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Abstract 1606: SON is a novel therapeutic target for pancreatic cancer

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Abstract To find novel therapeutic molecular targets for pancreatic cancer, we conducted a systematic knockdown screening of signaling-associated molecules in pancreatic cancer cells. During the course of screening, we found that knockdown of SON, a DNA binding protein of unknown function, by short interference RNA induced a strong inhibitory effect on proliferation of cultured pancreatic cancer cells in vitro. The colony formation assay employing the short hairpin RNA vector targeting SON (shRNA-SON) revealed a strong suppression of survival of cells. Flowcytometry analysis uncovered that the knockdown of SON induced G2/M arrest and apoptosis. Stable transfectants of cancer cells with shRNA-SON showed marked retardation of tumor formation in xenograft model. Knockdown of SON induced less suppressive effect on HPDE, the immortalized normal pancreatic duct epithelial cell, which indicated that the suppressive effect on proliferation was specific for cancer cells. We established 293-cell clones stably expressing EGFP-SON and found that SON was confined in speckles in intercalated nuclei and released in cytoplasm during mitosis. These results indicated that SON was a novel therapeutic target for pancreatic cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1606.
American Association for Cancer Research (AACR)
Title: Abstract 1606: SON is a novel therapeutic target for pancreatic cancer
Description:
Abstract To find novel therapeutic molecular targets for pancreatic cancer, we conducted a systematic knockdown screening of signaling-associated molecules in pancreatic cancer cells.
During the course of screening, we found that knockdown of SON, a DNA binding protein of unknown function, by short interference RNA induced a strong inhibitory effect on proliferation of cultured pancreatic cancer cells in vitro.
The colony formation assay employing the short hairpin RNA vector targeting SON (shRNA-SON) revealed a strong suppression of survival of cells.
Flowcytometry analysis uncovered that the knockdown of SON induced G2/M arrest and apoptosis.
Stable transfectants of cancer cells with shRNA-SON showed marked retardation of tumor formation in xenograft model.
Knockdown of SON induced less suppressive effect on HPDE, the immortalized normal pancreatic duct epithelial cell, which indicated that the suppressive effect on proliferation was specific for cancer cells.
We established 293-cell clones stably expressing EGFP-SON and found that SON was confined in speckles in intercalated nuclei and released in cytoplasm during mitosis.
These results indicated that SON was a novel therapeutic target for pancreatic cancer.
Citation Format: {Authors}.
{Abstract title} [abstract].
In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC.
Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1606.

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