PMID- 30115896
OWN - NLM
STAT- MEDLINE
DCOM- 20181116
LR  - 20181116
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 19
IP  - 8
DP  - 2018 Aug 16
TI  - Interaction between Tumor-Associated Dendritic Cells and Colon Cancer Cells 
      Contributes to Tumor Progression via CXCL1.
LID - 10.3390/ijms19082427 [doi]
LID - 2427
AB  - Crosstalk of a tumor with its microenvironment is a critical factor contributing 
      to cancer development. This study investigates the soluble factors released by 
      tumor-associated dendritic cells (TADCs) responsible for increasing cancer stem 
      cell (CSC) properties, cell mobility, and epithelial-to-mesenchymal transition 
      (EMT). Dendritic cells (DCs) of colon cancer patients were collected for 
      phenotype and CXCL1 expression by flow cytometry and Luminex assays. The 
      transcriptome of CXCL1-treated cancer cells was established by next generation 
      sequencing. Inflammatory chemokine CXCL1, present in large amounts in DCs 
      isolated from colon cancer patients, and SW620-conditioned TADCs, enhance CSC 
      characteristics in cancer, supported by enhanced anchorage-independent growth, 
      CD133 expression and aldehyde dehydrogenase activity. Additionally, CXCL1 
      increases the metastatic ability of a cancer by enhancing cell migration, matrix 
      metalloproteinase-7 expression and EMT. The enhanced CXCL1 expression in DCs is 
      also noted in mice transplanted with colon cancer cells. Transcriptome analysis 
      of CXCL1-treated SW620 cells indicates that CXCL1 increases potential oncogene 
      expression in colon cancer, including PTHLH, TYRP1, FOXO1, TCF4 and ZNF880. 
      Concurrently, CXCL1 displays a specific microRNA (miR) upregulated by the 
      prototypical colon cancer onco-miR miR-105. Analysis of publicly available data 
      reveals CXCL1-driven oncogenes and miR-105 have a negative prognostic impact on 
      the outcome of colon cancer. This study indicates a new mechanism by which the 
      colon cancer milieu exploits DC plasticity to support cancer progression.
FAU - Hsu, Ya-Ling
AU  - Hsu YL
AD  - Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical 
      University, Kaohsiung 807, Taiwan. hsuyl326@gmail.com.
FAU - Chen, Yi-Jen
AU  - Chen YJ
AD  - Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical 
      University, Kaohsiung 807, Taiwan. chernkmu@gmail.com.
AD  - Department of Physical Medicine and Rehabilitation, Kaohsiung Medical University 
      Hospital, Kaohsiung 807, Taiwan. chernkmu@gmail.com.
FAU - Chang, Wei-An
AU  - Chang WA
AD  - Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical 
      University, Kaohsiung 807, Taiwan. 960215kmuh@gmail.com.
AD  - Division of Pulmonary and Critical Care Medicine, Kaohsiung Medical University 
      Hospital, Kaohsiung 807, Taiwan. 960215kmuh@gmail.com.
FAU - Jian, Shu-Fang
AU  - Jian SF
AD  - Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical 
      University, Kaohsiung 807, Taiwan. chienfang1216@gmail.com.
FAU - Fan, Hsiao-Li
AU  - Fan HL
AD  - Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical 
      University, Kaohsiung 807, Taiwan. puffmilkian@gmail.com.
FAU - Wang, Jaw-Yuan
AU  - Wang JY
AUID- ORCID: 0000-0002-7705-2621
AD  - Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical 
      University, Kaohsiung 807, Taiwan. cy614112@ms14.hinet.net.
AD  - Division of Colorectal Surgery, Department of Surgery, Kaohsiung Medical 
      University Hospital, Kaohsiung 807, Taiwan. cy614112@ms14.hinet.net.
FAU - Kuo, Po-Lin
AU  - Kuo PL
AD  - Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical 
      University, Kaohsiung 807, Taiwan. kuopolin@seed.net.tw.
AD  - Center for Infectious Disease and Cancer Research, Kaohsiung Medical University, 
      Kaohsiung 807, Taiwan. kuopolin@seed.net.tw.
LA  - eng
PT  - Journal Article
DEP - 20180816
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (CXCL1 protein, human)
RN  - 0 (Chemokine CXCL1)
SB  - IM
MH  - Animals
MH  - Cell Line, Tumor
MH  - Cell Movement/genetics
MH  - Chemokine CXCL1/genetics/*metabolism
MH  - Colonic Neoplasms/genetics/*pathology
MH  - Dendritic Cells/*metabolism/*pathology
MH  - *Disease Progression
MH  - Epithelial-Mesenchymal Transition/genetics
MH  - Gene Expression Profiling
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Male
MH  - Mice, Inbred BALB C
MH  - Models, Biological
MH  - Neoplastic Stem Cells/metabolism/pathology
MH  - Phenotype
MH  - Transcriptome/genetics
MH  - Treatment Outcome
MH  - Up-Regulation/genetics
PMC - PMC6121631
OTO - NOTNLM
OT  - CXCL1
OT  - Parathyroid hormone-related protein
OT  - colon cancer
OT  - dendritic cells
OT  - miR-105
COIS- The authors declare no conflict of interest.
EDAT- 2018/08/18 06:00
MHDA- 2018/11/18 06:00
PMCR- 2018/08/01
CRDT- 2018/08/18 06:00
PHST- 2018/07/02 00:00 [received]
PHST- 2018/07/27 00:00 [revised]
PHST- 2018/08/13 00:00 [accepted]
PHST- 2018/08/18 06:00 [entrez]
PHST- 2018/08/18 06:00 [pubmed]
PHST- 2018/11/18 06:00 [medline]
PHST- 2018/08/01 00:00 [pmc-release]
AID - ijms19082427 [pii]
AID - ijms-19-02427 [pii]
AID - 10.3390/ijms19082427 [doi]
PST - epublish
SO  - Int J Mol Sci. 2018 Aug 16;19(8):2427. doi: 10.3390/ijms19082427.