THUMPD3‐AS1
inhibits ovarian cancer cell apoptosis through the
miR‐320d/ARF1
axis
Abstract
Ovarian cancer is one of the most common gynecologic malignancies that has a poor prognosis.
THUMPD3‐AS1
is an oncogenic long noncoding RNA (lncRNA) in several cancers. Moreover,
miR‐320d
is downregulated and inhibited proliferation in ovarian cancer cells, whereas
ARF1
was upregulated and promoted the malignant progression in epithelial ovarian cancer. Nevertheless, the role of
THUMPD3‐AS1
in ovarian cancer and the underlying mechanism has yet to be elucidated. Human normal ovarian epithelial cells (IOSE80) and ovarian cancer cell lines (CAVO3, A2780, SKOV3, OVCAR3, and HEY) were adopted for in vitro experiments. The functional roles of
THUMPD3‐AS1
in cell viability and apoptosis were determined using CCK‐8, flow cytometry, and TUNEL assays. Western blot was performed to assess the protein levels of
ARF1
,
Bax
,
Bcl‐2
, and
caspase 3
, whereas RT‐qPCR was applied to measure
ARF1
mRNA,
THUMPD3‐AS1
, and
miR‐320d
levels. The targeting relationship between
miR‐320d
and
THUMPD3‐AS1
or
ARF1
was validated with dual luciferase assay.
THUMPD3‐AS1
and
ARF1
were highly expressed in ovarian cancer cells, whereas
miR‐320d
level was lowly expressed.
THUMPD3‐AS1
knockdown was able to repress cell viability and accelerate apoptosis of OVCAR3 and SKOV3 cells. Also,
THUMPD3‐AS1
acted as a sponge of
miR‐320d
, preventing the degradation of
ARF1
.
MiR‐320d
downregulation reversed the tumor suppressive function induced by
THUMPD3‐AS1
depletion. Additionally, miR‐320d overexpression inhibited ovarian cancer cell viability and accelerated apoptosis, which was overturned by overexpression of
ARF1
.
THUMPD3‐AS1
inhibited ovarian cancer cell apoptosis by modulation of
miR‐320d
/
ARF1
axis. The discoveries might provide a prospective target for ovarian cancer treatment.
