TGF-beta signalling in colon carcinogenesis

Lampropoulos, Pavlos; Zizi-Sermpetzoglou, Adamantia; Rizos, Spyros; Kostakis, Alkiviadis; Nikiteas, Nikolaos; Papavassiliou, Athanasios G.

doi:10.1016/j.canlet.2011.09.041

Cited by 128 publications

(118 citation statements)

References 51 publications

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“…The requirement for the 15-PGDH pathway in mediating the antiproliferative and tumor suppressor actions of calcitriol is an area for further investigation. Our data implicate application, as the Markowitz lab and others have reported that approximately 30% of human colorectal cancers have TGF-β type II receptor mutations and over half of all human colorectal cancers have signaling defects downstream of the receptors (18,42,43). However, it is important to note that this emerging class of cancer chemopreventive agents includes small molecules that are multifunctional and thus not selective for a specific target.…”

Section: Discussionsupporting

confidence: 52%

“…The loss of 15-PGDH expression may also result from impaired TGF-β signaling, a common event in colon and gastric cancers (42)(43)(44). While published data support the concept that 15-PGDH plays a direct role in controlling epithelial cell proliferation and colony-forming capacity, it has also been suggested that disruption of 15-PGDH expression may be a required or important step for cancer cell adaptation to the hypoxic tumor microenvironment and may promote survival under the microenvironmental stress of glucose deprivation (11,15).…”

Section: Methodsmentioning

confidence: 99%

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Synthetic triterpenoid induces 15-PGDH expression and suppresses inflammation-driven colon carcinogenesis

Choi¹,

Kim²,

Robinson³

et al. 2014

J. Clin. Invest.

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Colitis-associated colon cancer (CAC) develops as a result of inflammation-induced epithelial transformation, which occurs in response to inflammatory cytokine-dependent downregulation of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) and subsequent suppression of prostaglandin metabolism. Agents that both enhance 15-PGDH expression and suppress cyclooxygenase-2 (COX-2) production may more effectively prevent CAC. Synthetic triterpenoids are a class of small molecules that suppress COX-2 as well as inflammatory cytokine signaling. Here, we found that administration of the synthetic triterpenoid 2-cyano-3,12-dioxooleana-1,9 (11)

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Section: Discussionsupporting

confidence: 52%

Section: Methodsmentioning

confidence: 99%

Synthetic triterpenoid induces 15-PGDH expression and suppresses inflammation-driven colon carcinogenesis

Choi¹,

Kim²,

Robinson³

et al. 2014

J. Clin. Invest.

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“…Two another proteins, vimentin and MMP-9, are necessary for tumor cells to invade and expand into the surrounding stroma. In addition, higher gene expression levels of vimentin and MMP-9 are correlated with a higher tumor malignancy grade (Lampropoulos et al, 2012;Sipos and Galamb, 2012). The results of the present study showed that TanIIA strongly increased the expression of E-cadherin and decreased the expression of vimentin and MMP-9 in colon cancer cells, thereby inhibiting colon cancer cell invasion and metastasis.…”

Section: Discussionsupporting

confidence: 56%

In vitro inhibition of invasion and metastasis in colon cancer cells by TanIIA

Zhang¹,

Liu²,

Xie³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. The purpose of this study was to investigate the effect of the traditional Chinese medicine TanIIA on the viability, invasion, and metastasis of SW480 cells. SW480 cells were treated with TanIIA for 24 h, and MTT assays were performed to determine the effect of TanIIA on cell viability. Transwell transmembrane experiments were applied to test the effect of 1.0 mg/mL TanIIA on SW480 cell invasion and metastasis abilities. Western blotting was performed to determine the expression of the tumor cell metastasis proteins E-cadherin, vimentin, and MMP-9. The cell growth inhibition rates were 0%, 26 ± 4.3%, 43.47 ± 4.0%, 63.0 ± 5.5%, and 76.8 ± 7.8% for treatment with 0, 0.5, 1.0, 2.0, and 5.0 mg/L TanIIA, respectively. The differences in the cell viability inhibitory rates among all groups were statistically significant (P < 0.05). The Transwell assay results indicated that SW620 cell invasion and metastasis abilities were strongly inhibited by 1.0 mg/mL TanII. The western blotting results showed that the expression of E-cadherin was significantly increased and that the expression levels of vimentin and MMP-9 were significantly decreased after treatment with 1.0 mg/mL TanII for 24 h (P < 0.05). Tan II can effectively inhibit the biological activity of colon cancer in vitro and prevent the invasion of colon cancer cells.

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“…To determine the effect of TGF-␤ on HGF secretion from myofibroblasts with Epim deletion, Epim Ϫ/Ϫ and WT myofibroblasts (n ϭ 3 primary myofibroblast cultures from each genotype) were incubated with TGF-␤3 for 24 h (20). Each primary culture was also treated with IL-1␤, which stimulates HGF secretion, as a normalizing control.…”

Section: /Epimmentioning

confidence: 99%

Epimorphin deletion inhibits polyposis in theApc^min/+mouse model of colon carcinogenesis via decreased myofibroblast HGF secretion

Swietlicki

Bala²,

Lü³

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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TGF-beta signalling in colon carcinogenesis

Cited by 128 publications

References 51 publications

Synthetic triterpenoid induces 15-PGDH expression and suppresses inflammation-driven colon carcinogenesis

Synthetic triterpenoid induces 15-PGDH expression and suppresses inflammation-driven colon carcinogenesis

In vitro inhibition of invasion and metastasis in colon cancer cells by TanIIA

Epimorphin deletion inhibits polyposis in theApc^min/+mouse model of colon carcinogenesis via decreased myofibroblast HGF secretion

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TGF-beta signalling in colon carcinogenesis

Cited by 128 publications

References 51 publications

Synthetic triterpenoid induces 15-PGDH expression and suppresses inflammation-driven colon carcinogenesis

Synthetic triterpenoid induces 15-PGDH expression and suppresses inflammation-driven colon carcinogenesis

In vitro inhibition of invasion and metastasis in colon cancer cells by TanIIA

Epimorphin deletion inhibits polyposis in theApcmin/+mouse model of colon carcinogenesis via decreased myofibroblast HGF secretion

Contact Info

Product

Resources

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Epimorphin deletion inhibits polyposis in theApc^min/+mouse model of colon carcinogenesis via decreased myofibroblast HGF secretion