Data from: Downregulation of endometrial mesenchymal marker SUSD2 causes cell senescence and cell death in endometrial carcinoma cells

The cause of death among the majority of endometrial cancer patients
involves migration of cancer cells within the peritoneal cavity and
subsequent implantation of cancer spheroids into neighbouring organs. It
is, thereby, important to identify factors that mediate metastasis. Cell
adhesion and migration are modified by the mesenchymal stem cell (MSC)
marker Sushi domain containing 2 (SUSD2), a type I transmembrane protein
that participates in the orchestration of cell adhesion and migration
through interaction with its partner Galactosidase-binding soluble-1
(LGALS1). MSCs have emerged as attractive targets in cancer therapy. Human
endometrial adenocarcinoma (Ishikawa) cells were treated with TGFβ
(10ng/ml) for 72h. SUSD2, LGALS1 and MKI67 transcript levels were
quantified using qRT-PCR. The proportion of SUSD2 positive (SUSD2+) cells
and SMAD2/3 abundance were quantified by FACS and Western blotting,
respectively. Senescent cells were identified with β-galactosidase
staining; cell cycle and cell death were quantified using Propidium Iodide
staining. Treatment of endometrial cancer cells (Ishikawa cells) with TGFβ
(10ng/ml) significantly decreased SUSD2 transcript levels and the
proportion of SUSD2 positive cells. Silencing of SUSD2 using siRNA
resulted in senescence and cell death of Ishikawa cells via activation of
SMAD2/3. These findings suggest that SUSD2 counteracts senescence and cell
death and is thus a potential chemotherapeutic target in human endometrial
cancer.