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« Back to Contents CERVICAL CANCER

LiFE re

Literature for ENYGO

Emerging molecular-targeted therapies or early preclinical trials
in cervical cancer

Editor Marcin Mardas 7. S hao et al. reported that EM23, a natural sesquiterpene lactone,
exhibited anti-cancer activity in human cervical cancer cell lines
Descriptive summary by inducing apoptosis as indicated by caspase 3 activation, XIAP
downregulation, and mitochondrial dysfunction. Additionally,
1. Xie et al. reported that volasertib (BI 6727), a highly selective EM23 inhibited the Akt/mTOR pathway and induced autophagy,
and potent inhibitor of PLK1, can markedly induce cell growth which was observed to be proapoptotic and mediated by ROS.
inhibition, cell cycle arrest at G2/M phase and apoptosis with the
decreased protein expressions of PLK1 substrates survivin and 8. Z aman et al. reported a poly(lactic-co-glycolic acid)-based cur-
wee1 in human cervical cancer cells. Furthermore, volasertib also cumin nanoparticle formulation (Nano-CUR). In comparison to free
enhances the intracellular reactive oxidative species and signifi- curcumin, Nano-CUR effectively inhibited cell growth, induced
cantly potentiates the activity of cisplatin to inhibit the growth of apoptosis, and arrested the cell cycle in cervical cancer cell
cervical cancer in vitro and in vivo. lines. Nano-CUR treatment modulated entities such as miRNAs,
transcription factors, and proteins associated with carcinogenesis.
2. J i et al. reported unique nanoparticles with a size less than <200 nm Moreover, Nano-CUR effectively reduced the tumour burden in a
(FPCC) prepared for the selective delivery of carboplatin to the cervi- preclinical orthotopic mouse.
cal cancer cells. FPCC showed a superior cytotoxic effect - the IC50
(concentration of the drug required to kill 50 % of the cells) value of 9. L ee et al. reported that snake venom toxin (SVT) inhibited the
FPCC was 0.65 μg/ml comparing to 2.35 μg/ml for free carboplatin. growth of cervical cancer cells by the induction of apoptotic cell
death through the inhibition of NF-κB. In vivo study also showed
3. L in et al. evaluated the antitumor effect of the fisetin, combined that SVT (0.5 and 1 mg/kg) inhibited tumour growth by inactiva-
with sorafenib, against human cervical cancer cells in vitro and in tion of NF-κB.
vivo. Apoptosis induction was achieved by caspase-3 and caspase-8
activation. In vivo studies revealed that the combination of fisetin
and sorafenib was superior to sorafenib treatment alone.

4. Milosevic et al. evaluated the role of sorafenib in patients with
cervical cancer receiving radical radiotherapy and concurrent
cisplatin. Sorafenib was administered daily for 7 days before the
start of standard therapy in patients with early-stage, low-risk dis-
ease and also during radiochemotherapy in patients with high-risk
disease. Sorafenib alone reduced tumour perfusion/permeability
and an increase in hypoxia. This would make the tumour rather
resistant to chemoradiation and lead to tumour growth rather than
tumour control. The results led to early closure of the study.

5. Zhang et al. reported that propofol significantly decreased cell via-
bility and increased cell apoptosis in Hela, Caski, and C-33A cells,
while HOTAIR overexpression promoted cell viability and inhibited
cell apoptosis. In vivo, propofol inhibited the tumour size but had
no inhibition effect in HOTAIR overexpression group.

6. Pandurangan et al. investigated the cytotoxicity of copper oxide
nanorods in human cervical carcinoma cells. They showed the cell
rounding and nuclear fragmentation following the exposure of
copper oxide nanorods. mRNA expression of p53 and caspase 3
was increased, confirming apoptosis at the transcriptional level.

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International Journal of Gynecological Cancer, Volume 26, Supplement #1 Page 40