PMID- 35557905
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231105
IS  - 2046-2069 (Electronic)
IS  - 2046-2069 (Linking)
VI  - 8
IP  - 71
DP  - 2018 Dec 4
TI  - LncRNA CASC2 inhibits autophagy and promotes apoptosis in non-small cell lung 
      cancer cells via regulating the miR-214/TRIM16 axis.
PG  - 40846-40855
LID - 10.1039/c8ra09573f [doi]
AB  - Background: Dysregulated long noncoding RNAs (lncRNAs) have been frequently 
      observed in various cancers including non-small cell lung cancer (NSCLC) and are 
      closely associated with cancer progression. Previous studies also found that low 
      expression of lncRNA cancer susceptibility candidate 2 (CASC2) functioned as a 
      tumor suppressor in NSCLC. Our study aimed to explore the detailed molecular 
      mechanism of CASC2 involved in NSCLC progression. Methods: The expressions of 
      CASC2, tripartite motif-containing protein 16 (TRIM16) and miR-214 in NSCLC 
      tissues and cells were detected by reverse transcription-quantitative polymerase 
      chain reaction (RT-qPCR) or western blot. Flow cytometry analysis was performed 
      to evaluate apoptosis. Autophagy was assessed using green fluorescent protein 
      microtubule-associated protein 1 light chain 3alpha (GFP-LC3) puncta analysis, 
      acridine orange (AO) staining and western blot. Luciferase reporter assay, RNA 
      immunoprecipitation (RIP), RNA pull-down and immunofluorescence staining were 
      employed to explore the association between CASC2, TRIM16 and miR-214. Results: 
      CASC2 and TRIM16 expressions were significantly downregulated and miR-214 
      expression was dramatically upregulated in NSCLC tissues and cells. 
      Overexpression of CASC2 induced apoptosis and inhibited autophagy in NSCLC cells. 
      miR-214 was bound to CASC2 and its knockdown reversed the regulatory effect of 
      CASC2 inhibition on apoptosis and autophagy in NSCLC cells. Moreover, TRIM16 was 
      validated as a target of miR-214 and its interference attenuated miR-214 
      knockdown-mediated promotion of apoptosis and inhibition of autophagy. Besides, 
      CASC2 enhanced TRIM16 expression through functioning as a competing endogenous 
      RNA (ceRNA) for miR-214 in NSCLC cells. Conclusion: lncRNA CASC2 inhibited 
      autophagy and promoted apoptosis in NSCLC cells via regulating the miR-214/TRIM16 
      axis, shedding light on the mechanism underlying NSCLC carcinogenesis.
CI  - This journal is (c) The Royal Society of Chemistry.
FAU - Li, Qian
AU  - Li Q
AD  - Department of Respiratory, People's Hospital of Rizhao 276800 China.
FAU - Chen, Kai
AU  - Chen K
AD  - Department of Respiratory, People's Hospital of Rizhao 276800 China.
FAU - Dong, Rong
AU  - Dong R
AD  - Department of Respiratory, People's Hospital of Rizhao 276800 China.
FAU - Lu, Hengxiao
AU  - Lu H
AD  - Department of Thoracic Surgery, Weifang People's Hospital No.151, Guangwen 
      Street, Kuiwen District Weifang 261041 China xheng45698@sina.com 
      +86-0536-8192133.
LA  - eng
PT  - Journal Article
DEP - 20181205
PL  - England
TA  - RSC Adv
JT  - RSC advances
JID - 101581657
ECI - RSC Adv. 2022 Feb 16;12(10):5890. PMID: 35427090
PMC - PMC9091572
COIS- There is no conflict of interest regarding the publication of this paper.
EDAT- 2018/12/05 00:00
MHDA- 2018/12/05 00:01
CRDT- 2022/05/13 18:08
PHST- 2018/11/21 00:00 [received]
PHST- 2018/11/22 00:00 [accepted]
PHST- 2022/05/13 18:08 [entrez]
PHST- 2018/12/05 00:00 [pubmed]
PHST- 2018/12/05 00:01 [medline]
AID - c8ra09573f [pii]
AID - 10.1039/c8ra09573f [doi]
PST - epublish
SO  - RSC Adv. 2018 Dec 5;8(71):40846-40855. doi: 10.1039/c8ra09573f. eCollection 2018 
      Dec 4.