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CXCL1 induces senescence of cancer-associated fibroblasts via autocrine loops in oral squamous cell carcinoma.

Abstract Cancer-associated fibroblasts (CAFs) have emerged as one of the main factors related to cancer progression, however, the conversion mechanism of normal fibroblasts (NOFs) to CAFs has not been well elucidated. The aim of this study was to investigate the underlying mechanism of CAF transformation from NOFs in oral squamous cell carcinoma (OSCC). This study found that NOFs exposed to OSCC cells transformed to senescent cells. The cytokine antibody array showed the highest secretion levels of IL-6 and CXCL1 in NOFs co-cultured with OSCC cells. Despite that both IL-6 and CXCL1 induced the senescent phenotype of CAFs, CXCL1 secretion showed a cancer-specific response to transform NOFs into CAFs in OSCC, whereas IL-6 secretion was eventuated by common co-culture condition. Further, CXCL1 was released from NOFs co-cultured with OSCC cells, however, CXCL1 was undetectable in mono-cultured NOFs or co-cultured OSCC cells with NOFs. Taken together, this study demonstrates that CXCL1 can transform NOFs into senescent CAFs via an autocrine mechanism. These data might contribute to further understanding of CAFs and to development of a potential therapeutic approach targeting cancer cells-CAFs interactions.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title plos one
Publication Year Start




PMID- 29360827
OWN - NLM
STAT- MEDLINE
DCOM- 20180206
LR  - 20180206
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 13
IP  - 1
DP  - 2018
TI  - CXCL1 induces senescence of cancer-associated fibroblasts via autocrine loops in 
      oral squamous cell carcinoma.
PG  - e0188847
LID - 10.1371/journal.pone.0188847 [doi]
AB  - Cancer-associated fibroblasts (CAFs) have emerged as one of the main factors
      related to cancer progression, however, the conversion mechanism of normal
      fibroblasts (NOFs) to CAFs has not been well elucidated. The aim of this study
      was to investigate the underlying mechanism of CAF transformation from NOFs in
      oral squamous cell carcinoma (OSCC). This study found that NOFs exposed to OSCC
      cells transformed to senescent cells. The cytokine antibody array showed the
      highest secretion levels of IL-6 and CXCL1 in NOFs co-cultured with OSCC cells.
      Despite that both IL-6 and CXCL1 induced the senescent phenotype of CAFs, CXCL1
      secretion showed a cancer-specific response to transform NOFs into CAFs in OSCC, 
      whereas IL-6 secretion was eventuated by common co-culture condition. Further,
      CXCL1 was released from NOFs co-cultured with OSCC cells, however, CXCL1 was
      undetectable in mono-cultured NOFs or co-cultured OSCC cells with NOFs. Taken
      together, this study demonstrates that CXCL1 can transform NOFs into senescent
      CAFs via an autocrine mechanism. These data might contribute to further
      understanding of CAFs and to development of a potential therapeutic approach
      targeting cancer cells-CAFs interactions.
FAU - Kim, Eun Kyoung
AU  - Kim EK
AD  - Oral Cancer Research Institute, Department of Oral Pathology, Yonsei University
      College of Dentistry, Seoul, Republic of Korea.
FAU - Moon, Sook
AU  - Moon S
AD  - Oral Cancer Research Institute, Department of Oral Pathology, Yonsei University
      College of Dentistry, Seoul, Republic of Korea.
AD  - Department of Dental hygiene, College of nursing Healthcare, Sorabol college,
      Gyeongju, Republic of Korea.
FAU - Kim, Do Kyeong
AU  - Kim DK
AD  - Oral Cancer Research Institute, Department of Oral Pathology, Yonsei University
      College of Dentistry, Seoul, Republic of Korea.
FAU - Zhang, Xianglan
AU  - Zhang X
AD  - Oral Cancer Research Institute, Department of Oral Pathology, Yonsei University
      College of Dentistry, Seoul, Republic of Korea.
AD  - Department of pathology, Yanbian University Hospital, Yanji City, Jilin Province,
      China.
FAU - Kim, Jin
AU  - Kim J
AUID- ORCID: 0000-0001-5398-8989
AD  - Oral Cancer Research Institute, Department of Oral Pathology, Yonsei University
      College of Dentistry, Seoul, Republic of Korea.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180123
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (CXCL1 protein, human)
RN  - 0 (Chemokine CXCL1)
RN  - 0 (Cytokines)
RN  - 0 (Reactive Oxygen Species)
SB  - IM
MH  - Blotting, Western
MH  - Carcinoma, Squamous Cell/metabolism/*pathology
MH  - Cellular Senescence/*physiology
MH  - Chemokine CXCL1/*physiology
MH  - Coculture Techniques
MH  - Cytokines/metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Fibroblasts/pathology
MH  - Humans
MH  - Mouth Neoplasms/metabolism/*pathology
MH  - Neoplasm Invasiveness
MH  - Reactive Oxygen Species/metabolism
MH  - Real-Time Polymerase Chain Reaction
MH  - Reverse Transcriptase Polymerase Chain Reaction
PMC - PMC5779641
EDAT- 2018/01/24 06:00
MHDA- 2018/02/07 06:00
CRDT- 2018/01/24 06:00
PHST- 2017/05/25 00:00 [received]
PHST- 2017/11/14 00:00 [accepted]
PHST- 2018/01/24 06:00 [entrez]
PHST- 2018/01/24 06:00 [pubmed]
PHST- 2018/02/07 06:00 [medline]
AID - 10.1371/journal.pone.0188847 [doi]
AID - PONE-D-17-20044 [pii]
PST - epublish
SO  - PLoS One. 2018 Jan 23;13(1):e0188847. doi: 10.1371/journal.pone.0188847.
      eCollection 2018.