Sil overexpression in lung cancer characterizes tumors with increased mitotic activity

Ayelet Erez; Marina Perelman; Stephen M. Hewitt; Gadi Cojacaru; Iris Goldberg; Iris Shahar; Pnina Yaron; Inna Muler; Stefano Campaner; Ninette Amariglio; Gideon Rechavi; Ilan R. Kirsch; Meir Krupsky; Naftali Kaminski; Shai Izraeli

doi:10.1038/sj.onc.1207685

Sil overexpression in lung cancer characterizes tumors with increased mitotic activity

Ayelet Erez, Marina Perelman, Stephen M. Hewitt, Gadi Cojacaru, Iris Goldberg, Iris Shahar, Pnina Yaron, Inna Muler, Stefano Campaner, Ninette Amariglio, Gideon Rechavi, Ilan R. Kirsch, Meir Krupsky, Naftali Kaminski, Shai Izraeli

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

50 Scopus citations

Abstract

Sil (SCL interrupting locus) was cloned from the most common chromosomal rearrangement in T-cell acute lymphoblastic leukemia. It is an immediate early gene whose expression is associated with cell proliferation. Sil protein levels are tightly regulated during the cell cycle, reaching peak levels in mitosis and disappearing on transition to G1. A recent study found Sil to be one of 17 genes whose overexpression in primary adenocarcinomas predicts metastatic spread. We hypothesized that Sil might have a role in carcinogenesis. To address this question, we utilized several approaches. Using a multitumor tissue array, we found that Sil protein expression was increased mostly in lung cancer, but also at lower levels, in a subset of other tumors. Microarray gene expression analysis and immunohistochemistry of lung cancer samples verified these observations. Sil gene expression in lung cancer correlated with the expression of several kinetochore check-point genes and with the histopathologic mitotic index. These observations suggest that overexpression of the Sil gene characterizes tumors with increased mitotic activity.

Original language	English
Pages (from-to)	5371-5377
Number of pages	7
Journal	Oncogene
Volume	23
Issue number	31
DOIs	https://doi.org/10.1038/sj.onc.1207685
State	Published - 8 Jul 2004
Externally published	Yes

Bibliographical note

Funding Information:
We thank Sergey Nemez for the statistical analysis. This study was supported by research grants from the Israel Science Foundation, the Israel Cancer Research foundation and from Tel-Aviv University Recanati foundation to S Izraeli. N Kaminski is the Dorothy P and Richard P Simmons chair of Interstitial Lung Diseases at the University of Pittsburgh Medical School. G Rechavi holds the Gregorio and Dora Shapiro Chair for Hematology Malignancies, Sackler School of Medicine, Tel-Aviv University. This work was preformed in partial fulfillment of the requirements for the PhD degree of Ayelet Erez, Sackler Faculty of Medicine, Tel-Aviv University.

Funding

We thank Sergey Nemez for the statistical analysis. This study was supported by research grants from the Israel Science Foundation, the Israel Cancer Research foundation and from Tel-Aviv University Recanati foundation to S Izraeli. N Kaminski is the Dorothy P and Richard P Simmons chair of Interstitial Lung Diseases at the University of Pittsburgh Medical School. G Rechavi holds the Gregorio and Dora Shapiro Chair for Hematology Malignancies, Sackler School of Medicine, Tel-Aviv University. This work was preformed in partial fulfillment of the requirements for the PhD degree of Ayelet Erez, Sackler Faculty of Medicine, Tel-Aviv University.

Funders	Funder number
Tel-Aviv University Recanati foundation
National Cancer Institute	Z01SC010364
Israel Cancer Research Fund
Israel Science Foundation

Keywords

Carcinogenesis
Lung cancer
Mitosis
Sil

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1038/sj.onc.1207685

Cite this

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title = "Sil overexpression in lung cancer characterizes tumors with increased mitotic activity",

abstract = "Sil (SCL interrupting locus) was cloned from the most common chromosomal rearrangement in T-cell acute lymphoblastic leukemia. It is an immediate early gene whose expression is associated with cell proliferation. Sil protein levels are tightly regulated during the cell cycle, reaching peak levels in mitosis and disappearing on transition to G1. A recent study found Sil to be one of 17 genes whose overexpression in primary adenocarcinomas predicts metastatic spread. We hypothesized that Sil might have a role in carcinogenesis. To address this question, we utilized several approaches. Using a multitumor tissue array, we found that Sil protein expression was increased mostly in lung cancer, but also at lower levels, in a subset of other tumors. Microarray gene expression analysis and immunohistochemistry of lung cancer samples verified these observations. Sil gene expression in lung cancer correlated with the expression of several kinetochore check-point genes and with the histopathologic mitotic index. These observations suggest that overexpression of the Sil gene characterizes tumors with increased mitotic activity.",

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note = "Funding Information: We thank Sergey Nemez for the statistical analysis. This study was supported by research grants from the Israel Science Foundation, the Israel Cancer Research foundation and from Tel-Aviv University Recanati foundation to S Izraeli. N Kaminski is the Dorothy P and Richard P Simmons chair of Interstitial Lung Diseases at the University of Pittsburgh Medical School. G Rechavi holds the Gregorio and Dora Shapiro Chair for Hematology Malignancies, Sackler School of Medicine, Tel-Aviv University. This work was preformed in partial fulfillment of the requirements for the PhD degree of Ayelet Erez, Sackler Faculty of Medicine, Tel-Aviv University.",

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AU - Cojacaru, Gadi

AU - Goldberg, Iris

AU - Shahar, Iris

AU - Yaron, Pnina

AU - Muler, Inna

AU - Campaner, Stefano

AU - Amariglio, Ninette

AU - Rechavi, Gideon

AU - Kirsch, Ilan R.

AU - Krupsky, Meir

AU - Kaminski, Naftali

AU - Izraeli, Shai

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Sil overexpression in lung cancer characterizes tumors with increased mitotic activity

Abstract

Bibliographical note

Funding

Keywords

UN SDGs

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