PMID- 35723199
OWN - NLM
STAT- MEDLINE
DCOM- 20221018
LR  - 20221018
IS  - 0028-2685 (Print)
IS  - 0028-2685 (Linking)
VI  - 69
IP  - 5
DP  - 2022 Sep
TI  - Exosomes from M2 macrophages promoted glycolysis in FaDu cells by inhibiting 
      PDLIM2 expression to stabilize PFKL.
PG  - 1041-1053
LID - 220426N455 [pii]
LID - 10.4149/neo_2022_220426N455 [doi]
AB  - Laryngeal squamous cell carcinoma (LSCC) is one of the most prevalent malignant 
      diseases worldwide. LSCC patients suffer from a severe decline in life quality, 
      due to the essential roles of the larynx in basic functions in the human body. 
      The overarching goal of the present study is to explore whether exosome from M2 
      macrophages promotes LSCC by targeting glycolysis. In the current study, the 
      expression of PDLIM2, an E3 ubiquitin ligase, in clinical samples was monitored 
      by quantitative PCR and immunohistochemical examination. Extracellular 
      acidification rate (ECAR) and oxygen consumption rate (OCR) were measured by the 
      Seahorse machine. Cell proliferation was measured by using Cell Counting Kit-8. A 
      luciferase assay was performed to verify the regulation of miRNA on its target 
      gene. The results showed that PDLIM2 exhibited downregulation in LSCC clinical 
      samples and was associated with stage and differentiation of tumors in patients. 
      In FaDu cell line, PDLIM2 inhibited cell proliferation and glycolysis but 
      promoted the ubiquitination of PFKL. Exosomes from M2-type macrophages delivered 
      miR-222-3p into LSCC cells to suppress PDLIM2 expression, leading to the elevated 
      expression of PFKL and enhanced glycolysis which accelerated the proliferation of 
      FaDu cells. The findings from cultured cells were supported by a subcutaneous 
      tumor growth model in nude mice. Collectively, our data provided a snapshot of 
      the miR-222-3p/PDLIM2/PFKL axis in LSCC tumorigenesis, and in concert with the 
      importance of TAM exosomes and glycolysis, could be potentially translated to 
      LSCC clinics.
FAU - Wang, Peng
AU  - Wang P
AD  - Department of Otorhinolaryngology, Head and Neck Surgery, Zhongshan Hospital, 
      Fudan University, Shanghai, China.
FAU - Li, Guang-Yao
AU  - Li GY
AD  - Department of Otorhinolaryngology, Head and Neck Surgery, Zhongshan Hospital, 
      Fudan University, Shanghai, China.
FAU - Zhou, Lei
AU  - Zhou L
AD  - Department of Otorhinolaryngology, Head and Neck Surgery, Zhongshan Hospital, 
      Fudan University, Shanghai, China.
FAU - Jiang, Huai-Li
AU  - Jiang HL
AD  - Department of Otorhinolaryngology, Head and Neck Surgery, Zhongshan Hospital, 
      Fudan University, Shanghai, China.
FAU - Yang, Yue
AU  - Yang Y
AD  - ENT institute and Department of Otorhinolaryngology, Eye & ENT Hospital, Fudan 
      University, Shanghai, China.
FAU - Wu, Hai-Tao
AU  - Wu HT
AD  - ENT institute and Department of Otorhinolaryngology, Eye & ENT Hospital, Fudan 
      University, Shanghai, China.
LA  - eng
PT  - Journal Article
DEP - 20220620
PL  - Slovakia
TA  - Neoplasma
JT  - Neoplasma
JID - 0377266
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (LIM Domain Proteins)
RN  - 0 (MicroRNAs)
RN  - 0 (Microfilament Proteins)
RN  - 0 (PDLIM2 protein, human)
RN  - 0 (Pdlim2 protein, mouse)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
SB  - IM
MH  - Adaptor Proteins, Signal Transducing
MH  - Animals
MH  - *Carcinoma, Squamous Cell/genetics
MH  - Cell Line, Tumor
MH  - Cell Proliferation/genetics
MH  - *Exosomes
MH  - Gene Expression Regulation, Neoplastic
MH  - Glycolysis
MH  - *Head and Neck Neoplasms/genetics
MH  - Humans
MH  - LIM Domain Proteins
MH  - *Laryngeal Neoplasms/pathology
MH  - Macrophages
MH  - Mice
MH  - Mice, Nude
MH  - *MicroRNAs/genetics/metabolism
MH  - Microfilament Proteins/genetics/metabolism
MH  - Squamous Cell Carcinoma of Head and Neck/genetics
MH  - Ubiquitin-Protein Ligases/genetics
EDAT- 2022/06/21 06:00
MHDA- 2022/10/19 06:00
CRDT- 2022/06/20 07:03
PHST- 2022/04/26 00:00 [received]
PHST- 2022/06/06 00:00 [accepted]
PHST- 2022/06/21 06:00 [pubmed]
PHST- 2022/10/19 06:00 [medline]
PHST- 2022/06/20 07:03 [entrez]
AID - 220426N455 [pii]
AID - 10.4149/neo_2022_220426N455 [doi]
PST - ppublish
SO  - Neoplasma. 2022 Sep;69(5):1041-1053. doi: 10.4149/neo_2022_220426N455. Epub 2022 
      Jun 20.