2007
DOI: 10.1002/ijc.22393
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Antitumor activity of ALK1 in pancreatic carcinoma cells

Abstract: In this study, the authors investigated the expression of activin receptor-like kinase 1 (ALK1) in pancreatic carcinoma and evaluated its potential role as a tumor suppressor in vitro and in vivo. Endogenous ALK1 expression was demonstrated by immunohistochemistry in both pancreatic tumor tissue and peritumoral normal tissue from 6 patients and by RT-PCR in 8/12 established pancreatic cancer cell lines. Ectopic expression of a constitutively active (ca) ALK1 mutant in TGF-b sensitive PANC-1 and COLO-357 cells … Show more

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Cited by 10 publications
(7 citation statements)
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“…Our data are in agreement with the increased migratory activity and invasive behavior in vitro following stimulation of PANC-1 cells with TGF-b1 (Ellenrieder et al, 2001a, b). Notably, following xenotransplantation of PANC-1 cells into mouse pancreas ALK5-TD strongly induced hepatic metastasis, while neither the Smadbinding-defective mutant (this study) nor a kinase-active mutant of the related ALK1, which signals through Smad1/5, was capable to do so (Ungefroren et al, 2007). This suggests a crucial role for Smad2/3 in TGF-bdriven metastasis of pancreatic carcinoma cells to the liver and resembles the situation in MDA-MB-231 breast cancer cells where Smads are required for metastasis to bone (Kang et al, 2005;Deckers et al, 2006).…”
Section: Tgf-b Receptor Type I In Tgf-b-induced Tumor Suppressionmentioning
confidence: 53%
“…Our data are in agreement with the increased migratory activity and invasive behavior in vitro following stimulation of PANC-1 cells with TGF-b1 (Ellenrieder et al, 2001a, b). Notably, following xenotransplantation of PANC-1 cells into mouse pancreas ALK5-TD strongly induced hepatic metastasis, while neither the Smadbinding-defective mutant (this study) nor a kinase-active mutant of the related ALK1, which signals through Smad1/5, was capable to do so (Ungefroren et al, 2007). This suggests a crucial role for Smad2/3 in TGF-bdriven metastasis of pancreatic carcinoma cells to the liver and resembles the situation in MDA-MB-231 breast cancer cells where Smads are required for metastasis to bone (Kang et al, 2005;Deckers et al, 2006).…”
Section: Tgf-b Receptor Type I In Tgf-b-induced Tumor Suppressionmentioning
confidence: 53%
“…Finally, because ALK1 is reported to be expressed by, and possibly functionally important for, lymphatic ECs, cells of the pituitary gland, hepatic stellate cells, chondrocytes, and pancreatic ductal cells, special care should be taken to record adverse events from the treatment of ALK1 inhibitors related to processes regulated by these particular tissues. 21,55,70,83,84 …”
Section: Possible Side Effects From Alk1 Inhibitionmentioning
confidence: 99%
“…TβRI, a serine/threonine kinase, subsequently phosphorylates SMAD2 and SMAD3, which form heterotrimers with SMAD4 and translocate to the nucleus, where they interact with DNA-binding transcription factors and either activate or repress transcription. TGFβ signaling in EMT is complicated by the fact that the type I receptors ALK1, ALK2, and ALK5 have distinct and sometimes opposing functions: Whereas, for example, the principal ALK5 receptor mediates EMT, ALK1 can counteract this effect [17]. Moreover, the TGFβ signal can be relayed in a non-canonical, i.e.…”
Section: Emt Signaling Pathwaysmentioning
confidence: 99%