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Cancer Congress 2019
Journal of Cancer Immunology &Therapy | Volume 2
Page 22
July 22-23, 2019 | Brussels, Belgium
OF EXCELLENCE
IN INTERNATIONAL
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CANCER SCIENCE AND THERAPY
2
nd
Global Congress on
A SURVIVIN REGULATED ONCOLYTIC ADENOVIRUS CAN IMPROVE THERAPEUTIC OUT-
COME IN CHEMOTHERAPY RESISTANT LUNG CANCER
Sakhawat A, Muhammad Tahir, Ma Ling, Aamir Ali Khan, Xue Chai Chen
and
Yinghui Huang
Beijing University of Technology, China
T
he treatment of advanced lung cancer is restricted due to chemotherapy resistance even in the patients
which initially show a good response. Author previously investigated a surviving promoter regulated condi-
tionally replicating adenovirus (Sur-P-CRAd) for its anti-tumor potential along with cisplatin in three lung can-
cer cell lines; A549, H292 and H661 and found it very efficient. Also, surprisingly, CRAd in monotherapy proved
very lethal against chemotherapy resistant sublines of above mentioned cells. They have suggested cispla-
tin-driven up regulation of CAR as a selective vulnerability of chemotherapy-resistant cancers. Keeping in mind
the heterogeneity of lung cancer, this study employed two different lung cancer cells, H23 and H2126 and
their resistant sublines H23/CPR, H2126/CPR, which were developed in our lab. RT-PCR and western blotting
analysis confirmed that ABCB1 (MDR1) gene was overexpressed at both mRNA and protein levels in resistant
sublines. Also, cocksackie-adenovirus receptor (CAR) expression found significantly up regulated in resistant
cells as compared to chemo-sensitive cells. Resistant cells exhibited enhanced adenoviral transduction efficacy
in X-gal staining assay which validated the up regulation of CAR. MTT assay, flow cytometry and scratch assays
showed that cisplatin significantly decreases the viability of chemo-sensitive cells and its combination with
CRAd synergistically inhibited cancer cell survival. Moreover, transwell assay revealed that CRAd pre-treatment
restricts migratory ability of cancer cells. Epithelial to mesenchymal transition (EMT) markers investigation dis-
played that CRAd-treatment could reverse EMT event, but its molecular mechanism needs further elucidation.
CRAd monotherapy experiments with resistant cells recapitulated similar results which established our hy-
pothesis that CRAd alone is a very potent anticancer agent for resistant and metastatic tumors. These insights
may prove to be a timely opportunity for the application of CRAd in recurrent drug-resistant cancers. Further
studies are warranted to confirm the possible use of this innovative treatment approach in clinics and to move
it from bench to bedside.
J Cancer Immunol Ther 2019, Volume 2