PMID- 30575946
OWN - NLM
STAT- MEDLINE
DCOM- 20200114
LR  - 20211204
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 22
IP  - 24
DP  - 2018 Dec
TI  - Significant association of DIRC1 overexpression with tumor progression and poor 
      prognosis in gastric cancer.
PG  - 8682-8689
LID - 16633 [pii]
LID - 10.26355/eurrev_201812_16633 [doi]
AB  - OBJECTIVE: DIRC1, Disrupted in Renal Cancer 1, was identified as a 
      breakpoint-spanning gene in a chromosomal translocation, which was associated 
      with the onset and progression of some cancers. However, the expression in human 
      gastric cancer (GC) and the role of DIRC1 in human gastric tumorigenesis are 
      unknown. Thereby, the main purpose of this study was to unearth the association 
      of DIRC1 with GC. MATERIALS AND METHODS: By analyzing The Cancer Genome Atlas 
      (TCGA) datasets, the expression of DIRC1 in GC and normal gastric tissues were 
      compared. Besides, its association with clinicopathological significance, overall 
      survival (OS) and independent prognosis were analyzed by Pearson's x2 test, 
      Kaplan-Meier method and Cox proportional hazards model, respectively. 
      Functionally, the knockdown of DIRC1 was performed by siRNA method; moreover, its 
      effects on the proliferation and metastasis of GC cells were examined by CCK-8 
      and transwell assays. Furthermore, the key markers of protein kinase B 
      (AKT)/mammalian target of rapamycin (mTOR) signaling were tested by Western blot 
      assay. RESULTS: The results showed that high expression of DIRC1 was found in GC 
      tissues compared with normal gastric tissues. High expression of DIRC1 was 
      associated with more cases of severer tumor malignancy and shorter OS; besides, 
      high-level of DIRC1 was suggested to be an independent prognostic factor for GC. 
      Furthermore, the knockdown of DIRC1 inhibited SGC-7901 GC cells proliferation, 
      migration and invasion. Mechanically, the activity of AKT/mTOR signaling was 
      suppressed by the knockdown of DIRC1. CONCLUSIONS: These findings offer clinical 
      associations and an in vitro evidence showing that the knockdown of DIRC1 impeded 
      the GC carcinogenicity possibly via suppression of AKT/mTOR signaling. This work 
      might provide a potential therapeutic target for GC treatment.
FAU - Li, Z
AU  - Li Z
AD  - Department of Radiotherapy, Qilu Hospital of Shandong University, Jinan, 
      Shandong, P.R. China. shaozhenyusdu@163.com.
FAU - Yang, A-J
AU  - Yang AJ
FAU - Wei, F-M
AU  - Wei FM
FAU - Zhao, X-H
AU  - Zhao XH
FAU - Shao, Z-Y
AU  - Shao ZY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (DIRC1 lncRNA, human)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (RNA, Small Interfering)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Carcinogenesis/pathology
MH  - Cell Movement
MH  - Cell Proliferation
MH  - Datasets as Topic
MH  - Disease Progression
MH  - Female
MH  - Gene Knockdown Techniques
MH  - Humans
MH  - Kaplan-Meier Estimate
MH  - Male
MH  - Middle Aged
MH  - Neoplasm Invasiveness/pathology
MH  - Neoplasm Proteins/*metabolism
MH  - Prognosis
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - RNA, Long Noncoding
MH  - RNA, Small Interfering/metabolism
MH  - Stomach/pathology
MH  - Stomach Neoplasms/mortality/*pathology
MH  - TOR Serine-Threonine Kinases/metabolism
EDAT- 2018/12/24 06:00
MHDA- 2020/01/15 06:00
CRDT- 2018/12/22 06:00
PHST- 2018/12/22 06:00 [entrez]
PHST- 2018/12/24 06:00 [pubmed]
PHST- 2020/01/15 06:00 [medline]
AID - 16633 [pii]
AID - 10.26355/eurrev_201812_16633 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2018 Dec;22(24):8682-8689. doi: 
      10.26355/eurrev_201812_16633.