Highlights
- •PCMT1 knockdown inhibited proliferation and the invasive ability in breast cancer cells.
- •PCMT1 silencing triggered apoptosis in breast cancer cells.
- •miR-195 was identified as the only upstream miRNA of PCMT1 in breast cancer.
- •SNHG16 was screened out as the only upstream lncRNA of miR-195 in breast cancer.
Abstract
Background
Protein L-isoaspartate (D-aspartate) O-methyltransferase (PCMT1) is a highly conserved
protein repair enzyme that participates in regulating the progression of human cancers.
We therefore studied the function and the related mechanisms of PCMT1 in breast cancer
cells.
Methods
Expression profile and prognostic analysis of PCMT1 in breast cancer patients were
analyzed using online databases. PCMT1 expression in breast cancer cells was detected
by western blot analysis. Cell proliferation was determined by CCK-8 and colony formation
assays. Apoptosis was evaluated using flow cytometry analysis and caspase-3/7 activity
assay. Cell invasion was assessed by Transwell invasion assay. The small nucleolar
RNA host gene 16 (SNHG16)/miR-195/PCMT1 regulatory axis was identified using bioinformatics
analysis.
Results
PCMT1 expression was increased in breast cancer tissues and cells. High PCMT1 expression
was correlated with poor prognosis in breast cancer patients. PCMT1 knockdown suppressed
cell proliferation and colony formation ability in breast cancer cells. Moreover,
PCMT1 knockdown induced apoptosis and restrained the invasive ability in breast cancer
cells. PCMT1 overexpression increased the proliferative and invasive abilities of
breast cancer cells. miR-195 was identified as the unique upstream miRNA of PCMT1.
SNHG16 was identified as the unique upstream lncRNA of miR-195. SNHG16 knockdown downregulated
PCMT1 by increasing miR-195 expression. Breast cancer cell proliferation was regulated
by the SNHG16/miR-195/PCMT1 axis.
Conclusion
PCMT1 silencing inhibited cell proliferation and invasion and induced apoptosis in
breast cancer cells and the SNHG16/miR-195/PCMT1 regulatory axis might serve as a
potential therapeutic target for breast cancer.
Keywords
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Article info
Publication history
Published online: December 23, 2022
Accepted:
December 19,
2022
Received in revised form:
August 11,
2022
Received:
March 25,
2022
Identification
Copyright
© 2022 Elsevier Inc. All rights reserved.
