More with some of the missing ones 5) (More)

More with some of the missing ones


5) (More) Melanoma
New Cases: 96k Deaths: 7k
Nov 2018
https://onlinelibrary.wiley.com/doi/abs/10.1002/path.5207
High expression of CCR5 in melanoma enhances epithelial–mesenchymal transition and metastasis via TGFβ1
We found that CCR5 was more abundant in melanoma cells than normal cells and was positively associated with tumor malignancy in clinical patients. Animal experiments suggested that CCR5 deficiency in B16/F10 or A375 cells suppressed primary tumor growth and lung metastasis, whereas CCR5 overexpression in B16/F0 cells enhanced primary tumor growth and lung metastasis. CCR5 played a critical role in proliferation and migration of melanoma cells in vitro. Importantly, CCR5 was required for maintenance of the mesenchymal phenotype of metastatic melanoma cells. Mechanistically, CCR5 positively regulated expression of TGFβ1, which in turn induced epithelial–mesenchymal transition and migration via PI3K/AKT/GSK3β signaling. Collectively, our results establish a critical role of CCR5 expressed by melanoma cells in cancer progression and reveal the novel mechanisms controlling this process, which suggests the prognostic value of CCR5 in melanoma patients and provides novel insights into CCR5‐targeted strategies for melanoma treatment.

10)Leukemia
New Cases: 62k Deaths: 23k
April 2017
https://www.ncbi.nlm.nih.gov/pubmed/28469959
Treatment with the C-C chemokine receptor type 5 (CCR5)-inhibitor maraviroc suppresses growth and induces apoptosis of acute lymphoblastic leukemia cells.

Here we report that CCR5 selective inhibitor significantly inhibited ALL cells SUP-B15 growth and induced SUP-B15 cells to undergo cell apoptosis. This cell apoptosis was associated with increased levels of cleavage of caspase-3 and caspase-9, and Poly (ADP-ribose) polymerase (PARP). Moreover, we demonstrated that maraviroc strongly inhibited SUP-B15 cells migration to C-X-C motif chemokine ligand 12 (CXCL12) and CXCL13, and adhesion to fibronectin and vascular cell adhesion molecule 1 (VCAM-1) in vitro. Importantly, CCR5-activated signaling proteins Janus Kinase 1 (JAK1), JAK2 and signal transducer and activator of transcription (STAT3) were inhibited by maraviroc. Finally, maraviroc suppressed the growth of SUP-B15 xenograft tumors in athymic mice. Collectively, this study demonstrated that CCR5 inhibition by maraviroc has the potential for the treatment of human ALL.

11) More with Pancreatic
New Cases: 57k Deaths: 46k
Jan 2018
https://www.nature.com/articles/s41598-018-19643-0
CCR5/CCL5 axis interaction promotes migratory and invasiveness of pancreatic cancer cells


13) Liver
New Cases: 42k Deaths: 31k
Sept 2013
https://www.ncbi.nlm.nih.gov/pubmed/23526353
Inflammation-induced hepatocellular carcinoma is dependent on CCR5 in mice.
Our results indicate that CCR5 has a critical role in both the development and progression of liver cancer. Therefore, we propose that a CCR5 antagonist can serve for HCC cancer prevention and treatment.

Cervical
New Cases: 12k Deaths: 4k
Feb 2016
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4734227/
Downregulation of CCR5 inhibits the proliferation and invasion of cervical cancer cells and is regulated by microRNA-107

Aug 2014
https://academic.oup.com/molehr/article/20/11/1144/2459719
CCR5 expression is elevated in cervical cancer cells and is up-regulated by seminal plasma