scholarly journals Dual role of DR5 in death and survival signaling leads to TRAIL resistance in cancer cells

2017 ◽  
Vol 8 (8) ◽  
pp. e3025-e3025 ◽  
Author(s):  
Yelyzaveta Shlyakhtina ◽  
Valeria Pavet ◽  
Hinrich Gronemeyer
Author(s):  
Svetlana N. Rubtsova ◽  
Irina Y. Zhitnyak ◽  
Natalya A. Gloushankova
Keyword(s):  

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1299 ◽  
Author(s):  
Marek Nowak ◽  
Magdalena Klink

Tumor-associated macrophages (TAMs) constitute the main population of immune cells present in the ovarian tumor microenvironment. These cells are characterized by high plasticity and can be easily polarized by colony-stimulating factor-1, which is released by tumor cells, into an immunosuppressive M2-like phenotype. These cells are strongly implicated in both the progression and chemoresistance of ovarian cancer. The main pro-tumoral function of M2-like TAMs is the secretion of a variety of cytokines, chemokines, enzymes and exosomes that reach microRNAs, directly inducing the invasion potential and chemoresistance of ovarian cancer cells by triggering their pro-survival signaling pathways. The M2-like TAMs are also important players in the metastasis of ovarian cancer cells in the peritoneum through their assistance in spheroid formation and attachment of cancer cells to the metastatic area—the omentum. Moreover, TAMs interplay with other immune cells, such as lymphocytes, natural killer cells, and dendritic cells, to inhibit their responsiveness, resulting in the development of immunosuppression. The detrimental character of the M2-like type of TAMs in ovarian tumors has been confirmed by a number of studies, demonstrating the positive correlation between their high level in tumors and low overall survival of patients.


2004 ◽  
Vol 22 (14_suppl) ◽  
pp. 3143-3143
Author(s):  
T. Hata ◽  
H. Yamamoto ◽  
M. Ikeda ◽  
M. Yasui ◽  
I. Seshimo ◽  
...  

2018 ◽  
Vol 6 (4) ◽  
pp. 813-819 ◽  
Author(s):  
Sheng-Jen Cheng ◽  
Hsien-Yi Chiu ◽  
Priyank V. Kumar ◽  
Kuan Yu Hsieh ◽  
Jia-Wei Yang ◽  
...  

The capability of GO to simultaneously play the dual-role of a: (i) cellular imaging agent and (ii) drug delivery agent in cancer cells without the need for additional fluorescent protein labeling.


2004 ◽  
Vol 22 (14_suppl) ◽  
pp. 3143-3143
Author(s):  
T. Hata ◽  
H. Yamamoto ◽  
M. Ikeda ◽  
M. Yasui ◽  
I. Seshimo ◽  
...  

2009 ◽  
Vol 30 (9) ◽  
pp. 1497-1506 ◽  
Author(s):  
Peng Wang ◽  
Zhen Chen ◽  
Zhi-Qiang Meng ◽  
Jie Fan ◽  
Jian-Min Luo ◽  
...  

Biomolecules ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 126
Author(s):  
Rosa Fontana ◽  
Daniela Guidone ◽  
Tiziana Angrisano ◽  
Viola Calabrò ◽  
Alessandra Pollice ◽  
...  

Background: The ARF tumour suppressor plays a well-established role as a tumour suppressor, halting cell growth by both p53-dependent and independent pathways in several cellular stress response circuits. However, data collected in recent years challenged the traditional role of this protein as a tumour suppressor. Cancer cells expressing high ARF levels showed that its expression, far from being dispensable, is required to guarantee tumour cell survival. In particular, ARF can promote autophagy, a self-digestion pathway that helps cells cope with stressful growth conditions arising during both physiological and pathological processes. Methods: We previously showed that ARF is regulated through the activation of the protein kinase C (PKC)-dependent pathway and that an ARF phospho-mimetic mutant on the threonine residue 8, ARF-T8D, sustains cell proliferation in HeLa cells. We now explored the role of ARF phosphorylation in both basal and starvation-induced autophagy by analysing autophagic flux in cells transfected with either WT and ARF phosphorylation mutants by immunoblot and immunofluorescence. Results: Here, we show that endogenous ARF expression in HeLa cells is required for starvation-induced autophagy. Further, we provide evidence that the hyper-expression of ARF-T8D appears to inhibit autophagy in both HeLa and lung cancer cells H1299. This effect is due to the cells’ inability to elicit autophagosomes formation upon T8D expression. Conclusions: Our results lead to the hypothesis that ARF phosphorylation could be a mechanism through which the protein promotes or counteracts autophagy. Several observations underline how autophagy could serve a dual role in cancer progression, either protecting healthy cells from damage or aiding cancerous cells to survive. Our results indicate that ARF phosphorylation controls protein’s ability to promote or counteract autophagy, providing evidence of the dual role played by ARF in cancer progression.


Sign in / Sign up

Export Citation Format

Share Document