Decreased TumorigenicityIn VivoWhen Transforming Growth Factor β Treatment Causes Cancer Cell Senescence

2003 ◽  
Vol 67 (4) ◽  
pp. 815-821 ◽  
Author(s):  
Yoshinori KATAKURA ◽  
Eriko NAKATA ◽  
Yukiko TABIRA ◽  
Takumi MIURA ◽  
Kiichiro TERUYA ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cancer Cell ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Cell Senescence

scholarly journals N6-Isopentenyladenosine promoted HeLa cell apoptosis through inhibitions of AKT and transforming growth factor β–activated kinase 1 activation

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769596 ◽  
Author(s):  
Miao Li ◽  
Yonghao Qi ◽  
Jing Wei ◽  
Lulu Lu ◽  
Xuan Zhao ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Cancer Cell ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Tumor Necrosis Factor Receptor ◽  
Transforming Growth Factor Β ◽  
Associated Factor ◽  
New Gene ◽  
Necrosis Factor

N6-Isopentenyladenosine, a member of the family of plant hormones, possesses anti-cancer activities on a number of cancer cell lines. However, its mode of action in cervical cancer cell remains poorly understood. Our computational docking studies showed that N6-Isopentenyladenosine could bind with the really interesting new gene domain of tumor necrosis factor receptor–associated factor 6, which is an ubiquitination E3 ligase. Tumor necrosis factor receptor–associated factor 6–mediated ubiquitination is known to activate both protein kinase B (also known as AKT) and transforming growth factor β–activated kinase 1, and the really interesting new gene domain comprises the core of the ubiquitin ligase catalytic domain. First, we evaluated the effects of iPA on cervical cancer cell line HeLa using MTT and flow cytometry. Second, we examined the effects of iPA on activation of tumor necrosis factor receptor–associated factor 6–mediated downstream targets using western blot or immunoprecipitation. iPA could reduce HeLa cell proliferation through apoptosis, and such anti-cancer activity is associated with inhibitions of both AKT and transforming growth factor β–activated kinase 1 signaling pathways. In addition, suppression of the anti-apoptotic protein Bcl-2 and elevation of the pro-apoptotic protein Bax were also observed. Anti-proliferation properties of iPA are likely due to its binding at the really interesting new gene domain of tumor necrosis factor receptor–associated factor 6 and loss of AKT and transforming growth factor β–activated kinase 1 activities as a result of functional modulations of tumor necrosis factor receptor–associated factor 6. These results support the emerging notion that tumor necrosis factor receptor–associated factor 6 could serve as a viable target for developing new cancer therapeutics.

scholarly journals Transforming Growth Factor-β and Oxidative Stress in Cancer: A Crosstalk in Driving Tumor Transformation

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 3093
Author(s):  
Valeria Ramundo ◽  
Giuliana Giribaldi ◽  
Elisabetta Aldieri
Keyword(s):  
Oxidative Stress ◽  
Growth Factor ◽  
Cancer Cell ◽  
Transforming Growth Factor ◽  
Cell Metabolism ◽  
Transforming Growth Factor Β ◽  
Ros Production ◽  
Redox Imbalance ◽  
Cancer Cell Metabolism ◽  
And Oxidative Stress

Cancer metabolism involves different changes at a cellular level, and altered metabolic pathways have been demonstrated to be heavily involved in tumorigenesis and invasiveness. A crucial role for oxidative stress in cancer initiation and progression has been demonstrated; redox imbalance, due to aberrant reactive oxygen species (ROS) production or deregulated efficacy of antioxidant systems (superoxide dismutase, catalase, GSH), contributes to tumor initiation and progression of several types of cancer. ROS may modulate cancer cell metabolism by acting as secondary messengers in the signaling pathways (NF-kB, HIF-1α) involved in cellular proliferation and metastasis. It is known that ROS mediate many of the effects of transforming growth factor β (TGF-β), a key cytokine central in tumorigenesis and cancer progression, which in turn can modulate ROS production and the related antioxidant system activity. Thus, ROS synergize with TGF-β in cancer cell metabolism by increasing the redox imbalance in cancer cells and by inducing the epithelial mesenchymal transition (EMT), a crucial event associated with tumor invasiveness and metastases. Taken as a whole, this review is addressed to better understanding this crosstalk between TGF-β and oxidative stress in cancer cell metabolism, in the attempt to improve the pharmacological and therapeutic approach against cancer.

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