PMID- 31724498
OWN - NLM
STAT- MEDLINE
DCOM- 20201201
LR  - 20201201
IS  - 1875-533X (Electronic)
IS  - 0929-8673 (Linking)
VI  - 27
IP  - 33
DP  - 2020
TI  - The CXCL12-CXCR4 Signaling Axis Plays a Key Role in Cancer Metastasis and is a 
      Potential Target for Developing Novel Therapeutics against Metastatic Cancer.
PG  - 5543-5561
LID - 10.2174/0929867326666191113113110 [doi]
AB  - Metastasis is the main cause of death in cancer patients; there is currently no 
      effective treatment for cancer metastasis. This is primarily due to our 
      insufficient understanding of the metastatic mechanisms in cancer. An increasing 
      number of studies have shown that the C-X-C motif chemokine Ligand 12 (CXCL12) is 
      overexpressed in various tissues and organs. It is a key niche factor that 
      nurtures the pre-metastatic niches (tumorigenic soil) and recruits tumor cells 
      (oncogenic "seeds") to these niches, thereby fostering cancer cell aggression and 
      metastatic capabilities. However, the C-X-C motif chemokine Receptor 4 (CXCR4) is 
      aberrantly overexpressed in various cancer stem/progenitor cells and functions as 
      a CXCL12 receptor. CXCL12 activates CXCR4 as well as multiple downstream multiple 
      tumorigenic signaling pathways, promoting the expression of various oncogenes. 
      Activation of the CXCL12-CXCR4 signaling axis promotes Epithelial-Mesenchymal 
      Transition (EMT) and mobilization of cancer stem/progenitor cells to 
      pre-metastatic niches. It also nurtures cancer cells with high motility, 
      invasion, and dissemination phenotypes, thereby escalating multiple proximal or 
      distal cancer metastasis; this results in poor patient prognosis. Based on this 
      evidence, recent studies have explored either CXCL12- or CXCR4-targeted 
      anti-cancer therapeutics and have achieved promising results in the preclinical 
      trials. Further exploration of this new strategy and its potent therapeutics 
      effect against metastatic cancer through the targeting of the CXCL12- CXCR4 
      signaling axis may lead to a novel therapy that can clean up the tumor 
      microenvironment ("soil") and kill the cancer cells, particularly the cancer 
      stem/progenitor cells ("seeds"), in cancer patients. Ultimately, this approach 
      has the potential to effectively treat metastatic cancer.
CI  - Copyright(c) Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - Yang, Ping
AU  - Yang P
AD  - Department of Pathophysiology, School of Medicine (School of Nursing), Nantong 
      University, Nantong, Jiangsu 226000, China.
FAU - Hu, Yae
AU  - Hu Y
AD  - Department of Pathophysiology, School of Medicine (School of Nursing), Nantong 
      University, Nantong, Jiangsu 226000, China.
FAU - Zhou, Quansheng
AU  - Zhou Q
AD  - Cyrus Tang Hematology Center, Jiangsu Institute of Hematology, Soochow 
      University; Suzhou, Jiangsu 215123, China.
LA  - eng
GR  - 81703595; 81572257; 81772535 , 81503304/National Natural Science Foundation of 
      China/International
PT  - Journal Article
PL  - United Arab Emirates
TA  - Curr Med Chem
JT  - Current medicinal chemistry
JID - 9440157
RN  - 0 (CXCL12 protein, human)
RN  - 0 (CXCR4 protein, human)
RN  - 0 (Chemokine CXCL12)
RN  - 0 (Receptors, CXCR4)
SB  - IM
MH  - Cell Movement
MH  - Chemokine CXCL12
MH  - Epithelial-Mesenchymal Transition
MH  - Humans
MH  - Neoplasm Invasiveness
MH  - Neoplasm Metastasis
MH  - *Neoplasms
MH  - Receptors, CXCR4
MH  - *Signal Transduction
MH  - Tumor Microenvironment
OTO - NOTNLM
OT  - CXCL12
OT  - CXCR4
OT  - cancer metastasis
OT  - cancer therapy
OT  - signaling axis
OT  - therapeutics
EDAT- 2019/11/15 06:00
MHDA- 2020/12/02 06:00
CRDT- 2019/11/15 06:00
PHST- 2018/10/31 00:00 [received]
PHST- 2019/10/07 00:00 [revised]
PHST- 2019/10/25 00:00 [accepted]
PHST- 2019/11/15 06:00 [pubmed]
PHST- 2020/12/02 06:00 [medline]
PHST- 2019/11/15 06:00 [entrez]
AID - CMC-EPUB-102306 [pii]
AID - 10.2174/0929867326666191113113110 [doi]
PST - ppublish
SO  - Curr Med Chem. 2020;27(33):5543-5561. doi: 10.2174/0929867326666191113113110.