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Poster lunch

2048 - PARK2 deficiency promotes Cervical Tumorigenesis by deregulation in cyclin activity via P53 dependent pathway (5P)


18 Nov 2017


Poster lunch


Cancer Biology;  Cervical Cancer




Annals of Oncology (2017) 28 (suppl_10): x1-x6. 10.1093/annonc/mdx652


Z.B. Hafeez, K.U. Fakhri, Z. Iqbal, M.A. Rizvi

Author affiliations



Abstract 2048


Cervical cancer is the second most common cause of cancer in women worldwide. Genetic instability in cervical cancer is commonly associated with losses or gains of function of tumor suppressor genes/oncogenes. Parkin or PARK2 gene has been considered a new candidate tumor suppressor in various types of cancer. Mutation or deletion/inactivation of PARK2 has been identified frequently in human malignant tumors. It encodes an E3 ubiquitin ligase that targets a variety of candidate substrate proteins, resulting in proteosomal degradation. This study aimed to investigate the role of PARK2 in controlling the cell cycle regulatory protein cyclin. However, the underlying molecular mechanism by which PARK2 plays a role in cancer development remains to be fully understood.


PARK2 expression level was evaluated by immunohistochemical staining of 110 cases of cervix cancer tissue microarray (TMA) slide and 10 spot were normal adjacent tissue out of 110 spot. Further, PARK2 gene was specifically knocked down in a cervical cell line by using PARK2-specific SiRNA, then cell cycle study was performed by FACS and also evaluation of the expression levels of cyclin D, cyclin E and cyclin-dependent kinases and P53 by western blot in cervical cell line in vitro.


Immunohistochemical staining of cervix tissues showed mild PARK2 expression in 41% of cases. However in most cases we found loss of expression but in all normal adjacent tissue higher expression was seen. We also observed a decrease in the expression level of PARK2 cervix cancer cell lines. We examined the in vitro cell proliferation after knock down of PARK2 and found increased growth rate. Further study revealed that following knock down of PARK2, we observed a significant number of cells entering into S Phase of cell cycle and also decrease in the number of cells in G1 phase. Increase in expression levels of cyclin D and cyclin E was observed but there were no significant changes found in the level of cdk2 and cdk6. We further found a decrease in expression of P53 after blocking of PARK2 in western blot analysis.


These data suggest that PARK2 controls the regulation of cell cycle progression and loss of PARK2 expression links with increase in cervical cancer progression both in vitro and in vivo.

Clinical trial identification

Legal entity responsible for the study



Indian Council of Medical Research (ICMR) and UGC, India.


All authors have declared no conflicts of interest.

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