Inhibition and Promotion of Differentiated-Like Phenotype of a Human Lung Carcinoma in Athymic Mice by Natural and Recombinant Forms of Transforming Growth Factor-beta

Twardzik, D. R.; Ranchalis, Jane; McPherson, John M.; Ogawa, Yasushi; Gentry, L E; Purchio, A. F.; Plata, Ernest J.; Todaro, G. J.

doi:10.1093/jnci/81.15.1182

Cited by 33 publications

(14 citation statements)

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“…Transforming growth factor (TGF)-β inhibits the growth and induces differentiation of several lung and other carcinoma cells (Twardzik et al, 1989;Chakrabarty et al, 1990;Schroy et al, 1990). Glucocorticoids synergistically inhibit the growth of monocytoid leukaemia cells in combination with a low concentration of TGF-β (Kanatani et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Vesnarinone and glucocorticoids cooperatively induce G1 arrest and have an anti-tumour effect on human non-small cell lung carcinoma cells grown in nude mice

1999

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Vesnarinone, an oral cardiotonic, inhibited the growth of several human non-small cell lung carcinoma cell lines, and its anti-proliferative effects in vitro and in vivo were greatly enhanced by combination with glucocorticoids, but not other steroids. Simultaneous treatment with vesnarinone and dexamethasone is the most effective to evoke the synergistic effect in the growth inhibition of lung carcinoma EBC-1 cells. Dexamethasone and other glucocorticoids induced morphological changes in EBC-1 cells and these agents together with vesnarinone induced alkaline phosphatase activity, which is a typical marker of type II pneumocyte maturation. This treatment arrested the growth of the cells at the G 1 phase, indicating that this treatment is cytostatic rather than cytotoxic. These results suggest that vesnarinone plus glucocorticoid might be useful in lung cancer therapy. © 1999 Cancer Research Campaign

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Section: Discussionmentioning

confidence: 99%

Vesnarinone and glucocorticoids cooperatively induce G1 arrest and have an anti-tumour effect on human non-small cell lung carcinoma cells grown in nude mice

1999

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“…These solid tumors include neuroblastoma [13], glioma [14], pheochromocytoma [15], retinoblastoma [16], melanoma [17], teratoma [18], salivary gland tumor [8][9][10][11][12], breast cancer [19], colon cancer [20][21][22], lung cancer [23][24][25][26], pancreatic cancer [27], uterine cervical cancer [28], skin cancer [29], laryngeal cancer [30], rhabdomyosarcoma [31], and liposarcoma [32]. Differentiation inducers on solid tumors ( Table 1) can be divided in to two categories.…”

Section: Differentiation Of Several Solid Tumor Cells By Several Diffmentioning

confidence: 99%

Differentiation-Inducing Therapy for Solid Tumors

Kawamata

Tachibana²,

Fujimori³

et al. 2006

CPD

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Treating malignant tumor through the induction of cell differentiation has been an attractive concept, but clinical development of differentiation-inducing agents to treat malignant tumor, especially for solid tumors has been limited to date. Nerve growth factor, all trans retinoic acid, dimethyl sulfoxide, active form vitamin D(3), peroxisome proliferator-activated receptorgamma, 12-0-tetradecanoylphorbol 13-acetate, hexamethylene-bis-acetamide, transforming growth factor-beta, butyric acid, cAMP, and vesnarinone are known to have a differentiation-inducing capability on solid tumors in vitro and/or in vivo. Moreover some of the differentiation-inducing agents have been used for treating patients with solid tumor, but the therapeutic effect of the differentiation-inducing agents on solid tumor is not strong when compared with that of conventional chemotherapeutic agents. However, because most of the differentiation-inducing agents can potentiate the effect of conventional chemotherapy or radiation therapy, combination of differentiation-inducing therapy with conventional chemotherapy or radiation therapy might be used as a second- or third-line therapy in patients with advanced cancer. Furthermore, analysis of the molecular mechanisms of the tumor differentiation therapy might provide selective and targeted molecules for novel cancer therapy.

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“…Other proteases are known to either activate the small latent complex and/or proteolytically cleave LTBP1. Initial studies were performed using recombinant small latent TGFb1 and TGFb2 from CHO cell conditioned medium as described previously (Gentry et al, 1987;Twardzik et al, 1989). Plasmin was used as a positive control for the activation of small latent TGFb1 (Fig.…”

Section: Activation Of Latent Tgfb2 By Psamentioning

confidence: 99%

Preferential production of latent transforming growth factor β‐2 by primary prostatic epithelial cells and its activation by prostate‐specific antigen

Dallas

Zhao

Cramer

et al. 2004

Journal Cellular Physiology

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Three mammalian isoforms of transforming growth factor-beta (TGFbeta) are known, TGFbeta1, 2, and 3, that have non-overlapping functions during development. However, their specific roles in cancers such as prostate cancer are less clear. Here we show that primary cultures of prostatic epithelial cells preferentially produce and activate the latent TGFbeta2 isoform. Paired cultures of normal and malignant prostate cells from prostate cancer patients produced predominantly the TGFbeta2 isoform, with 30- to 70-fold less TGFbeta1. By mono-Q ion exchange chromatography, three major peaks of latent TGFbeta2 activity were observed corresponding to the known small latent TGFbeta2 complex, the known large latent TGFbeta2 complex and a novel eluting peak of latent TGFbeta2. Although prostate cells are known to activate latent TGFbeta, the mechanism for activation is currently unclear. We investigated whether prostate specific antigen (PSA), a serine protease used as a clinical marker for prostate cancer, could play a role in the activation of latent TGFbeta. Unlike plasmin, a known activator of both latent TGFbeta1 and 2, PSA specifically activated the recombinant small latent form of TGFbeta2, but not TGFbeta1. Prostate epithelial cells, therefore, preferentially produce the TGFbeta2 isoform and PSA, a protease produced by the prostate, specifically targets the activation of this TGFbeta isoform. PSA-mediated activation of latent TGFbeta2 may be an important mechanism for autocrine TGFbeta regulation in the prostate and may potentially contribute to the formation of osteoblastic lesions in bone metastatic prostate cancer.

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Inhibition and Promotion of Differentiated-Like Phenotype of a Human Lung Carcinoma in Athymic Mice by Natural and Recombinant Forms of Transforming Growth Factor-beta

Cited by 33 publications

References 0 publications

Vesnarinone and glucocorticoids cooperatively induce G1 arrest and have an anti-tumour effect on human non-small cell lung carcinoma cells grown in nude mice

Vesnarinone and glucocorticoids cooperatively induce G1 arrest and have an anti-tumour effect on human non-small cell lung carcinoma cells grown in nude mice

Differentiation-Inducing Therapy for Solid Tumors

Preferential production of latent transforming growth factor β‐2 by primary prostatic epithelial cells and its activation by prostate‐specific antigen

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