isoforms during physiological and neoplastic changes in the mouse mammary gland

Tetsuya Tsukamoto; Jakyoung Yoo; Soo In Hwang; Raphael C. Guzman; Yoshifumi Hirokawa; Yu Chien Chou; Sumaiya Olatunde; Tony Huang; Tapan K. Bera; Jason Yang; Satyabrata Nandi

doi:10.1016/S0304-3835(99)00350-X

Expression of MAT1/PEA-15 mRNA isoforms during physiological and neoplastic changes in the mouse mammary gland

Tetsuya Tsukamoto, Jakyoung Yoo, Soo In Hwang, Raphael C. Guzman, Yoshifumi Hirokawa, Yu Chien Chou, Sumaiya Olatunde, Tony Huang, Tapan K. Bera, Jason Yang, Satyabrata Nandi

Research output: Contribution to journal › Article › peer-review

20 Citations (Scopus)

Abstract

MAT1 is a novel transforming gene which was cloned from a mouse mammary tumor induced by N-methyl-N-nitrosourea in vitro in the presence of lithium as a mitogen. Later, it was found to be identical to the 3' untranslated region (UTR) of the 2.5 kb isoform of PEA-15 (phosphoprotein enriched in astrocytes-15 kDa). We re-cloned MAT1/PEA-15 cDNAs and showed 2.5, 2.0 and 1.8 kb isoforms and confirmed MAT1 localization as reported. The 2.0 and 1.8 kb isoforms were produced by alternative splicing and alternative polyadenylation at the 3' UTR, respectively. To analyze the role of MAT1/PEA- 15, we examined the expression of MAT1/PEA-15 mRNA in normal mammary tissues and in mammary tumors. The mammary gland during pregnancy, lactation and weaning showed weak but stable expression. Compared with normal mammary gland, mammary tumors showed stronger expression. Aberrant expression of MAT1/PEA-15 isoforms was found in mouse mammary epithelial cell lines, FSK7 and TM6, which lost the 2.5/2.0 and 2.5 kb isoforms, respectively. In contrast to other oncogenes like c-myc, MAT1/PEA-15 mRNA was extremely stable after actinomycin D and cycloheximide treatments suggesting that other protein expression is prerequisite for degradation of MAT1/PEA-15 mRNA. It evoked the possibility of the 3' UTR of MAT1/PEA-15 (designated as MAT1-T) as a riboregulator in mammary tumorigenesis and necessity for further analysis of human breast cancers as well as mouse mammary tumors. (C) 2000 Elsevier Science Ireland Ltd.

Original language	English
Pages (from-to)	105-113
Number of pages	9
Journal	Cancer Letters
Volume	149
Issue number	1-2
DOIs	https://doi.org/10.1016/S0304-3835(99)00350-X
Publication status	Published - 28-02-2000
Externally published	Yes

All Science Journal Classification (ASJC) codes

Oncology
Cancer Research

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@article{ab37db5131384b8e9f6939d3525a6a9c,

title = "Expression of MAT1/PEA-15 mRNA isoforms during physiological and neoplastic changes in the mouse mammary gland",

abstract = "MAT1 is a novel transforming gene which was cloned from a mouse mammary tumor induced by N-methyl-N-nitrosourea in vitro in the presence of lithium as a mitogen. Later, it was found to be identical to the 3' untranslated region (UTR) of the 2.5 kb isoform of PEA-15 (phosphoprotein enriched in astrocytes-15 kDa). We re-cloned MAT1/PEA-15 cDNAs and showed 2.5, 2.0 and 1.8 kb isoforms and confirmed MAT1 localization as reported. The 2.0 and 1.8 kb isoforms were produced by alternative splicing and alternative polyadenylation at the 3' UTR, respectively. To analyze the role of MAT1/PEA- 15, we examined the expression of MAT1/PEA-15 mRNA in normal mammary tissues and in mammary tumors. The mammary gland during pregnancy, lactation and weaning showed weak but stable expression. Compared with normal mammary gland, mammary tumors showed stronger expression. Aberrant expression of MAT1/PEA-15 isoforms was found in mouse mammary epithelial cell lines, FSK7 and TM6, which lost the 2.5/2.0 and 2.5 kb isoforms, respectively. In contrast to other oncogenes like c-myc, MAT1/PEA-15 mRNA was extremely stable after actinomycin D and cycloheximide treatments suggesting that other protein expression is prerequisite for degradation of MAT1/PEA-15 mRNA. It evoked the possibility of the 3' UTR of MAT1/PEA-15 (designated as MAT1-T) as a riboregulator in mammary tumorigenesis and necessity for further analysis of human breast cancers as well as mouse mammary tumors. (C) 2000 Elsevier Science Ireland Ltd.",

author = "Tetsuya Tsukamoto and Jakyoung Yoo and Hwang, {Soo In} and Guzman, {Raphael C.} and Yoshifumi Hirokawa and Chou, {Yu Chien} and Sumaiya Olatunde and Tony Huang and Bera, {Tapan K.} and Jason Yang and Satyabrata Nandi",

note = "Funding Information: We thank Dr Daniel Medina (Baylor College of Medicine, Houston, TX) for mouse mammary epithelial cell lines and Dr Anthony Anisowicz (Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA) for 36B4 probe. We also thank Dr Masae Tatematsu (Laboratoy of Pathology, Aichi Cancer Center Research Institute, Nagoya, Japan) for critical review of the manuscript. This work was supported by grants CA-05388 and CA-63369 awarded by the National Institutes of Health.",

year = "2000",

month = feb,

day = "28",

doi = "10.1016/S0304-3835(99)00350-X",

language = "English",

volume = "149",

pages = "105--113",

journal = "Cancer Letters",

issn = "0304-3835",

publisher = "Elsevier Ireland Ltd",

number = "1-2",

}

Expression of MAT1/PEA-15 mRNA isoforms during physiological and neoplastic changes in the mouse mammary gland. / Tsukamoto, Tetsuya; Yoo, Jakyoung; Hwang, Soo In; Guzman, Raphael C.; Hirokawa, Yoshifumi; Chou, Yu Chien; Olatunde, Sumaiya; Huang, Tony; Bera, Tapan K.; Yang, Jason; Nandi, Satyabrata.

In: Cancer Letters, Vol. 149, No. 1-2, 28.02.2000, p. 105-113.

Research output: Contribution to journal › Article › peer-review

TY - JOUR

T1 - Expression of MAT1/PEA-15 mRNA isoforms during physiological and neoplastic changes in the mouse mammary gland

AU - Tsukamoto, Tetsuya

AU - Yoo, Jakyoung

AU - Hwang, Soo In

AU - Guzman, Raphael C.

AU - Hirokawa, Yoshifumi

AU - Chou, Yu Chien

AU - Olatunde, Sumaiya

AU - Huang, Tony

AU - Bera, Tapan K.

AU - Yang, Jason

AU - Nandi, Satyabrata

N1 - Funding Information: We thank Dr Daniel Medina (Baylor College of Medicine, Houston, TX) for mouse mammary epithelial cell lines and Dr Anthony Anisowicz (Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA) for 36B4 probe. We also thank Dr Masae Tatematsu (Laboratoy of Pathology, Aichi Cancer Center Research Institute, Nagoya, Japan) for critical review of the manuscript. This work was supported by grants CA-05388 and CA-63369 awarded by the National Institutes of Health.

PY - 2000/2/28

Y1 - 2000/2/28

N2 - MAT1 is a novel transforming gene which was cloned from a mouse mammary tumor induced by N-methyl-N-nitrosourea in vitro in the presence of lithium as a mitogen. Later, it was found to be identical to the 3' untranslated region (UTR) of the 2.5 kb isoform of PEA-15 (phosphoprotein enriched in astrocytes-15 kDa). We re-cloned MAT1/PEA-15 cDNAs and showed 2.5, 2.0 and 1.8 kb isoforms and confirmed MAT1 localization as reported. The 2.0 and 1.8 kb isoforms were produced by alternative splicing and alternative polyadenylation at the 3' UTR, respectively. To analyze the role of MAT1/PEA- 15, we examined the expression of MAT1/PEA-15 mRNA in normal mammary tissues and in mammary tumors. The mammary gland during pregnancy, lactation and weaning showed weak but stable expression. Compared with normal mammary gland, mammary tumors showed stronger expression. Aberrant expression of MAT1/PEA-15 isoforms was found in mouse mammary epithelial cell lines, FSK7 and TM6, which lost the 2.5/2.0 and 2.5 kb isoforms, respectively. In contrast to other oncogenes like c-myc, MAT1/PEA-15 mRNA was extremely stable after actinomycin D and cycloheximide treatments suggesting that other protein expression is prerequisite for degradation of MAT1/PEA-15 mRNA. It evoked the possibility of the 3' UTR of MAT1/PEA-15 (designated as MAT1-T) as a riboregulator in mammary tumorigenesis and necessity for further analysis of human breast cancers as well as mouse mammary tumors. (C) 2000 Elsevier Science Ireland Ltd.

AB - MAT1 is a novel transforming gene which was cloned from a mouse mammary tumor induced by N-methyl-N-nitrosourea in vitro in the presence of lithium as a mitogen. Later, it was found to be identical to the 3' untranslated region (UTR) of the 2.5 kb isoform of PEA-15 (phosphoprotein enriched in astrocytes-15 kDa). We re-cloned MAT1/PEA-15 cDNAs and showed 2.5, 2.0 and 1.8 kb isoforms and confirmed MAT1 localization as reported. The 2.0 and 1.8 kb isoforms were produced by alternative splicing and alternative polyadenylation at the 3' UTR, respectively. To analyze the role of MAT1/PEA- 15, we examined the expression of MAT1/PEA-15 mRNA in normal mammary tissues and in mammary tumors. The mammary gland during pregnancy, lactation and weaning showed weak but stable expression. Compared with normal mammary gland, mammary tumors showed stronger expression. Aberrant expression of MAT1/PEA-15 isoforms was found in mouse mammary epithelial cell lines, FSK7 and TM6, which lost the 2.5/2.0 and 2.5 kb isoforms, respectively. In contrast to other oncogenes like c-myc, MAT1/PEA-15 mRNA was extremely stable after actinomycin D and cycloheximide treatments suggesting that other protein expression is prerequisite for degradation of MAT1/PEA-15 mRNA. It evoked the possibility of the 3' UTR of MAT1/PEA-15 (designated as MAT1-T) as a riboregulator in mammary tumorigenesis and necessity for further analysis of human breast cancers as well as mouse mammary tumors. (C) 2000 Elsevier Science Ireland Ltd.

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U2 - 10.1016/S0304-3835(99)00350-X

DO - 10.1016/S0304-3835(99)00350-X

M3 - Article

C2 - 10737714

AN - SCOPUS:18844470235

VL - 149

SP - 105

EP - 113

JO - Cancer Letters

JF - Cancer Letters

SN - 0304-3835

IS - 1-2

ER -

Expression of MAT1/PEA-15 mRNA isoforms during physiological and neoplastic changes in the mouse mammary gland

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