sto-609 and Adenocarcinoma

sto-609 has been researched along with Adenocarcinoma* in 1 studies

Other Studies

1 other study(ies) available for sto-609 and Adenocarcinoma

Article	Year
CAMKK2 Promotes Prostate Cancer Independently of AMPK via Increased Lipogenesis. Cancer research, 2018, 12-15, Volume: 78, Issue:24 : New targets are required for treating prostate cancer, particularly castrate-resistant disease. Previous studies reported that calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) expression is increased in human prostate cancer. Here, we show that Camkk2 deletion or pharmacologic inhibition protects against prostate cancer development in a preclinical mouse model that lacks expression of prostate-specific Pten. In contrast, deletion of AMP-activated protein kinase (Ampk) β1 resulted in earlier onset of adenocarcinoma development. These findings suggest for the first time that Camkk2 and Ampk have opposing effects in prostate cancer progression. Loss of CAMKK2 Topics: Adenocarcinoma; AMP-Activated Protein Kinases; Animals; Benzimidazoles; Calcium-Calmodulin-Dependent Protein Kinase Kinase; Cell Cycle; Cell Line, Tumor; Cell Movement; Cell Proliferation; Cell Survival; CRISPR-Cas Systems; Female; Gene Deletion; Humans; Lipogenesis; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Naphthalimides; Neoplasm Invasiveness; Phosphorylation; Prostatic Neoplasms; Receptors, Androgen; Signal Transduction	2018

Article

Year

CAMKK2 Promotes Prostate Cancer Independently of AMPK via Increased Lipogenesis.

Cancer research, 2018, 12-15, Volume: 78, Issue:24

: New targets are required for treating prostate cancer, particularly castrate-resistant disease. Previous studies reported that calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) expression is increased in human prostate cancer. Here, we show that Camkk2 deletion or pharmacologic inhibition protects against prostate cancer development in a preclinical mouse model that lacks expression of prostate-specific Pten. In contrast, deletion of AMP-activated protein kinase (Ampk) β1 resulted in earlier onset of adenocarcinoma development. These findings suggest for the first time that Camkk2 and Ampk have opposing effects in prostate cancer progression. Loss of CAMKK2

Topics: Adenocarcinoma; AMP-Activated Protein Kinases; Animals; Benzimidazoles; Calcium-Calmodulin-Dependent Protein Kinase Kinase; Cell Cycle; Cell Line, Tumor; Cell Movement; Cell Proliferation; Cell Survival; CRISPR-Cas Systems; Female; Gene Deletion; Humans; Lipogenesis; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Naphthalimides; Neoplasm Invasiveness; Phosphorylation; Prostatic Neoplasms; Receptors, Androgen; Signal Transduction

2018