2021
DOI: 10.18632/aging.203697
|View full text |Cite
|
Sign up to set email alerts
|

Propofol suppresses the growth and invasion of cervical carcinoma cells by inhibiting MIR155HG

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1

Citation Types

0
2
0

Year Published

2022
2022
2024
2024

Publication Types

Select...
3

Relationship

0
3

Authors

Journals

citations
Cited by 3 publications
(2 citation statements)
references
References 35 publications
0
2
0
Order By: Relevance
“…17 Propofol is a widely used intravenous anesthetic, and increasing evidence has shown that at clinically relevant concentrations (10-100 μM), propofol significantly suppresses the malignant biological behaviors of cancer cells. [18][19][20] Du et al 21 demonstrated that 30-100 μM propofol reduced the viability of CaSki and SiHa cells in a dose-and time-dependent manner. However, our study demonstrated that 0-100 μM propofol had no effect on cell viability after treatment for 24 and 48 h and that 30 μM propofol did not affect the malignancy of HeLa and CaSki cells after treatment for 48 h. Mitosis is a necessary pathway for cancer cell proliferation.…”
Section: Discussionmentioning
confidence: 99%
“…17 Propofol is a widely used intravenous anesthetic, and increasing evidence has shown that at clinically relevant concentrations (10-100 μM), propofol significantly suppresses the malignant biological behaviors of cancer cells. [18][19][20] Du et al 21 demonstrated that 30-100 μM propofol reduced the viability of CaSki and SiHa cells in a dose-and time-dependent manner. However, our study demonstrated that 0-100 μM propofol had no effect on cell viability after treatment for 24 and 48 h and that 30 μM propofol did not affect the malignancy of HeLa and CaSki cells after treatment for 48 h. Mitosis is a necessary pathway for cancer cell proliferation.…”
Section: Discussionmentioning
confidence: 99%
“…In glioma U87 and U251 cells, RES upregulated NEAT1, MIR155HG, MEG3, and ST7OT1 during induction of apoptosis [ 201 ]. Since NEAT1 and MIR155HG are oncogenic [ 202 , 203 , 204 ] and MEG3 is tumor-suppressing [ 166 ], the effect of RES on MEG3 may be a predominant contributor to apoptosis of these cells. NEAT1 was demonstrated to activate ERK, which is a component molecule in RSTAPs ( Figure 1 ) [ 202 ].…”
Section: Involvements Of Lncrs In Rstapsmentioning
confidence: 99%