PMID- 32271416
OWN - NLM
STAT- MEDLINE
DCOM- 20210315
LR  - 20211204
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 24
IP  - 6
DP  - 2020 Mar
TI  - Promoting effect of PAX5-activated lncRNA UASR1 on growth of colorectal cancer by 
      regulating the mTOR pathway.
PG  - 2986-2993
LID - 20663 [pii]
LID - 10.26355/eurrev_202003_20663 [doi]
AB  - OBJECTIVE: To study the expression of long non-coding ribonucleic acid (lncRNA) 
      UNC5B antisense RNA 1 (UASR1) in colorectal cancer (CRC) and its biological 
      functions, and to discuss the regulatory effect of the transcription factor on 
      lncRNA UASR1. PATIENTS AND METHODS: The expressions of lncRNA UASR1 in the CRC 
      tissues and cells were detected via quantitative Reverse Transcription-Polymerase 
      Chain Reaction (qRT-PCR) assay. After the expression of lncRNA UASR1 was 
      interfered, the change in the CRC cell proliferation ability was investigated 
      through cell counting kit-8 (CCK-8) assay and colony formation assay, 
      respectively. Changes in cell cycle distribution and apoptosis rate in CRC cells 
      after transfection of small-interfering UASR1 (si-UASR1) were detected using flow 
      cytometry. Potential transcription factors binding UASR1 promoter region were 
      analyzed through bioinformatics. The change in the UASR1 expression was measured 
      through the qRT-PCR assay after the paired box 5 (PAX5) expression was 
      interfered. Following the interference in the expressions of PAX5 and UASR1, 
      expression changes in the molecular markers of the mammalian target of rapamycin 
      (mTOR) signaling pathway were detected via Western blotting assay. RESULTS: The 
      qRT-PCR results indicated that the UASR1 expression was up-regulated in 39/45 CRC 
      tissues, and it identically presented the up-regulated expression level in the 
      CRC cells. After the UASR1 expression was interfered, the CRC cell proliferation 
      ability was degraded according to the CCK-8 assay and colony formation assay. 
      Based on the flow cytometry results, compared with the small-interfering-negative 
      control (si-NC) group, the cell cycle was arrested in the G1/G0 phase in the 
      si-UASR1 group, and apoptosis rate increased. Bioinformatics and qRT-PCR results 
      showed that the transcription factor PAX5 regulated the UASR1 expression. The 
      Western blotting assay indicated that the expressions of the molecular markers of 
      the mTOR signaling pathway were changed after the expressions of PAX5 and UASR1 
      were interfered. CONCLUSIONS: The transcription factor PAX5 promotes the 
      expression of lncRNA UASR1 in CRC. The highly expressed UASR1 facilitates the 
      malignant proliferation of CRC via the mTOR signaling pathway.
FAU - Wang, W
AU  - Wang W
AD  - Department of Colorectal Surgery, Changhai Hospital, Shanghai, China. 
      xuli_ch@163.com.
FAU - Wang, Z
AU  - Wang Z
FAU - Wang, H
AU  - Wang H
FAU - Li, X
AU  - Li X
FAU - Wang, H-T
AU  - Wang HT
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 (PAX5 Transcription Factor)
RN  - 0 (PAX5 protein, human)
RN  - 0 (RNA, Long Noncoding)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - Colorectal Neoplasms/*metabolism/pathology
MH  - Humans
MH  - PAX5 Transcription Factor/genetics/*metabolism
MH  - RNA, Long Noncoding/genetics/*metabolism
MH  - TOR Serine-Threonine Kinases/genetics/*metabolism
EDAT- 2020/04/10 06:00
MHDA- 2021/03/16 06:00
CRDT- 2020/04/10 06:00
PHST- 2020/04/10 06:00 [entrez]
PHST- 2020/04/10 06:00 [pubmed]
PHST- 2021/03/16 06:00 [medline]
AID - 20663 [pii]
AID - 10.26355/eurrev_202003_20663 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2020 Mar;24(6):2986-2993. doi: 
      10.26355/eurrev_202003_20663.