Background:
Non-small cell lung cancer (NSCLC) consists of a class of heterogeneous
diseases.
Objective:
LncRNAs are exceedingly implicated in the pathogenesis of NSCLC. Herein, the current
study set out to illustrate the molecular mechanism of SH3BP5-AS1 in NSCLC cells.
Methods:
SH3BP5-AS1 expression in clinical NSCLC tissues and its impact on prognosis were analyzed
by bioinformatics database. SH3BP5-AS1 expression patterns in NSCLC cell lines
(A549/H1299/H1975/H460) and human normal lung epithelial cell lines (BEAS-2B) were examined
by RT-qPCR. SH3BP5-AS1 was overexpressed in A549 or silenced in H1975 cells through
transfection to assess its effect on proliferation, cell cycle distribution, and apoptosis, apoptosisrelated
protein (Cleaved Caspase-3, Bax, Bcl-2) levels, invasive, migratory, and healing capacity
through CCK-8, colony formation assay, flow cytometry, Western blot, Transwell, and cell scratch
test.
Results:
SH3BP5-AS1 was under-expressed in NSCLC clinical tissues, and NSCLC patients with
low SH3BP5-AS1 expression showed poor prognosis. A549/H1299/H1975/H460 cells had reduced
levels of SH3BP5-AS1, with the relative level lowest/highest expression in A549/H1975 cells, respectively.
SH3BP5-AS1 overexpression repressed A549 cell proliferation, slowed down cell cycle
progression, enhanced apoptosis, elevated Cleared Caspase-3, Bax, suppressed Bcl-2 protein levels,
and inhibited migratory, invasive, and scratch healing capacities, while SH3BP5-AS1 silencing
brought about the opposite results in H1975 cells.
Conclusion:
SH3BP5-AS1 could suppress NSCLC cell proliferation, slow down cell cycle progression,
stimulate apoptosis, and limit invasion and migration.