PMID- 33015790
OWN - NLM
STAT- MEDLINE
DCOM- 20210507
LR  - 20210719
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 24
IP  - 18
DP  - 2020 Sep
TI  - MiR-376b-3p functions as a tumor suppressor by targeting KLF15 in non-small cell 
      lung cancer.
PG  - 9480-9486
LID - 23033 [pii]
LID - 10.26355/eurrev_202009_23033 [doi]
AB  - OBJECTIVE: The aim of this study was to explore the regulatory effects of micro 
      ribonucleic acid (miR)-376b-3p on proliferation and apoptosis of non-small cell 
      lung cancer (NSCLC) cells by targeting Kruppel-like factor 15 (KLF15) and its 
      mechanism of action. PATIENTS AND METHODS: The expression of miR-376b-3p in NSCLC 
      and para-carcinoma normal tissues, as well as NSCLC cell lines, was detected via 
      quantitative Polymerase Chain Reaction (qPCR). The effects of miR-548-3p on the 
      proliferation, cycle distribution, and apoptosis of NSCLC cells were detected via 
      colony formation assay, flow cytometry, and terminal deoxynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) assay, respectively. The 
      interaction between miR-376b-3p and KLF15 was determined using Dual-Luciferase 
      reporter gene assay. In vivo tumorigenic ability of NSCLC cells was studied using 
      nude mouse tumorigenicity assay. Furthermore, the expression of Ki67 in tumor in 
      nude mice was detected via immunohistochemistry. RESULTS: The expression of 
      miR-376b-3p was significantly downregulated in NSCLC tissues when compared with 
      para-carcinoma normal tissues (p<0.05). MiR-376b-3p was lowly expressed in NSCLC 
      cells as well (p<0.05). After overexpression of miR-376b-3p, the proliferation 
      ability of NSCLC cells remarkably declined (p<0.05). The apoptosis rate rose, and 
      cell cycle was arrested in the G1/G0 phase. Dual-Luciferase reporter gene assay 
      confirmed that miR-376b-3p could specifically bind to KLF15 3'UTR to regulate the 
      expression activity of KLF15. After overexpression of miR-376b-3p, tumor volume 
      and weight were significantly reduced in tumor-bearing mice (p<0.05). 
      CONCLUSIONS: MiR-376b-3p plays an important role in the occurrence and 
      development of NSCLC, which affects the proliferation and apoptosis of NSCLC 
      cells by targeting KLF15.
FAU - Liu, X-W
AU  - Liu XW
AD  - Department of Internal Medicine, Linyi People's Hospital, Linyi, China. 
      964840322@qq.com.
FAU - Zhang, C-C
AU  - Zhang CC
FAU - Zhang, T
AU  - Zhang T
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (KLF15 protein, human)
RN  - 0 (Kruppel-Like Transcription Factors)
RN  - 0 (MIRN376C microRNA, human)
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Carcinoma, Non-Small-Cell Lung/*metabolism/pathology
MH  - Cell Proliferation
MH  - Female
MH  - Humans
MH  - Kruppel-Like Transcription Factors/genetics/*metabolism
MH  - Lung Neoplasms/*metabolism/pathology
MH  - Mice
MH  - Mice, Nude
MH  - MicroRNAs/genetics/*metabolism
MH  - Tumor Cells, Cultured
EDAT- 2020/10/06 06:00
MHDA- 2021/05/08 06:00
CRDT- 2020/10/05 06:25
PHST- 2020/10/05 06:25 [entrez]
PHST- 2020/10/06 06:00 [pubmed]
PHST- 2021/05/08 06:00 [medline]
AID - 23033 [pii]
AID - 10.26355/eurrev_202009_23033 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9480-9486. doi: 
      10.26355/eurrev_202009_23033.