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A n n u a l E u r o p e a n C o n f e r e n c e o n
Gastroenterology
Euro Gastro 2018
J u n e 1 9 - 2 0 , 2 0 1 8
P a r i s , F r a n c e
Page 43
Journal of Clinical Gastroenterology and Hepatology
ISSN 2575-7733
Biography
Nada Alaaeddine was the head of regenerative medicine
lab at the faculty of medicine at the University of St Joseph
Beirut Lebanon. Currently, she is an invited professor at the
immunology and inflammation lab at CHUM, University
of Montreal, Canada. She also works on cell therapy and
osteoarthritis and cancer such as hepatocellular carcinoma, as
well telomerase and cancer. She has won many awards such
as Phil Rosen awards, the awards of an outstanding woman
for innovation on stem cells, and recently she was chosen to
represent the Arab pioneer on stem cells to be mentioned on
Forbes.
nada.aladdin@gmail.comNada Alaaeddine
1
, Nagib Saliba
3
, George Hilal
2
, Mayssam
Moussa
2
, Ghada Hassan
1
, Riad Sarkis
3
, Marwan Nasr
3
, Oula El
Atat
2
, Charbel Khalil
2
and Rim Serhal
2
1
Centre Hospitalier de l'Universite de Montreal, Canada
2
Saint-Joseph University, Lebanon
3
Hotel-Dieu de France, Lebanon
Nada Alaaeddine et al., J Clin Gastroenterol Hepatol 2018, Volume: 2
DOI: 10.21767/2575-7733-C1-002
Effect of adipose derived mesenchymal stem cells on hepato-
cellular carcinoma: in vitro inhibition of carcinogenesis
Background:
Hepatocellular carcinoma (HCC) is a malignant, deadly disease
with higher incidence and no effective treatment. Adipose derived stem cells
(ADMSCs) have been shown to exhibit therapeutic efficacy in many diseases;
however, their therapeutic effect on cancer is not clear and controversial. In
this study, we investigated the effect of ADMSCs and their conditioned media
(CM) on biological responses of HCC cell lines, HepG2 and PLC-PRF-5 cells.
Methods:
Proliferation rate of cancer cells was measured using cell counting
kit-8. Apoptosis level was determined by flow cytometry. Protein and mRNA
expressions were measured by ELISA and real time PCR respectively. Migration
and invasion rates were detected by transwell migration and invasion assay.
Results:
Our data demonstrated that ADMSCs and their CM significantly
inhibited the proliferation and increased the apoptosis of HepG2 and PLC-
PRF-5 cells, along with an upregulation of the
p53/Retinoblastoma
mRNA
and a downregulation of
c-myc/hTERT
. Co-culturing HCC cell lines with
ADMSCs or treating them with ADMSCs CM also suppressed the expression
of alpha-fetoprotein and Des-γ-carboxyprothrombin, two important markers
of carcinogenicity in HCC. In addition, ADMSCs and ADMSCs CM diminished
migration and invasion levels of the HepG2 and PLC-PRF-5 cells, possibly
through increased expression of the tissue inhibitor metalloproteinases TIMP-
1, TIMP-2 and TIMP-3.
Conclusion:
These findings shed a new light on a protective role for ADMSCs
and their CM in controlling the invasiveness and carcinogenesis of HCC and
might be a new pathway to investigate in the treatment of this disease.