PMID- 32617295
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220415
IS  - 2305-5839 (Print)
IS  - 2305-5847 (Electronic)
IS  - 2305-5839 (Linking)
VI  - 8
IP  - 11
DP  - 2020 Jun
TI  - Downregulation of long non-coding RNA LINP1 inhibits the malignant progression of 
      esophageal squamous cell carcinoma.
PG  - 675
LID - 10.21037/atm-20-1009 [doi]
LID - 675
AB  - BACKGROUND: Long noncoding RNA (lncRNA) in non-homologous end joining pathway 1 
      (LINP1) contributes to tumorigenesis in various cancers. However, little has been 
      known about the role of LINP1 in esophageal squamous cell carcinoma (ESCC). 
      METHODS: LINP1 was selected as the target lncRNA by bioinformatics analysis. The 
      relationship between LINP1 expression and prognosis was analyzed in 122 ESCC 
      patients. LINP1 status was evaluated by fluorescence in situ hybridization (FISH) 
      and quantitative real-time PCR (qRT-PCR) in normal esophageal tissues, ESCC 
      tissues and EC9706 cells. Short hairpin RNA transfection was used to silence 
      LINP1 in EC9706 cells. Clone formation assay, transwell migration assay, flow 
      cytometry, and tumorigenesis experiment were performed to evaluate the malignant 
      phenotype of EC9706 cells. RESULTS: Bioinformatics analysis showed that LINP1 was 
      the most significantly differentially expressed lncRNA. Upregulation of LINP1 was 
      observed in ESCC tissues and EC9706 cells. High LINP1 expression had close 
      correlation with larger tumor size (P=0.009), tumor invasion (P=0.015), lymph 
      nodes metastasis (P=0.044), and advanced TNM stage (P=0.010). LINP1 
      overexpression was an independent prognostic factor of ESCC patients (P=0.034). 
      LINP1 knockdown decreased the proliferative and migratory abilities of EC9706 
      cells, and promoted apoptosis and cell cycle arrest at the G2/GM phase. 
      Epithelial-mesenchymal transition (EMT) related proteins such as N-cadherin, 
      vimentin, snail and slug were downregulated while E-cadherin was up-regulated 
      significantly in shRNA-LINP1 cells. In the xenograft model, knockdown of LINP1 
      suppressed ESCC tumorigenesis in vivo. CONCLUSIONS: LINP1 was prognostic 
      indicator of ESCC and silencing of LINP1 could inhibit the malignant behavior of 
      ESCC cells.
CI  - 2020 Annals of Translational Medicine. All rights reserved.
FAU - Lu, Tao
AU  - Lu T
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 
      China.
FAU - Ma, Ke
AU  - Ma K
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 
      China.
FAU - Zhan, Cheng
AU  - Zhan C
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 
      China.
FAU - Yang, Xiaodong
AU  - Yang X
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 
      China.
FAU - Shi, Yu
AU  - Shi Y
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 
      China.
FAU - Jiang, Wei
AU  - Jiang W
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 
      China.
FAU - Wang, Hao
AU  - Wang H
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 
      China.
FAU - Wang, Shuai
AU  - Wang S
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 
      China.
FAU - Wang, Qun
AU  - Wang Q
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 
      China.
FAU - Tan, Lijie
AU  - Tan L
AD  - Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 
      China.
LA  - eng
PT  - Journal Article
PL  - China
TA  - Ann Transl Med
JT  - Annals of translational medicine
JID - 101617978
PMC - PMC7327344
OTO - NOTNLM
OT  - LINP1
OT  - Long noncoding RNA (lncRNA)
OT  - esophageal cancer (EC)
OT  - prognosis
COIS- Conflicts of Interest: All authors have completed the ICMJE uniform disclosure 
      form (available at http://dx.doi.org/10.21037/atm-20-1009). SW serves as an 
      unpaid Section Editor of Annals of Translational Medicine from Oct 2019 to Sep 
      2020. The other authors have no conflicts of interest to declare.
EDAT- 2020/07/04 06:00
MHDA- 2020/07/04 06:01
PMCR- 2020/06/01
CRDT- 2020/07/04 06:00
PHST- 2020/07/04 06:00 [entrez]
PHST- 2020/07/04 06:00 [pubmed]
PHST- 2020/07/04 06:01 [medline]
PHST- 2020/06/01 00:00 [pmc-release]
AID - atm-08-11-675 [pii]
AID - 10.21037/atm-20-1009 [doi]
PST - ppublish
SO  - Ann Transl Med. 2020 Jun;8(11):675. doi: 10.21037/atm-20-1009.