PMID- 33015786
OWN - NLM
STAT- MEDLINE
DCOM- 20210507
LR  - 20210507
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 24
IP  - 18
DP  - 2020 Sep
TI  - Long noncoding RNA Linc00210 promotes non-small cell lung cancer progression via 
      sponging miR-16-5p/PTK2 axis.
PG  - 9438-9452
LID - 23029 [pii]
LID - 10.26355/eurrev_202009_23029 [doi]
AB  - OBJECTIVE: Long noncoding RNAs (lncRNAs) are important regulators involved in a 
      variety of cancer development. However, the role of Linc00210 in non-small cell 
      lung cancer (NSCLC) remains unknown. This study aims to investigate the clinical 
      value of Linc00210 in NSCLC patients and the biological functions of Linc00210 in 
      NSCLC. PATIENTS AND METHODS: Gene expression in NSCLC tissues and cell lines was 
      detected using qRT-PCR or Western blot. 
      3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and 
      colony formation assays were conducted to evaluate the effect of Linc00210 on 
      NSCLC cell proliferation. Transwell assay and annexin V-Fluorescein 
      5-isothiocyanate (FITC)/Propidium Iodide (PI) were done to analyze the effect of 
      Linc00210 on cancer cell invasion and apoptosis, respectively. Luciferase 
      reporter assay and RIP assay were performed to determine the target of Linc00210 
      and miR-16-5p. Besides, these assays were used to determine reciprocally 
      inhibition of each other-controlled NSCLC cell behaviors. In vivo tumorigenesis 
      experiments were applied to exhibit subcutaneous tumor growth. RESULTS: Linc0021 
      was highly expressed in NSCLC tissues and cell lines. Knockdown of Linc00210 
      inhibited cancer cell proliferation and invasion, and increased cell apoptosis, 
      and regulated the expression of Cyclin A1, proliferating cell nuclear antigen 
      (PCNA), E-cadherin, N-cadherin, Bax, and Bcl-2 in NSCLC cells. Further data 
      showed Linc00210 bound to and directly modulated the miR-16-5p levels. 
      Impressively, overexpression of miR-16-5p suppressed NSCLC cell proliferation and 
      invasion, but increased cell apoptosis, and these behaviors could be overturned 
      by overexpression of Linc00210 in vitro and in vivo. Finally, Linc00210 and 
      miR-16-5p cooperatively controlled expression of protein tyrosine kinase 2 
      (PTK2), a miR-16-5p target. CONCLUSIONS: Linc00210/miR-16-5p/PTK2 signaling 
      suggests a promising novel strategy for anti-NSCLC therapy.
FAU - Peng, Q
AU  - Peng Q
AD  - Department of Respiration, Shangluo Central Hospital, Shangluo, Shanxi, China. 
      natsci2019@yeah.net.
FAU - Chen, Y
AU  - Chen Y
FAU - Li, C-N
AU  - Li CN
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 (MIRN16 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
RN  - EC 2.7.10.2 (Focal Adhesion Kinase 1)
RN  - EC 2.7.10.2 (PTK2 protein, human)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Carcinoma, Non-Small-Cell Lung/*metabolism/pathology
MH  - Cell Proliferation
MH  - Focal Adhesion Kinase 1/*metabolism
MH  - Humans
MH  - Lung Neoplasms/*metabolism/pathology
MH  - Mice
MH  - Mice, Nude
MH  - MicroRNAs/*metabolism
MH  - Neoplasms, Experimental/metabolism/pathology
MH  - RNA, Long Noncoding/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 - 23029 [pii]
AID - 10.26355/eurrev_202009_23029 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9438-9452. doi: 
      10.26355/eurrev_202009_23029.