Transforming growth factor-β2 is an autocrine growth inhibitory factor for the MOSER human colon carcinoma cell line

Levine, Alan E.; Lewis, Laurie R.

doi:10.1016/0304-3835(93)90216-v

Cited by 8 publications

(5 citation statements)

References 28 publications

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“…First, it is likely that the driving force for Smad4 mutation in human cancer cell lines is the loss of responsiveness to TGF-␤. This conclusion is consistent with the many studies demonstrating that colorectal epithelial cells synthesize TGF-␤ and that this ligand functions in an autocrine loop to inhibit the growth of cells that are not fully transformed (41,42,(50)(51)(52)(53)(54). Second, our results provide compelling evidence that genetic inactivation of the components of TGF-␤ signaling occurs in human cancer cells.…”

supporting

confidence: 80%

Targeted deletion of Smad4 shows it is required for transforming growth factor β and activin signaling in colorectal cancer cells

Zhou

Buckhaults

Zawel

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

149

100

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Smad4 (DPC4) is a candidate tumor suppressor gene that has been hypothesized to be critical for transmitting signals from transforming growth factor (TGF) ␤ and related ligands. To directly test this hypothesis, the Smad4 gene was deleted through homologous recombination in human colorectal cancer cells. This deletion abrogated signaling from TGF-␤, as well as from the TGF-␤ family member activin. These results provide unequivocal evidence that mutational inactivation of Smad4 causes TGF-␤ unresponsiveness and provide a basis for understanding the physiologic role of this gene in tumorigenesis.

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supporting

confidence: 80%

Targeted deletion of Smad4 shows it is required for transforming growth factor β and activin signaling in colorectal cancer cells

Zhou

Buckhaults

Zawel

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

149

100

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“…43 Further studies have shown that TGF-β can inhibit cell proliferation and tumor growth via activation of Smad-dependent andindependent signaling pathways in normal and tumor cell lines. 44,45 Boulay et al 46 showed that TGFβ, is a tumor suppressor that stimulates apoptosis and inhibits cell growth through Smad7 overexpression. Another study conducted by Wang et al 47 showed that aspirin exerts its antitumor effects and stimulates apoptotic cell death, while suppresses cells proliferation through enhancement of TGF-β1 secretion.…”

Section: Tgf-β Signaling Pathwaymentioning

confidence: 99%

“…It has been reported that p21 expression is highly expressed in TGF‐β‐stimulated human colon cancer cells . Further studies have shown that TGF‐β can inhibit cell proliferation and tumor growth via activation of Smad‐dependent and ‐independent signaling pathways in normal and tumor cell lines . Boulay et al showed that TGFβ, is a tumor suppressor that stimulates apoptosis and inhibits cell growth through Smad7 overexpression.…”

Section: Introductionmentioning

confidence: 99%

Role of the transforming growth factor‐β signaling pathway in the pathogenesis of colorectal cancer

Soleimani

Pashirzad

Rezayi

et al. 2018

J of Cellular Biochemistry

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The transforming growth factor-β (TGF-β) signaling pathway plays an important role in cancer cell proliferation, growth, metastasis, and apoptosis. It has been shown that TGF-β acts as a tumor suppressor in the early stages of the disease, and as a tumor promoter in its late stages. Mutations in the TGF-β signaling components, the TGF-β receptors and cytoplasmic signaling transducers, are frequently observed in colorectal carcinomas. Exploiting specific TGF-β receptor agonist and antagonist with antitumor properties may be a way of controlling cancer progression. This review summarizes the regulatory role of TGF-β signaling in the pathogenesis of colorectal cancer.

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“…Ample evidence is available showing that TGF-␤ restrains the growth of colon cancer cells (Lamprecht et al, 1989;Levine and Lewis, 1993;Mulder and Brattain, 1989;Wu et al, 1992). The escape from this negative regulation is thought to contribute to tumor progression (Filmus and Kerbel, 1993;Fynan and Reiss, 1993;Lamprecht et al, 1989;Mulder and Brattain, 1989).…”

mentioning

confidence: 99%

“…The escape from this negative regulation is thought to contribute to tumor progression (Filmus and Kerbel, 1993;Fynan and Reiss, 1993;Lamprecht et al, 1989;Mulder and Brattain, 1989). Colon cancer cells resistant to the TGF-␤ inhibitory action are poorly differentiated whereas precancerous and moderately differentiated colon tumor cells retain their response to TGF-␤ 1 (Hossein et al, 1987;Lahm and Odartchenko, 1993;Lamprecht et al, 1989;Levine and Lewis, 1993;Manning et al, 1991;Markowitz and Roberts, 1996;Mulder and Brattain, 1989) The results showing that the growth-restraining action of TGF-␤ on colon cancer cells is related to definite stages of their malignant progression derive exclusively from in vitro studies and no observation was hitherto available pertaining to a suppressive effect of the cytokine on colorectal carcinogenesis in vivo.…”

mentioning

confidence: 99%

Controlled release of TGF‐β1 impedes rat colon carcinogenesis in vivo

et al. 1998

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Transforming growth factor ␤ 1 (TGF-␤ 1 ) is a cytokine known to play a key role in the control of cell growth. TGF-␤ 1 potently inhibits the proliferation of human and rodentderived epithelial cells. Colonic precancerous and moderately differentiated cancer cells are responsive to TGF-␤ 1 , whereas malignant colon cancer cells are resistant to the inhibitory action of the cytokine. These observations have been derived exclusively from in vitro studies. Therefore, the main aim of our study was to determine whether TGF-␤ 1 exerts a growth-restraining action on colon carcinogenesis in vivo. TGF-␤ 1 was sequestered into ethylene acetate copolymer matrices and ''loaded'' preparations were implanted intraperitoneally (i.p.) in rats. One week later, the animals were treated with dimethylhydrazine (DMH), a colon procarcinogen. Empty matrices devoid of TGF-␤ 1 but containing bovine serum albumin (BSA) carrier served as the appropriate control preparations. The number of aberrant crypt foci (ACF), considered to be preneoplastic lesions of the colon, was scored. Tumor formation and size were assessed at the appropriate times. TGF-␤ 1 released in a sustained manner from copolymer matrices: (i) markedly inhibited colonic ACF formation and the number of aberrant crypts and (ii) significantly reduced colonic tumor formation and size. Int. J. Cancer 78:618-623, 1998. Wiley-Liss, Inc.Transforming growth-factor ␤ (TGF-␤ 1 ), a multifunctional 25 kDa peptide, regulates a variety of cellular processes, including proliferation, differentiation, migration and adhesion (Lawrence, 1996;Massagué and Polyak, 1995;Roberts and Sporn, 1987). The cytokine potently inhibits proliferation of human and rodentderived intestinal epithelial cells (Barnard et al., 1989;Kurokowa et al., 1987;Lamprecht et al., 1989). TGF-␤ 1 exerts a suppressive effect on cell growth by interfering with critical events of the cell cycle (Alexandrow and Moses, 1995;Ravitz and Wenner, 1997).Ample evidence is available showing that TGF-␤ restrains the growth of colon cancer cells (Lamprecht et al., 1989;Levine and Lewis, 1993;Mulder and Brattain, 1989;Wu et al., 1992). The escape from this negative regulation is thought to contribute to tumor progression (Filmus and Kerbel, 1993;Fynan and Reiss, 1993;Lamprecht et al., 1989;Mulder and Brattain, 1989). Colon cancer cells resistant to the TGF-␤ inhibitory action are poorly differentiated whereas precancerous and moderately differentiated colon tumor cells retain their response to TGF-␤ 1 (Hossein et al., 1987;Lahm and Odartchenko, 1993;Lamprecht et al., 1989;Levine and Lewis, 1993;Manning et al., 1991;Markowitz and Roberts, 1996;Mulder and Brattain, 1989) The results showing that the growth-restraining action of TGF-␤ on colon cancer cells is related to definite stages of their malignant progression derive exclusively from in vitro studies and no observation was hitherto available pertaining to a suppressive effect of the cytokine on colorectal carcinogenesis in vivo.Daunting challenges to design rational protocols of sus...

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Transforming growth factor-β2 is an autocrine growth inhibitory factor for the MOSER human colon carcinoma cell line

Cited by 8 publications

References 28 publications

Targeted deletion of Smad4 shows it is required for transforming growth factor β and activin signaling in colorectal cancer cells

Targeted deletion of Smad4 shows it is required for transforming growth factor β and activin signaling in colorectal cancer cells

Role of the transforming growth factor‐β signaling pathway in the pathogenesis of colorectal cancer

Controlled release of TGF‐β1 impedes rat colon carcinogenesis in vivo

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