Expression of bcl-2 and bax in TGF-β1-induced apoptosis of L1210 leukemic cells

Motyl, T.; Grzelkowska, K.; Zimowska, Wioletta; Skierski, Janusz; Warȩski, Przemyslaw; Płoszaj, Tomasz; Trzeciak, Lech

doi:10.1016/s0171-9335(98)80070-8

Cited by 49 publications

(38 citation statements)

References 32 publications

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“…A role for p53 in the growth-inhibitory actions of TGF-␤1 on primitive hematopoietic cells was also recently suggested following the detection of a TGF-␤1-resistant subpopulation in HPP-CFC (very primitive progenitors) isolated from p53-deficient but not wild type mice (50). In contrast to the data obtained from Sasaki et al Recent studies on leukemic cell lines have suggested that the proapoptotic effects of TGF-␤1 may be mediated in part through the modulation of Bcl-2 family members (37)(38)(39). In this study, we have shown that TGF-␤1-induced apoptosis of FDCP-Mix cells is associated with a down-regulation in Bcl-2 but not Bcl-x L expression.…”

Section: Tgf-␤1-mediated Apoptosis Is Inhibited By Expression Of Bcl-mentioning

confidence: 97%

Transforming Growth Factor-β1 Induces Apoptosis Independently of p53 and Selectively Reduces Expression of Bcl-2 in Multipotent Hematopoietic Cells

Francis¹,

Heyworth²,

Spooncer³

et al. 2000

Journal of Biological Chemistry

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Section: Tgf-␤1-mediated Apoptosis Is Inhibited By Expression Of Bcl-mentioning

confidence: 97%

Transforming Growth Factor-β1 Induces Apoptosis Independently of p53 and Selectively Reduces Expression of Bcl-2 in Multipotent Hematopoietic Cells

Francis¹,

Heyworth²,

Spooncer³

et al. 2000

Journal of Biological Chemistry

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“…Radiation Causes an Increase in Bax mRNA and Protein Expression in MIA PaCa-2/RII Cells-TGF-␤ signaling has been implicated in the induction of apoptosis through a variety of mechanisms including the activation of caspases, the downregulation of Bcl-2 and related family members, and the induction of Bax (56). We determined whether these factors might play a role in enhancing radiation-induced apoptosis of MIA PaCa-2/RII transfectants.…”

Section: P21mentioning

confidence: 99%

Restoration of Transforming Growth Factor-β Signaling Enhances Radiosensitivity by Altering the Bcl-2/Bax Ratio in the p53 Mutant Pancreatic Cancer Cell Line MIA PaCa-2

Ahmed

Alcock

Damodaran³

et al. 2002

Journal of Biological Chemistry

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In this study, we investigated whether lack of transforming growth factor ␤ (TGF-␤) type II receptor (RII) expression and loss of TGF-␤ signaling played a role in radiation resistance of pancreatic cancer cells MIA PaCa-2 that possess a mutated p53 gene. Transfection of this cell line with a RII cDNA led to a stimulation of the transcriptional activity of p3TP-Lux, a TGF-␤؊respon-sive reporter construct. The RII transfectants (MIA PaCa-2/RII) showed a significant increase in sensitivity to radiation when compared with MIA PaCa-2/vector cells. The increase in sensitivity to radiation was reversed by neutralizing antibodies to TGF-␤, indicating that these changes were dependent on TGF-␤ signaling.

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“…Stimulation and inhibition of expression of proand anti-apoptotic Bcl family members, respectively, with subsequent caspase activation has been implicated in TGF-b-induced apoptosis (Fig. 3) (Motyl et al, 1998;Francis et al, 2000;Chipuk et al, 2001;Kim et al, 2001). In addition, TGF-b-mediated induction of Id3 expression in primary B lymphocyte progenitors (Kee et al, 2001), TIEG in mink lung epithelial and Hep3B cells (Chalaux et al, 1999;Ribeiro et al, 1999), and TGFb-stimulated clone 22 (TSC-22) in gastric carcinoma cells (Ohta et al, 1997), have been implicated in apoptosis.…”

Section: Regulation Of Apoptosis By Smadsmentioning

confidence: 99%

Regulation of cell proliferation by Smad proteins

Dijke

Goumans

Itoh

2002

Journal Cellular Physiology

399

278

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Transforming growth factor-b (TGF-b) family members which include TGF-bs, activins, and bone morphogenetic proteins (BMPs) regulate a broad spectrum of biological responses on a large variety of cell types. TGF-b family members initiate their cellular responses by binding to distinct receptors with intrinsic serine/ threonine kinase activity and activation of speci®c downstream intracellular effectors termed Smad proteins. Smads relay the signal from the cell membrane to the nucleus, where they affect the transcription of target genes. Smad activation, subcellular distribution, and stability have been found to be intricately regulated and a broad array of transcription factors have been identi®ed as Smad partners. Important activities of TGF-b are its potent anti-mitogenic and pro-apoptotic effects that, at least in part, are mediated via Smad proteins. Escape from TGF-b/ Smad-induced growth inhibition and apoptosis is frequently observed in tumors. Certain Smads have been found to be mutated in speci®c types of cancer and gene ablation of particular Smads in mice has revealed increased rate of tumorigenesis. In late stage tumors, TGF-b has been shown to function as a tumor promoter. TGFb can stimulate the de-differentiation of epithelial cells to malignant invasive and metastatic ®broblastic cells. Interestingly, TGF-b may mediate these effects directly on tumor cells via subverted Smad-dependent and/or Smad-independent pathways.

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Expression of bcl-2 and bax in TGF-β1-induced apoptosis of L1210 leukemic cells

Cited by 49 publications

References 32 publications

Transforming Growth Factor-β1 Induces Apoptosis Independently of p53 and Selectively Reduces Expression of Bcl-2 in Multipotent Hematopoietic Cells

Transforming Growth Factor-β1 Induces Apoptosis Independently of p53 and Selectively Reduces Expression of Bcl-2 in Multipotent Hematopoietic Cells

Restoration of Transforming Growth Factor-β Signaling Enhances Radiosensitivity by Altering the Bcl-2/Bax Ratio in the p53 Mutant Pancreatic Cancer Cell Line MIA PaCa-2

Regulation of cell proliferation by Smad proteins

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