Menée in vitro, cette étude met en évidence un mécanisme par lequel la nicotine, en perturbant les réactions d'oxydoréduction intracellulaires et en altérant la fonction de la protéine p53, favorise la tumorigenèse pulmonaire

Nicotine exposure potentiates lung tumorigenesis by perturbing cellular surveillance

Zhang, Qiang ; Ganapathy, Suthakar ; Avraham, Hava ; Nishioka, Takashi ; Chen, Changyan

Background : Nicotine is a major tobacco component and found at circulating concentrations in smokers’ bloodstreams. Although considered a non-carcinogenic substance, nicotine rapidly defuses to tissues after being inhaled, inviting effects on cellular physiology, particularly in the lung. Widespread increased use of nicotine-based e-cigarettes, especially in younger adults, creates an urgent need for improved understanding of nicotine’s potential to impact human health. Methods : Biological [...]

Menée sur des lignées cellulaires de cancer mammaire et à l'aide d'échantillons tumoraux humains, cette étude met en évidence un mécanisme par lequel l'acide lipoïque (un cofacteur impliqué dans le métabolisme oxydatif), réduit la prolifération des cellules cancéreuses en inhibant le récepteur de l'IGF1 via la diminution de l'expression de la furine, une convertase impliquée dans la maturation de ce récepteur

Lipoic acid decreases breast cancer cell proliferation by inhibiting IGF-1R via furin downregulation

Farhat, Diana ; Léon, Sophie ; Ghayad, Sandra E. ; Gadot, Nicolas ; Icard, Philippe ; Le Romancer, Muriel ; Hussein, Nader ; Lincet, Hubert

Background : Breast cancer is the second most common cancer in the world. Despite advances in therapies, the mechanisms of resistance remain the underlying cause of morbidity and mortality. Lipoic acid (LA) is an antioxidant and essential cofactor in oxidative metabolism. Its potential therapeutic effects have been well documented, but its mechanisms of action (MOA) are not fully understood. Methods : The aim of this study is to validate the inhibitory LA effect on the proliferation of various [...]

Menée in vitro et à l'aide d'un modèle murin de cancer du sein métastatique, cette étude met en évidence un mécanisme par lequel la kinase AKAP8, une protéine liant l'ARN, supprime le développement de métastases tumorales en inhibant l'épissage alternatif associé à la transition épithélio-mésenchymateuse

The RNA-binding protein AKAP8 suppresses tumor metastasis by antagonizing EMT-associated alternative splicing

Hu, Xiaohui ; Harvey, Samuel E. ; Zheng, Rong ; Lyu, Jingyi ; Grzeskowiak, Caitlin L. ; Powell, Emily ; Piwnica-Worms, Helen ; Scott, Kenneth L. ; Cheng, Chonghui

Alternative splicing has been shown to causally contribute to the epithelial–mesenchymal transition (EMT) and tumor metastasis. However, the scope of splicing factors that govern alternative splicing in these processes remains largely unexplored. Here we report the identification of A-Kinase Anchor Protein (AKAP8) as a splicing regulatory factor that impedes EMT and breast cancer metastasis. AKAP8 not only is capable of inhibiting splicing activity of the EMT-promoting splicing regulator hnRNPM [...]

Menée in vitro et à l'aide de xénogreffes sur un modèle murin, cette étude met en évidence un mécanisme par lequel HSP47, une protéine chaperon facilitant la sécrétion et le dépôt de collagène, favorise le développement de métastases en augmentant l'interaction entre les plaquettes sanguines et les cellules cancéreuses

Hsp47 promotes cancer metastasis by enhancing collagen-dependent cancer cell-platelet interaction

Xiong, Gaofeng ; Chen, Jie ; Zhang, Guoying ; Wang, Shike ; Kawasaki, Kunito ; Zhu, Jieqing ; Zhang, Yan ; Nagata, Kazuhiro ; Li, Zhenyu ; Zhou, Binhua P. ; Xu, Ren

Cancer cell–platelet interaction is crucial for cancer metastasis; however, how this interaction is regulated remains largely unknown. We have identified Hsp47 as an EMT inducer and showed that Hsp47 and its dependent collagen secretion enhanced cancer cell–platelet interaction. Importantly, Hsp47-induced cancer cell–platelet interaction enhanced cancer cell clustering, which is crucial for cancer cell colonization at distant sites. We also found that Hsp47 gene amplification and expression [...]

Menée in vitro, cette étude met en évidence le rôle de l'isocitrate déshydrogénase, de la protéine TAU et du récepteur de l'EGFR dans le caractère agressif des gliomes diffus

The IDH-TAU-EGFR triad defines the neovascular landscape of diffuse gliomas

Gargini, Ricardo ; Segura-Collar, Berta ; Herránz, Beatriz ; García-Escudero, Vega ; Romero-Bravo, Andrés ; Nunez, Felipe J. ; García-Pérez, Daniel ; Gutiérrez-Guamán, Jacqueline ; Ayuso-Sacido, Angel ; Seoane, Joan ; Perez-Nuñez, Angel ; Sepulveda-Sanchez, Juan M. ; Hernández-Laín, Aurelio ; Castro, Maria G. ; Garcia-Escudero, Ramon ; Ávila, Jesús ; Sánchez-Gómez, Pilar

Gliomas, brain tumors originating in glial cells, are classified according to histologic as well as genetic features. Mutations in the IDH1/2 genes are associated with more favorable prognosis, whereas mutations in EGFR are characteristic of aggressive tumors. How these genes affect the microenvironment is not completely clear. Now, Gargini et al. show that TAU protein, classically associated with neurodegenerative disorders, is increased in less aggressive tumors. TAU inhibited the transition [...]

Cet article passe en revue les connaissances concernant le cycle de vie dans le stroma tumoral des fibroblastes associés au cancer, analyse les implications cliniques liées à leur activation ainsi que les stratégies thérapeutiques ciblant cette activation

The life cycle of cancer-associated fibroblasts within the tumour stroma and its importance in disease outcome

D’Arcangelo, Elisa ; Wu, Nila C. ; Cadavid, Jose L. ; McGuigan, Alison P.

The tumour microenvironment (TME) determines vital aspects of tumour development, such as tumour growth, metastases and response to therapy. Cancer-associated fibroblasts (CAFs) are abundant and extremely influential in this process and interact with cellular and matrix TME constituents such as endothelial and immune cells and collagens, fibronectin and elastin, respectively. However, CAFs are also the recipients of signals—both chemical and physical—that are generated by the TME, and their [...]