To determine the relationships between
miR-96-5p/
-182-5p and
GPC1 in pancreatic cancer (PC), we conducted the population and in vitro studies. We followed 38 pancreatic cancer patients, measured and compared the expression of
miR-96-5p/
-182-5p,
GPC1, characteristics and patients’
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To determine the relationships between
miR-96-5p/
-182-5p and
GPC1 in pancreatic cancer (PC), we conducted the population and in vitro studies. We followed 38 pancreatic cancer patients, measured and compared the expression of
miR-96-5p/
-182-5p,
GPC1, characteristics and patients’ survival time of different
miR-96-5p/
-182-5p expression levels in PC tissues. In an
in vitro study, we investigated the proliferation, cycle and apotosis in cells transfected with mimics/inhibitors of the two miRNAs, and determine their effects on
GPC1 by dual-luciferase assay. In the follow-up study, we found that the expressions of
miR-96-5p/
-182-5p were lower/higher in PC tissues; patients with lower/higher levels of
miR-96-5p/
-182-5p suffered poorer characteristics and decreased survival time. In the
in vitro study, the expressions of
miR-96-5p/
-182-5p were different in cells. Proliferation of cells transfected with
miR-96-5p mimics/inhibitors was lower/higher in Panc-1/BxPC-3; when transfected with
miR-182-5p mimics/inhibitors, proliferation of cells were higher/lower in AsPC-1/Panc-1. In a cell cycle study, panc-1 cells transfected with
miR-96-5p mimics was arrested at G0/G1; BxPC-3 cells transfected with
miR-96-5p inhibitors showed a significantly decrease at G0/G1; AsPC-1 cells transfected with
miR-182-5p mimics was arrested at S; Panc-1 cells transfected with
miR-182-5p inhibitors showed a decrease at S.
MiR-96-5p mimics increased the apoptosis rate in Panc-1 cells, and its inhibitors decreased the apoptosis rate in BxPC-3. Dual luciferase assay revealed that
GPC1 was regulated by
miR-96-5p, not
-182-5p. We found that
miR-96-5p/
-182-5p as good markers for PC;
miR-96-5p, rather than
-182-5p, inhibits
GPC1 to suppress proliferation of PC cells.
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