RelB promotes the migration and invasion of prostate cancer DU145 cells via exosomal ICAM1 in vitro

Li, Wenjing; Xu, Jingjing; Cheng, Li; Zhao, Chenyi; Zhang, Lianjun; Shao, Qiang; Guo, Feng

doi:10.1016/j.cellsig.2021.110221

Cited by 11 publications

(11 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This may suggest that exosomes derived from pathological contexts, in this case PCa, can promote the migration capacity of tumoral cells. These results agree with those observed by Li et al in 2022, where they showed that intracellular adhesion molecule 1 (ICAM‐1), whose presence has been described in PCa exosomes, is able to promote PCa DU145 cell migration by interacting with RelB, a component of the NF‐κB pathway 33 . From a clinical point of view, it is interesting to note that castration‐resistant cell lines, regardless of the degree of cell differentiation in prostate cancer patients, develop the ability to migrate.…”

Section: Discussionsupporting

confidence: 92%

“…These results agree with those observed by Li et al in 2022, where they showed that intracellular adhesion molecule 1 (ICAM-1), whose presence has been described in PCa exosomes, is able to promote PCa DU145 cell migration by interacting with RelB, a component of the NF-κB pathway. 33 From a clinical point of view, it is interesting to note that castration-resistant cell lines, regardless of the degree of cell differentiation in prostate cancer patients, develop the ability to migrate. In this respect, it should be noted that the samples from the patients with more poorly differentiated International Society of Urological Pathology (ISUP) five grades were mostly metastatic.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Induction of more aggressive tumoral phenotypes in LNCaP and PC3 cells by serum exosomes from prostate cancer patients

Huertas‐Lárez

Muñoz‐Moreno

Recio‐Aldavero

et al. 2023

Intl Journal of Cancer

View full text Add to dashboard Cite

Prostate cancer (PCa) is the second most frequent and sixth most fatal cancer in men worldwide. Despite its high prevalence, our understanding of its etiology and the molecular mechanisms involved in the progression of the disease is substantially limited. In recent years, the potential participation of exosomes in this process has been suggested. Therefore, we aim to study the effect of exosomes isolated from the serum of patients with PCa on various cellular processes associated with increased tumor aggressiveness in two PCa cell lines: LNCaP‐FGC and PC3. The exosomes were isolated by filtration wand ultracentrifugation. Their presence was confirmed by immunodetection of specific markers and their size distribution was analyzed by Dynamic Light Scattering (DLS). The results obtained demonstrated that serum exosomes from PCa patients increased migration of PC3 cells and neuroendocrine differentiation of LNCaP‐FGC cells regardless of the grade of the tumor. PCa serum exosomes also enhanced the secretion of enzymes related to invasiveness and resistance to chemotherapeutics, such as extracellular matrix metalloproteases 2 and 9, and gamma‐glutamyltransferase in both cell lines. Altogether, these findings support the pivotal participation of exosomes released by tumoral cells in the progression of PCa. Future studies on the molecular mechanisms involved in the observed changes could provide crucial information on this disease and help in the discovery of new therapeutic targets.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Induction of more aggressive tumoral phenotypes in LNCaP and PC3 cells by serum exosomes from prostate cancer patients

Huertas‐Lárez

Muñoz‐Moreno

Recio‐Aldavero

et al. 2023

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…(2) Intracellular Adhesion Molecule 1 (ICAM-1) has been correlated with M2-macrophage polarization, as identified in lung cancer [ 42 ]. In addition, migration and invasion of mutant p53 PC cells is promoted by their exosomal packaging of ICAM-1 [ 43 ]. This data suggests that at 12 weeks, Trp53 (R245W/R245W) tumours exhibit a novel GOF linked to the accumulation of tumour associated macrophage-monocyte populations.…”

Section: Resultsmentioning

confidence: 99%

Modelling aggressive prostate cancers of young men in immune-competent mice, driven by isogenic Trp53 alterations and Pten loss

et al. 2022

View full text Add to dashboard Cite

Understanding prostate cancer onset and progression in order to rationally treat this disease has been critically limited by a dire lack of relevant pre-clinical animal models. We have generated a set of genetically engineered mice that mimic human prostate cancer, initiated from the gland epithelia. We chose driver gene mutations that are specifically relevant to cancers of young men, where aggressive disease poses accentuated survival risks. An outstanding advantage of our models are their intact repertoires of immune cells. These mice provide invaluable insight into the importance of immune responses in prostate cancer and offer scope for studying treatments, including immunotherapies. Our prostate cancer models strongly support the role of tumour suppressor p53 in functioning to critically restrain the emergence of cancer pathways that drive cell cycle progression; alter metabolism and vasculature to fuel tumour growth; and mediate epithelial to mesenchymal-transition, as vital to invasion. Importantly, we also discovered that the type of p53 alteration dictates the specific immune cell profiles most significantly disrupted, in a temporal manner, with ramifications for disease progression. These new orthotopic mouse models demonstrate that each of the isogenic hotspot p53 amino acid mutations studied (R172H and R245W, the mouse equivalents of human R175H and R248W respectively), drive unique cellular changes affecting pathways of proliferation and immunity. Our findings support the hypothesis that individual p53 mutations confer their own particular oncogenic gain of function in prostate cancer.

show abstract

“…ETS1, the founder of the large ETS transcription factor family, functions primarily as a transcriptional activator and drives key events in advanced cancer progression [ 34 ]. According to previous studies, transcription factors can influence the expression of nucleic acids or proteins in tumor cell exosomes, thereby altering tumorigenesis and progression [ 35 – 37 ]. However, the effects of ETS1 on the release and composition of exosomes derived from ovarian cancer cells remain unknown.…”

Section: Discussionmentioning

confidence: 99%

Laminins in tumor-derived exosomes upregulated by ETS1 reprogram omental macrophages to promote omental metastasis of ovarian cancer

Zeng

Shu

et al. 2022

Cell Death Dis

View full text Add to dashboard Cite

Tumor-derived exosomes participate in omental metastatic colonization of ovarian cancer by inducing an adaptive response in the tumor microenvironment. However, cell–cell communication via exosomes between primary tumor cells and the microenvironment of distant omentum and the mechanism of pre-metastatic niche formation are poorly understood. Here, we demonstrated that ETS1-overexpressing ovarian cancer cells secreted larger exosomes with higher laminin levels. In addition, ovarian cancer exosomes could be taken up by omental macrophages through integrin and laminin interaction. Compared with control exosomes, exosomes derived from ETS1-overexpressing ovarian cancer cells (LV-ETS1 Exos) stimulated the polarization of more macrophages toward the M2 phenotype (CD163 marker), as well as the production of more CXCL5 and CCL2 in macrophages, via integrin αvβ5/AKT/Sp1 signaling. In vivo experiments showed that LV-ETS1 Exos promoted omental metastasis of ovarian cancer by mediating the tumor-promoting effect of macrophages, which could be neutralized by integrin ανβ5 inhibitor cilengitide. These results indicated that ETS1 could drive ovarian cancer cells to release exosomes with higher laminin levels, thereby accelerating the exosome-mediated pro-metastatic effects of omental macrophages via the integrin αvβ5/AKT/Sp1 signaling pathway, and the integrin ανβ5 inhibitor cilengitide could inhibit omental metastasis of ovarian cancer driven by tumor-derived exosomes.

show abstract

RelB promotes the migration and invasion of prostate cancer DU145 cells via exosomal ICAM1 in vitro

Cited by 11 publications

References 30 publications

Induction of more aggressive tumoral phenotypes in LNCaP and PC3 cells by serum exosomes from prostate cancer patients

Induction of more aggressive tumoral phenotypes in LNCaP and PC3 cells by serum exosomes from prostate cancer patients

Modelling aggressive prostate cancers of young men in immune-competent mice, driven by isogenic Trp53 alterations and Pten loss

Laminins in tumor-derived exosomes upregulated by ETS1 reprogram omental macrophages to promote omental metastasis of ovarian cancer

Contact Info

Product

Resources

About