Functional characterization of Trip10 in cancer cell growth and survival

Chia Chen Hsu, Yu Wei Leu, Min Jen Tseng, Kuan Der Lee, Tzen Yu Kuo, Jia Yi Yen, Yen Ling Lai, Yi Chen Hung, Wei Sheng Sun, Chien Min Chen, Pei Yi Chu, Kun Tu Yeh, Pearlly S. Yan, Yu Sun Chang, Tim H.M. Huang, Shu Huei Hsiao

Research output: Contribution to journalArticle

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Abstract

Background. The Cdc42-interacting protein-4, Trip10 (also known as CIP4), is a multi-domain adaptor protein involved in diverse cellular processes, which functions in a tissue-specific and cell lineage-specific manner. We previously found that Trip10 is highly expressed in estrogen receptor-expressing (ER +) breast cancer cells. Estrogen receptor depletion reduced Trip10 expression by progressively increasing DNA methylation. We hypothesized that Trip10 functions as a tumor suppressor and may be involved in the malignancy of ER-negative (ER-) breast cancer. To test this hypothesis and evaluate whether Trip10 is epigenetically regulated by DNA methylation in other cancers, we evaluated DNA methylation of Trip10 in liver cancer, brain tumor, ovarian cancer, and breast cancer. Methods. We applied methylation-specific polymerase chain reaction and bisulfite sequencing to determine the DNA methylation of Trip10 in various cancer cell lines and tumor specimens. We also overexpressed Trip10 to observe its effect on colony formation and in vivo tumorigenesis. Results. We found that Trip10 is hypermethylated in brain tumor and breast cancer, but hypomethylated in liver cancer. Overexpressed Trip10 was associated with endogenous Cdc42 and huntingtin in IMR-32 brain tumor cells and CP70 ovarian cancer cells. However, overexpression of Trip10 promoted colony formation in IMR-32 cells and tumorigenesis in mice inoculated with IMR-32 cells, whereas overexpressed Trip10 substantially suppressed colony formation in CP70 cells and tumorigenesis in mice inoculated with CP70 cells. Conclusions. Trip10 regulates cancer cell growth and death in a cancer type-specific manner. Differential DNA methylation of Trip10 can either promote cell survival or cell death in a cell type-dependent manner.

Original languageEnglish
Article number12
JournalJournal of Biomedical Science
Volume18
Issue number1
DOIs
Publication statusPublished - 2011
Externally publishedYes

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Cell growth
Tumors
Cell Survival
Cells
DNA Methylation
Brain Neoplasms
Growth
Brain
Breast Neoplasms
Cell death
Neoplasms
Estrogen Receptors
Liver
Carcinogenesis
Liver Neoplasms
Methylation
Ovarian Neoplasms
Polymerase chain reaction
cdc42 GTP-Binding Protein
Cell Death

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology
  • Biochemistry, medical
  • Pharmacology (medical)

Cite this

Hsu, C. C., Leu, Y. W., Tseng, M. J., Lee, K. D., Kuo, T. Y., Yen, J. Y., ... Hsiao, S. H. (2011). Functional characterization of Trip10 in cancer cell growth and survival. Journal of Biomedical Science, 18(1), [12]. https://doi.org/10.1186/1423-0127-18-12

Functional characterization of Trip10 in cancer cell growth and survival. / Hsu, Chia Chen; Leu, Yu Wei; Tseng, Min Jen; Lee, Kuan Der; Kuo, Tzen Yu; Yen, Jia Yi; Lai, Yen Ling; Hung, Yi Chen; Sun, Wei Sheng; Chen, Chien Min; Chu, Pei Yi; Yeh, Kun Tu; Yan, Pearlly S.; Chang, Yu Sun; Huang, Tim H.M.; Hsiao, Shu Huei.

In: Journal of Biomedical Science, Vol. 18, No. 1, 12, 2011.

Research output: Contribution to journalArticle

Hsu, CC, Leu, YW, Tseng, MJ, Lee, KD, Kuo, TY, Yen, JY, Lai, YL, Hung, YC, Sun, WS, Chen, CM, Chu, PY, Yeh, KT, Yan, PS, Chang, YS, Huang, THM & Hsiao, SH 2011, 'Functional characterization of Trip10 in cancer cell growth and survival', Journal of Biomedical Science, vol. 18, no. 1, 12. https://doi.org/10.1186/1423-0127-18-12
Hsu, Chia Chen ; Leu, Yu Wei ; Tseng, Min Jen ; Lee, Kuan Der ; Kuo, Tzen Yu ; Yen, Jia Yi ; Lai, Yen Ling ; Hung, Yi Chen ; Sun, Wei Sheng ; Chen, Chien Min ; Chu, Pei Yi ; Yeh, Kun Tu ; Yan, Pearlly S. ; Chang, Yu Sun ; Huang, Tim H.M. ; Hsiao, Shu Huei. / Functional characterization of Trip10 in cancer cell growth and survival. In: Journal of Biomedical Science. 2011 ; Vol. 18, No. 1.
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abstract = "Background. The Cdc42-interacting protein-4, Trip10 (also known as CIP4), is a multi-domain adaptor protein involved in diverse cellular processes, which functions in a tissue-specific and cell lineage-specific manner. We previously found that Trip10 is highly expressed in estrogen receptor-expressing (ER +) breast cancer cells. Estrogen receptor depletion reduced Trip10 expression by progressively increasing DNA methylation. We hypothesized that Trip10 functions as a tumor suppressor and may be involved in the malignancy of ER-negative (ER-) breast cancer. To test this hypothesis and evaluate whether Trip10 is epigenetically regulated by DNA methylation in other cancers, we evaluated DNA methylation of Trip10 in liver cancer, brain tumor, ovarian cancer, and breast cancer. Methods. We applied methylation-specific polymerase chain reaction and bisulfite sequencing to determine the DNA methylation of Trip10 in various cancer cell lines and tumor specimens. We also overexpressed Trip10 to observe its effect on colony formation and in vivo tumorigenesis. Results. We found that Trip10 is hypermethylated in brain tumor and breast cancer, but hypomethylated in liver cancer. Overexpressed Trip10 was associated with endogenous Cdc42 and huntingtin in IMR-32 brain tumor cells and CP70 ovarian cancer cells. However, overexpression of Trip10 promoted colony formation in IMR-32 cells and tumorigenesis in mice inoculated with IMR-32 cells, whereas overexpressed Trip10 substantially suppressed colony formation in CP70 cells and tumorigenesis in mice inoculated with CP70 cells. Conclusions. Trip10 regulates cancer cell growth and death in a cancer type-specific manner. Differential DNA methylation of Trip10 can either promote cell survival or cell death in a cell type-dependent manner.",
author = "Hsu, {Chia Chen} and Leu, {Yu Wei} and Tseng, {Min Jen} and Lee, {Kuan Der} and Kuo, {Tzen Yu} and Yen, {Jia Yi} and Lai, {Yen Ling} and Hung, {Yi Chen} and Sun, {Wei Sheng} and Chen, {Chien Min} and Chu, {Pei Yi} and Yeh, {Kun Tu} and Yan, {Pearlly S.} and Chang, {Yu Sun} and Huang, {Tim H.M.} and Hsiao, {Shu Huei}",
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T1 - Functional characterization of Trip10 in cancer cell growth and survival

AU - Hsu, Chia Chen

AU - Leu, Yu Wei

AU - Tseng, Min Jen

AU - Lee, Kuan Der

AU - Kuo, Tzen Yu

AU - Yen, Jia Yi

AU - Lai, Yen Ling

AU - Hung, Yi Chen

AU - Sun, Wei Sheng

AU - Chen, Chien Min

AU - Chu, Pei Yi

AU - Yeh, Kun Tu

AU - Yan, Pearlly S.

AU - Chang, Yu Sun

AU - Huang, Tim H.M.

AU - Hsiao, Shu Huei

PY - 2011

Y1 - 2011

N2 - Background. The Cdc42-interacting protein-4, Trip10 (also known as CIP4), is a multi-domain adaptor protein involved in diverse cellular processes, which functions in a tissue-specific and cell lineage-specific manner. We previously found that Trip10 is highly expressed in estrogen receptor-expressing (ER +) breast cancer cells. Estrogen receptor depletion reduced Trip10 expression by progressively increasing DNA methylation. We hypothesized that Trip10 functions as a tumor suppressor and may be involved in the malignancy of ER-negative (ER-) breast cancer. To test this hypothesis and evaluate whether Trip10 is epigenetically regulated by DNA methylation in other cancers, we evaluated DNA methylation of Trip10 in liver cancer, brain tumor, ovarian cancer, and breast cancer. Methods. We applied methylation-specific polymerase chain reaction and bisulfite sequencing to determine the DNA methylation of Trip10 in various cancer cell lines and tumor specimens. We also overexpressed Trip10 to observe its effect on colony formation and in vivo tumorigenesis. Results. We found that Trip10 is hypermethylated in brain tumor and breast cancer, but hypomethylated in liver cancer. Overexpressed Trip10 was associated with endogenous Cdc42 and huntingtin in IMR-32 brain tumor cells and CP70 ovarian cancer cells. However, overexpression of Trip10 promoted colony formation in IMR-32 cells and tumorigenesis in mice inoculated with IMR-32 cells, whereas overexpressed Trip10 substantially suppressed colony formation in CP70 cells and tumorigenesis in mice inoculated with CP70 cells. Conclusions. Trip10 regulates cancer cell growth and death in a cancer type-specific manner. Differential DNA methylation of Trip10 can either promote cell survival or cell death in a cell type-dependent manner.

AB - Background. The Cdc42-interacting protein-4, Trip10 (also known as CIP4), is a multi-domain adaptor protein involved in diverse cellular processes, which functions in a tissue-specific and cell lineage-specific manner. We previously found that Trip10 is highly expressed in estrogen receptor-expressing (ER +) breast cancer cells. Estrogen receptor depletion reduced Trip10 expression by progressively increasing DNA methylation. We hypothesized that Trip10 functions as a tumor suppressor and may be involved in the malignancy of ER-negative (ER-) breast cancer. To test this hypothesis and evaluate whether Trip10 is epigenetically regulated by DNA methylation in other cancers, we evaluated DNA methylation of Trip10 in liver cancer, brain tumor, ovarian cancer, and breast cancer. Methods. We applied methylation-specific polymerase chain reaction and bisulfite sequencing to determine the DNA methylation of Trip10 in various cancer cell lines and tumor specimens. We also overexpressed Trip10 to observe its effect on colony formation and in vivo tumorigenesis. Results. We found that Trip10 is hypermethylated in brain tumor and breast cancer, but hypomethylated in liver cancer. Overexpressed Trip10 was associated with endogenous Cdc42 and huntingtin in IMR-32 brain tumor cells and CP70 ovarian cancer cells. However, overexpression of Trip10 promoted colony formation in IMR-32 cells and tumorigenesis in mice inoculated with IMR-32 cells, whereas overexpressed Trip10 substantially suppressed colony formation in CP70 cells and tumorigenesis in mice inoculated with CP70 cells. Conclusions. Trip10 regulates cancer cell growth and death in a cancer type-specific manner. Differential DNA methylation of Trip10 can either promote cell survival or cell death in a cell type-dependent manner.

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