PMID- 32395291
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220414
IS  - 2072-1439 (Print)
IS  - 2077-6624 (Electronic)
IS  - 2072-1439 (Linking)
VI  - 12
IP  - 4
DP  - 2020 Apr
TI  - miR-107 inhibited malignant biological behavior of non-small cell lung cancer 
      cells by regulating the STK33/ERK signaling pathway in vivo and vitro.
PG  - 1540-1551
LID - 10.21037/jtd.2020.03.103 [doi]
AB  - BACKGROUND: The role of miRNAs in non-small cell lung cancer (NSCLC) has been 
      broadly studied and confirmed, and miR-107 has attracted an ever-growing level of 
      attention. This study set out to research the mechanism of the effect of miR-107 
      on the malignant biological behavior of NSCLC in vivo and vitro. METHODS: The 
      expression of miRNAs related to the development of NSCLC was detected by RT-qPCR. 
      Western blotting was carried out to detect expression levels of serine/threonine 
      kinase 33 (STK33) and proteins related to the extracellular regulated protein 
      kinases (ERK) signaling pathway, while cell proliferation was detected using cell 
      counting kit-8 (CCK-8). The cell apoptosis rate was measured using flow 
      cytometry. The invasion ability was detected by Transwell assay. In vivo tumor 
      growth assays were performed on mice. The expression ERK signaling 
      pathway-related proteins in vivo was evaluated by immunohistochemistry staining. 
      The targeted relationship between miR-107 and STK33 was confirmed by the dual 
      luciferase reporter gene. RESULTS: In NSCLC cell lines and tissues, miR-107 was 
      downregulated. Overexpression of miR-107 inhibited malignant biological behavior 
      of NSCLC cell lines, and suppressed tumor growth in vivo. In addition, STK33 is 
      one of the target genes of miR-107. Therefore, miR-107 suppressed cell 
      proliferation and invasion and promoted tumor growth in vivo and cell apoptosis 
      of NSCLC in vitro. The mechanism was found to be miR-107 targeting STK33, and a 
      lack of STK33 led to the activation of ERK signaling pathway. CONCLUSIONS: 
      miR-107 inhibited malignant biological behavior of NSCLC through regulation of 
      the STK33/ERK signaling pathway.
CI  - 2020 Journal of Thoracic Disease. All rights reserved.
FAU - Wei, Xueqiang
AU  - Wei X
AD  - Kunming Medical University, Kunming 650500, China.
AD  - Department of Thoracic Surgery Iota, the Third Affiliated Hospital of Kunming 
      Medical University/Yunnan Cancer Hospital, Yunnan Cancer Center, The 
      International Cooperation Key Laboratory of Regional Tumor in High Altitude Area, 
      Kunming 650118, China.
FAU - Lei, Yujie
AU  - Lei Y
AD  - Department of Thoracic Surgery Iota, the Third Affiliated Hospital of Kunming 
      Medical University/Yunnan Cancer Hospital, Yunnan Cancer Center, The 
      International Cooperation Key Laboratory of Regional Tumor in High Altitude Area, 
      Kunming 650118, China.
FAU - Li, Minjie
AU  - Li M
AD  - Kunming Medical University, Kunming 650500, China.
AD  - Department of Thoracic Surgery Iota, the Third Affiliated Hospital of Kunming 
      Medical University/Yunnan Cancer Hospital, Yunnan Cancer Center, The 
      International Cooperation Key Laboratory of Regional Tumor in High Altitude Area, 
      Kunming 650118, China.
FAU - Zhao, Guangqiang
AU  - Zhao G
AD  - Department of Thoracic Surgery Iota, the Third Affiliated Hospital of Kunming 
      Medical University/Yunnan Cancer Hospital, Yunnan Cancer Center, The 
      International Cooperation Key Laboratory of Regional Tumor in High Altitude Area, 
      Kunming 650118, China.
FAU - Zhou, Yongchun
AU  - Zhou Y
AD  - Department of Thoracic Surgery Iota, the Third Affiliated Hospital of Kunming 
      Medical University/Yunnan Cancer Hospital, Yunnan Cancer Center, The 
      International Cooperation Key Laboratory of Regional Tumor in High Altitude Area, 
      Kunming 650118, China.
FAU - Ye, Lianhua
AU  - Ye L
AD  - Department of Thoracic Surgery Iota, the Third Affiliated Hospital of Kunming 
      Medical University/Yunnan Cancer Hospital, Yunnan Cancer Center, The 
      International Cooperation Key Laboratory of Regional Tumor in High Altitude Area, 
      Kunming 650118, China.
FAU - Huang, Yunchao
AU  - Huang Y
AD  - Department of Thoracic Surgery Iota, the Third Affiliated Hospital of Kunming 
      Medical University/Yunnan Cancer Hospital, Yunnan Cancer Center, The 
      International Cooperation Key Laboratory of Regional Tumor in High Altitude Area, 
      Kunming 650118, China.
LA  - eng
PT  - Journal Article
PL  - China
TA  - J Thorac Dis
JT  - Journal of thoracic disease
JID - 101533916
PMC - PMC7212150
OTO - NOTNLM
OT  - Non-small cell lung cancer (NSCLC)
OT  - STK33/ERK signaling pathway
OT  - cell apoptosis
OT  - cell invasion
OT  - cell proliferation
OT  - miR-107
OT  - tumor growth
COIS- Conflicts of Interest: All authors have completed the ICMJE uniform disclosure 
      form (available at http://dx.doi.org/10.21037/jtd.2020.03.103). The authors have 
      no conflicts of interest to declare.
EDAT- 2020/05/13 06:00
MHDA- 2020/05/13 06:01
PMCR- 2020/04/01
CRDT- 2020/05/13 06:00
PHST- 2020/05/13 06:00 [entrez]
PHST- 2020/05/13 06:00 [pubmed]
PHST- 2020/05/13 06:01 [medline]
PHST- 2020/04/01 00:00 [pmc-release]
AID - jtd-12-04-1540 [pii]
AID - 10.21037/jtd.2020.03.103 [doi]
PST - ppublish
SO  - J Thorac Dis. 2020 Apr;12(4):1540-1551. doi: 10.21037/jtd.2020.03.103.