PMID- 38149567
OWN - NLM
STAT- MEDLINE
DCOM- 20240104
LR  - 20240104
IS  - 0304-4920 (Print)
IS  - 0304-4920 (Linking)
VI  - 66
IP  - 6
DP  - 2023 Nov-Dec
TI  - Long non-coding RNA NBR2 suppresses the progression of colorectal cancer by 
      downregulating miR-19a to regulate M2 macrophage polarization.
PG  - 546-557
LID - 10.4103/cjop.CJOP-D-23-00064 [doi]
AB  - Colorectal cancer (CRC) is a malignant tumor of the gastrointestinal tract that 
      significantly impacts the health of patients and lacks promising methods of 
      diagnosis. Tumor-associated macrophages (TAMs) are involved in CRC progression, 
      and their function is regulated by long non-coding RNAs (lncRNAs). The lncRNA 
      NBR2 was recently reported as an oncogene, whose function in CRC remains 
      uncertain. The present study aimed to investigate the biological function of 
      lncRNA NBR2 in the progression of CRC and its underlying molecular mechanisms. 
      Ten pairs of clinical CRC and para-carcinoma tissues were collected to determine 
      the expression levels of lncRNA NBR2 and miR-19a, and the polarization state of 
      TAMs. Quantitative reverse transcriptase-polymerase chain reaction was used to 
      evaluate the expression of miR-19a, and western blotting was used to determine 
      the expression levels of tumor necrosis factor-alpha, human leukocyte antigen-DR, 
      arginase-1, CD163, CD206, interleukin-4, AMP-activated protein kinase (AMPK), 
      p-AMPK, hypoxia-inducible factor-1alpha (HIF-1alpha), protein kinase B (AKT), p-AKT, 
      mechanistic target of rapamycin (mTOR), and p-mTOR in TAMs. The proliferative 
      ability of HCT-116 cells was detected using the CCK8 assay, and the migratory 
      ability of HCT-116 cells was evaluated using the Transwell assay. The interaction 
      between lncRNA NBR2 and miR-19a was determined using the luciferase assay. The 
      lncRNA NBR2 was downregulated and miR-19a was highly expressed in CRC cells, 
      accompanied by a high M2 polarization. Downregulated miR-19a promoted M1 
      polarization, activated AMPK, suppressed HIF-1alpha and AKT/mTOR signaling pathways, 
      and promoted antitumor properties in NBR2-overexpressed TAMs, which were all 
      reversed by the introduction of the miR-19a mimic. LncRNA NBR2 was verified to 
      target miR-19a in macrophages according to the results of the luciferase assay. 
      Collectively, lncRNA NBR2 may suppress the progression of CRC by downregulating 
      miR-19a to regulate M2 macrophage polarization.
FAU - Yang, Xiaoting
AU  - Yang X
AD  - School of Medicine, Quzhou College of Technology, Quzhou, Zhejiang, China.
FAU - Luo, Ye
AU  - Luo Y
AD  - School of Medicine, Quzhou College of Technology, Quzhou, Zhejiang, China.
FAU - Li, Mengying
AU  - Li M
AD  - School of Medicine, Quzhou College of Technology, Quzhou, Zhejiang, China.
FAU - Jin, Zhan
AU  - Jin Z
AD  - School of Medicine, Quzhou College of Technology, Quzhou, Zhejiang, China.
FAU - Chen, Gao
AU  - Chen G
AD  - School of Medicine, Quzhou College of Technology, Quzhou, Zhejiang, China.
FAU - Gan, Chunchun
AU  - Gan C
AD  - School of Medicine, Quzhou College of Technology, Quzhou, Zhejiang, China.
LA  - eng
PT  - Journal Article
PL  - India
TA  - Chin J Physiol
JT  - The Chinese journal of physiology
JID - 7804502
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - EC 1.13.12.- (Luciferases)
RN  - 0 (MicroRNAs)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - 0 (RNA, Long Noncoding)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - 0 (NBR2 lncRNA, human)
SB  - IM
MH  - Humans
MH  - AMP-Activated Protein Kinases/metabolism
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - *Colorectal Neoplasms/genetics/pathology
MH  - Luciferases/metabolism
MH  - Macrophages
MH  - *MicroRNAs/genetics/metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - *RNA, Long Noncoding/genetics/metabolism
MH  - TOR Serine-Threonine Kinases/metabolism
OTO - NOTNLM
OT  - Colorectal cancer
OT  - long non-coding RNA NBR2
OT  - macrophage polarization
OT  - miR-19a
COIS- None
EDAT- 2023/12/27 12:42
MHDA- 2023/12/28 06:42
CRDT- 2023/12/27 06:46
PHST- 2023/12/28 06:42 [medline]
PHST- 2023/12/27 12:42 [pubmed]
PHST- 2023/12/27 06:46 [entrez]
AID - ChinJPhysiol_2023_66_6_546_391967 [pii]
AID - 10.4103/cjop.CJOP-D-23-00064 [doi]
PST - ppublish
SO  - Chin J Physiol. 2023 Nov-Dec;66(6):546-557. doi: 10.4103/cjop.CJOP-D-23-00064.