PMID- 35264069
OWN - NLM
STAT- MEDLINE
DCOM- 20220408
LR  - 20220606
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 13
IP  - 3
DP  - 2022 Mar
TI  - C-X-C motif chemokine ligand 12 (CXCL12)/C-X-C motif chemokine receptor 7(CXCR7) 
      regulates epithelial-mesenchymal transition process and promotes the metastasis 
      of esophageal cancer by activating signal transducer and activator of 
      transcription 3 (STAT3) pathway.
PG  - 7425-7438
LID - 10.1080/21655979.2022.2048984 [doi]
AB  - Esophageal cancer is a malignant tumor of the digestive system that is prone to 
      metastasis. Chemokines and their receptors act an essential role in the 
      occurrence and development of tumors. Here, we investigated the regulatory 
      mechanism of CXCL12/CXCR7 in the growth and metastasis of esophageal cancer. 
      CXCR7 was found highly expressed in clinical tissues and cells of esophageal 
      cancer. Knockdown of CXCR7 inhibited the proliferation, migration, invasion, and 
      epithelial-mesenchymal transition (EMT) process of esophageal cancer cells. The 
      knockdown of chemokine CXCL12 also inhibited the expression of EMT-related 
      proteins and the mesenchymal morphology changes of esophageal cancer cells, but 
      the knockdown of C-X-C motif chemokine receptor 4 (CXCR4) had no such effect. 
      Furthermore, the knockdown of CXCR7 attenuated the enhanced EMT process induced 
      by CXCL12 overexpression, while the knockdown of CXCR4 cannot inhibit this 
      process. In addition, overexpressed CXCL12/CXCR7 activated the downstream STAT3 
      pathway, but had little effect on the extracellular regulated protein kinase 
      (ERK) or serine-threonine kinase (AKT) pathways. Inhibition of the STAT3 pathway 
      using AZD9150 weakened the accelerated effects of CXCL12/CXCR7 on the growth and 
      metastasis of esophageal cancer in vitro and in vivo. In conclusion, our research 
      revealed that CXCL12/CXCR7 regulates EMT and other malignant processes by 
      activating the STAT3 pathway to accelerate the growth and metastasis of 
      esophageal cancer.
FAU - Guo, Jing
AU  - Guo J
AUID- ORCID: 0000-0001-9050-4947
AD  - Department of Thoracic Surgery, Ningbo First Hospital, Ningbo, Zhejiang province, 
      China.
FAU - Tong, Chang-Yong
AU  - Tong CY
AD  - Department of Thoracic Surgery, Ningbo First Hospital, Ningbo, Zhejiang province, 
      China.
FAU - Shi, Jian-Guang
AU  - Shi JG
AD  - Department of Thoracic Surgery, Ningbo First Hospital, Ningbo, Zhejiang province, 
      China.
FAU - Li, Xin-Jian
AU  - Li XJ
AD  - Department of Thoracic Surgery, Ningbo First Hospital, Ningbo, Zhejiang province, 
      China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (ACKR3 protein, human)
RN  - 0 (CXCL12 protein, human)
RN  - 0 (Chemokine CXCL12)
RN  - 0 (Ligands)
RN  - 0 (Receptors, CXCR)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (STAT3 protein, human)
SB  - IM
MH  - Cell Line, Tumor
MH  - Chemokine CXCL12/genetics/metabolism/pharmacology
MH  - Epithelial-Mesenchymal Transition/genetics
MH  - *Esophageal Neoplasms/genetics
MH  - Humans
MH  - Ligands
MH  - *Receptors, CXCR/genetics
MH  - STAT3 Transcription Factor/genetics/metabolism
PMC - PMC8973702
OTO - NOTNLM
OT  - CXCL12
OT  - CXCR7
OT  - Esophageal cancer
OT  - epithelial-mesenchymal transition
OT  - tumor metastasis
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2022/03/11 06:00
MHDA- 2022/04/09 06:00
PMCR- 2022/03/09
CRDT- 2022/03/10 05:32
PHST- 2022/03/10 05:32 [entrez]
PHST- 2022/03/11 06:00 [pubmed]
PHST- 2022/04/09 06:00 [medline]
PHST- 2022/03/09 00:00 [pmc-release]
AID - 2048984 [pii]
AID - 10.1080/21655979.2022.2048984 [doi]
PST - ppublish
SO  - Bioengineered. 2022 Mar;13(3):7425-7438. doi: 10.1080/21655979.2022.2048984.