PMID- 38309677
OWN - NLM
STAT- MEDLINE
DCOM- 20240226
LR  - 20240226
IS  - 1879-0712 (Electronic)
IS  - 0014-2999 (Linking)
VI  - 967
DP  - 2024 Mar 15
TI  - Advance in the role of chemokines/chemokine receptors in carcinogenesis: Focus on 
      pancreatic cancer.
PG  - 176357
LID - S0014-2999(24)00045-1 [pii]
LID - 10.1016/j.ejphar.2024.176357 [doi]
AB  - The chemokines/chemokine receptors pathway significantly influences cell 
      migration, particularly in recruiting immune cells to the tumor microenvironment 
      (TME), impacting tumor progression and treatment outcomes. Emerging research 
      emphasizes the involvement of chemokines in drug resistance across various tumor 
      therapies, including immunotherapy, chemotherapy, and targeted therapy. This 
      review focuses on the role of chemokines/chemokine receptors in pancreatic cancer 
      (PC) development, highlighting their impact on TME remodeling, immunotherapy, and 
      relevant signaling pathways. The unique immunosuppressive microenvironment formed 
      by the interaction of tumor cells, stromal cells and immune cells plays an 
      important role in the tumor proliferation, invasion, migration and therapeutic 
      resistance. Chemokines/chemokine receptors, such as chemokine ligand (CCL) 2, 
      CCL3, CCL5, CCL20, CCL21, C-X-C motif chemokine ligand (CXCL) 1, CXCL2, CXCL3, 
      CXCL4, CXCL5, CXCL8, CXCL9, CXCL10, CXCL11, CXCL12, CXCL13, CXCL14, CXCL16, 
      CXCL17, and C-X3-C motif chemokine ligand (CX3CL)1, derived mainly from leukocyte 
      cells, cancer-related fibroblasts (CAFs), pancreatic stellate cells (PSCs), and 
      tumor-associated macrophages (TAMs), contribute to PC progression and treatment 
      resistance. Chemokines recruit myeloid-derived suppressor cells (MDSC), 
      regulatory T cells (Tregs), and M2 macrophages, inhibiting the anti-tumor 
      activity of immune cells. Simultaneously, they enhance pathways like 
      epithelial-mesenchymal transition (EMT), Akt serine/threonine kinase (AKT), 
      extracellular regulated protein kinases (ERK) 1/2, and nuclear factor kappa-B 
      (NF-kappaB), etc., elevating the risk of PC metastasis and compromising the efficacy 
      of radiotherapy, chemotherapy, and anti-PD-1/PD-L1 immunotherapy. Notably, the 
      CCLx-CCR2 and CXCLx-CXCR2/4 axis emerge as potential therapeutic targets in PC. 
      This review integrates recent findings on chemokines and receptors in PC 
      treatment, offering valuable insights for innovative therapeutic approaches.
CI  - Copyright (c) 2024 Elsevier B.V. All rights reserved.
FAU - Song, Na
AU  - Song N
AD  - Department of Pathology, Xinxiang Key Laboratory of Precision Medicine, The First 
      Affiliated Hospital of Xinxiang Medical University, China; Department of 
      Pathology, Xinxiang Medical University, Xinxiang, 453000, China.
FAU - Cui, Kai
AU  - Cui K
AD  - Department of Pathology, Xinxiang Medical University, Xinxiang, 453000, China.
FAU - Zeng, Liqun
AU  - Zeng L
AD  - Department of Pathology, Xinxiang Medical University, Xinxiang, 453000, China.
FAU - Li, Mengxiao
AU  - Li M
AD  - Department of Pathology, Xinxiang Key Laboratory of Precision Medicine, The First 
      Affiliated Hospital of Xinxiang Medical University, China.
FAU - Fan, Yanwu
AU  - Fan Y
AD  - Department of Pathology, Xinxiang Medical University, Xinxiang, 453000, China.
FAU - Shi, Pingyu
AU  - Shi P
AD  - Department of Pathology, Xinxiang Medical University, Xinxiang, 453000, China.
FAU - Wang, Ziwei
AU  - Wang Z
AD  - Department of Pathology, Xinxiang Medical University, Xinxiang, 453000, China.
FAU - Su, Wei
AU  - Su W
AD  - Department of Pathology, Xinxiang Key Laboratory of Precision Medicine, The First 
      Affiliated Hospital of Xinxiang Medical University, China. Electronic address: 
      weisu_xxmu@163.com.
FAU - Wang, Haijun
AU  - Wang H
AD  - Department of Pathology, Xinxiang Key Laboratory of Precision Medicine, The First 
      Affiliated Hospital of Xinxiang Medical University, China; Department of 
      Pathology, Xinxiang Medical University, Xinxiang, 453000, China. Electronic 
      address: wnavy@xxmu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20240201
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (Receptors, Chemokine)
RN  - 0 (Ligands)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - 0 (Chemokines)
SB  - IM
MH  - Humans
MH  - *Receptors, Chemokine/metabolism
MH  - Ligands
MH  - Proto-Oncogene Proteins c-akt
MH  - Chemokines/metabolism
MH  - *Pancreatic Neoplasms/therapy
MH  - Carcinogenesis
MH  - Tumor Microenvironment
OTO - NOTNLM
OT  - Carcinogenesis
OT  - Chemokine receptors
OT  - Chemokines
OT  - Immunotherapy
OT  - Microenvironment
OT  - Pancreatic cancer
COIS- Declaration of competing interest The authors declare no potential conflicts of 
      interest with respect to the research, authorship, and/or publication of this 
      article.
EDAT- 2024/02/04 00:42
MHDA- 2024/02/26 06:45
CRDT- 2024/02/03 19:35
PHST- 2023/09/13 00:00 [received]
PHST- 2024/01/17 00:00 [revised]
PHST- 2024/01/23 00:00 [accepted]
PHST- 2024/02/26 06:45 [medline]
PHST- 2024/02/04 00:42 [pubmed]
PHST- 2024/02/03 19:35 [entrez]
AID - S0014-2999(24)00045-1 [pii]
AID - 10.1016/j.ejphar.2024.176357 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2024 Mar 15;967:176357. doi: 10.1016/j.ejphar.2024.176357. Epub 
      2024 Feb 1.