Convergence of eicosanoid and integrin biology: Role of Src in 12-LOX activation

Dilly, Ashok K.; Tang, Keqin; Guo, Yande; Joshi, Sangeeta; Ekambaram, Prasanna; Maddipati, Krishna Rao; Cai, Yinlong; Tucker, Stephanie C.; Honn, Kenneth V.

doi:10.1016/j.yexcr.2016.12.011

Cited by 7 publications

(3 citation statements)

References 69 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Overexpression of the platelet 12-LOX in PC-3 prostate cancer cells results in 12(S)-HETE production which leads to the activation of transcription factors such as NF-κB resulting in increased MMP9 expression and in hypoxia inducible factor-1alpha (HIF-1alpha)-mediated in VEGF expression [ 71 , 72 , 117 ]. There is also evidence that platelet 12-LOX-mediated AA metabolism is responsible for radioresistance of prostate cancer cells and metastatic potential of melanoma cells [ 118 ].…”

Section: Platelet-associated Molecules and Therapymentioning

confidence: 99%

Antiplatelet agents for cancer treatment: a real perspective or just an echo from the past?

Wojtukiewicz

Hempel²,

Sierko

et al. 2017

Cancer Metastasis Rev

Self Cite

View full text Add to dashboard Cite

The association between coagulation and cancer development has been observed for centuries. However, the connection between inflammation and malignancy is also well-recognized. The plethora of evidence indicates that among multiple hemostasis components, platelets play major roles in cancer progression by providing surface and granular contents for several interactions as well as behaving like immune cells. Therefore, the anticancer potential of anti-platelet therapy has been intensively investigated for many years. Anti-platelet agents may prevent cancer, decrease tumor growth, and metastatic potential, as well as improve survival of cancer patients. On the other hand, there are suggestions that antiplatelet treatment may promote solid tumor development in a phenomenon described as “cancers follow bleeding.” The controversies around antiplatelet agents justify insight into the subject to establish what, if any, role platelet-directed therapy has in the continuum of anticancer management.

show abstract

Section: Platelet-associated Molecules and Therapymentioning

confidence: 99%

Antiplatelet agents for cancer treatment: a real perspective or just an echo from the past?

Wojtukiewicz

Hempel²,

Sierko

et al. 2017

Cancer Metastasis Rev

Self Cite

View full text Add to dashboard Cite

show abstract

“…In turn, these autonomously-generated gradients cause self-organization of the cells, such that they migrate as a group [ 46 , 47 ]. Although we have not detected differences in mRNA expression of the 12-S-HETE biosynthetic proteins, or the 12-S-HETE receptor (GPR31) between winner and loser GSCs, in human prostate cancer expression levels of GPR31 and 12-S-HETE both positively correlate with metastasis [ 48 , 49 ]. The link between relay signaling, clustering and competition is the subject of current studies.…”

Section: Discussionmentioning

confidence: 99%

Increased collective migration correlates with germline stem cell competition in a basal chordate

Fentress,

De Tomaso

2023

PLoS ONE

View full text Add to dashboard Cite

Cell competition is a process that compares the relative fitness of progenitor cells, resulting in winners, which contribute further to development, and losers, which are excluded, and is likely a universal quality control process that contributes to the fitness of an individual. Cell competition also has pathological consequences, and can create super-competitor cells responsible for tumor progression. We are studying cell competition during germline regeneration in the colonial ascidian, Botryllus schlosseri. Germline regeneration is due to the presence of germline stem cells (GSCs) which have a unique property: a competitive phenotype. When GSCs from one individual are transplanted into another, the donor and recipient cells compete for germline development. Often the donor GSCs win, and completely replace the gametes of the recipient- a process called germ cell parasitism (gcp). gcp is a heritable trait, and winner and loser genotypes can be found in nature and reared in the lab. However, the molecular and cellular mechanisms underlying gcp are unknown. Using an ex vivo migration assay, we show that GSCs isolated from winner genotypes migrate faster and in larger clusters than losers, and that cluster size correlates with expression of the Notch ligand, Jagged. Both cluster size and jagged expression can be manipulated simultaneously in a genotype dependent manner: treatment of loser GSCs with hepatocyte growth factor increases both jagged expression and cluster size, while inhibitors of the MAPK pathway decrease jagged expression and cluster size in winner GSCs. Live imaging in individuals transplanted with labeled winner and loser GSCs reveal that they migrate to the niche, some as small clusters, with the winners having a slight advantage in niche occupancy. Together, this suggests that the basis of GSC competition resides in a combination in homing ability and niche occupancy, and may be controlled by differential utilization of the Notch pathway.

show abstract

“…12-LOX has been identified as a crucial player in diabetes, skin diseases, thrombosis and cancers 15,22–27. There is increasing evidence that 12-LOX and 12-HETE promote tumor angiogenesis, growth and metastasis 28. Genetic studies suggest that mutations of 12-LOX are closely associated with tumorigenesis 29.…”

Section: Discussionmentioning

confidence: 99%

<p>12-Lipoxygenase promotes epithelial–mesenchymal transition via the Wnt/β-catenin signaling pathway in gastric cancer cells</p>

Yang¹,

Zhuang²,

Xie³

et al. 2019

OTT

View full text Add to dashboard Cite

Background 12-Lipoxygenase (12-LOX) plays a major role in the progression and metastasis of various types of cancer. In gastric cancer (GC), the expression level of 12-LOX is significantly up-regulated; however, its function, and underlying mechanism of action remain unclear. Methods The mRNA and protein expression levels of 12-LOX were assessed using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot analyses, respectively, in GC cell lines. 12-LOX expression was stably up-regulated using lentiviral vector in BGC823 and MGC803 cells, and cell-counting kit-8 (CCK8), colony formation, and invasion assays were performed to verify the function of 12-LOX in proliferation and metastasis. In addition, the expression levels of epithelial-mesenchymal transition (EMT) differentiation markers and downstream targets of the Wnt/β-catenin signaling pathway were examined by Western blotting. A nude mouse model of tumor growth and metastasis was established to investigate the role of 12-LOX in vivo. Results Our findings demonstrate that 12-LOX mRNA and protein were highly expressed in GC cell lines. 12-LOX overexpression promoted GC cell proliferation, migration, and invasion both in vitro and in vivo. In addition, up-regulation of 12-LOX promoted the EMT in GC cells, as reflected by a decrease in E-cadherin expression and an increase in N-cadherin and Snail expression. 12-LOX overexpression in GC cells also increased the expression of multiple downstream targets of the Wnt/β-catenin signaling pathway. Conclusion These findings revealed that 12-LOX functions as an oncogene in promoting GC cell proliferation and metastasis in vitro and in vivo. In addition, 12-LOX might regulate the EMT via the Wnt/β-catenin signaling pathway, indicating a potential role for 12-LOX as a target in GC treatment.

show abstract

Convergence of eicosanoid and integrin biology: Role of Src in 12-LOX activation

Cited by 7 publications

References 69 publications

Antiplatelet agents for cancer treatment: a real perspective or just an echo from the past?

Antiplatelet agents for cancer treatment: a real perspective or just an echo from the past?

Increased collective migration correlates with germline stem cell competition in a basal chordate

<p>12-Lipoxygenase promotes epithelial–mesenchymal transition via the Wnt/β-catenin signaling pathway in gastric cancer cells</p>

Contact Info

Product

Resources

About