Page 102 - Book of Abstracts

th
8 Biannual Conference on Chemistry - CHEM 08

MiR-520c-3p Modulates Doxorubicin-chemosensitivity in
HepG2 cells

Mohamed A. Ragheb , Marwa H. Soliman , Emad M. Elzayat , Mervat S.
1†
2
1†
Mohamed , Nada El-Ekiaby , Ahmed I. Abdelaziz , Abdelhady A.
4
1,3
4
Abdelwahab *
5,
1 Department of Chemistry (Biochemistry Division), Faculty of Science, Cairo
University, Giza, Egypt. Department of Zoology, Faculty of Science, Cairo
2
University, Giza, Egypt. Department of Biochemistry, Faculty of Science,
3
University of Tabuk, Tabuk, Kingdom of Saudi Arabia. School of Medicine,
4
NewGiza University (NGU), NewGiza, Cairo, Egypt. Department of Cancer
5
Biology, National Cancer Institute, Cairo University, Cairo, Egypt.
Email: abdelhady.abdelwahab@nci.cu.edu.eg.

ABSTRACT
Background: Doxorubicin (DOX) is the most common drugs used in cancer
therapy, including hepatocellular carcinoma (HCC). Drug resistance, is one of
chemotherapy’s significant problems. Emerging studies have shown that
microRNAs (miRNAs) could participate in regulating this mechanism.
Nevertheless, the impact of miRNAs on HCC chemoresistance is still enigmatic.
Objective: Investigating the role of miR-520c-3p in enhancement of anti-tumor
effect of DOX against HepG2 cells.
Methods: Expression profile for liver related miRNAs (384 miRNAs) has been
analyzed on HepG2 cells treated with DOX using qRT-PCR. miR-520c-3p, the
most deregulated miRNA, was selected for combination treatment with DOX.
Expression level for LEF1, CDK2, CDH1, VIM, Mcl-1 and TP53 was evaluated in
miR-520c-3p transfected cells. Cell viability, colony formation, wound healing as
well as apoptosis assays have been demonstrated. Furthermore, Mcl-1 protein
level was measured using western blot technique.
Results: The present data indicated that miR-520c-3p overexpression could
render HepG2 cells chemo-sensitive to DOX through enhancing its suppressive
effects on proliferation, migration, and induction of apoptosis. The suppressive
effect of miR-520c-3p involved altering the expression levels of some key
regulators of cell cycle, proliferation, migration and apoptosis including LEF1,
CDK2, CDH1, VIM, Mcl-1 and TP53. Interestingly, Mcl-1 was found to be one of
the potential targets of miR-520c-3p, and its protein expression level was down-
regulated upon miR-520c-3p overexpression.
Conclusion: Our data referred to the tumor suppressor function of miR-520c-3p
that could modulate chemosensitivity of HepG2 cells toward DOX treatment,
providing a promising therapeutic strategy in HCC.
Keywords: Hepatocellular carcinoma, miR-520c-3p, Doxorubicin,
Chemotherapy, Drug resistance, Mcl-1.

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