لخّصلي

Lung cancer is statistically one of the most
common diseases worldwide, and presents a serious threat to human health and life1,2. In recent
decades, lung cancer death rates have increased
yearly in an apparent trend, particularly nonsmall-cell lung cancer (NSCLC)3
. NSCLC is the
most common type of lung cancer. At present,
chemotherapy is one of the most common methods for NSCLC treatment4,5. However, many chemotherapeutic drugs produce debilitating side
effects on the human body, and hence, are limited
in clinical application.
Recent attention has focused on phytochemicals as anticancer agents. Curcumin is a yellow
pigment found in turmeric rhizomes, reported to
exhibit various anti-inflammatory, anti-angiogenic, anti-proliferative, and antioxidant properties.
More importantly, it was found to not induce
cytotoxic effects in healthy cells6,7. Many reports8,9 have suggested that curcumin may induce
apoptosis in malignant cells, indicating potential
use in the treatment of tumors. Apoptosis is a
programmed cell death process related to tumor
malignancy, and is very important in embryonic
development and tissue homeostasis. Little is
currently known about the effects of curcumin
on NSCLC, or the mechanism through which
such effects would be induced. Therefore, in this
study, we explored the effects of curcumin on
NSCLC and investigated the associated mechanisms.
Oxidative stress is one of the most common
causes of cellular damage, mostly due to the
build-up of reactive oxygen species (ROS) free
radicals through impairments to antioxidative
enzymes, such as superoxide dismutase (SOD).
Dysregulated oxidative metabolism may lead to
cell death, an important reason for increased
proliferation, with several studies10-12 showing
the involvement of oxidative stress in cell proliferation. Therefore, we explored the relationship
between oxidative stress and cell proliferation in
curcumin-treated NSCLC cells.
The Wnt/β-catenin pathway determines the
development of vertebrates and invertebrates by
regulating cell destiny13. Wnt is a secreted glycoprotein which binds to Frizzled receptors. β-catenin, which is deregulated in many cancers, is
a multifunctional adaptor protein/transcription
factor. In the absence of Wnt binding (off-state),
β-catenin is downregulated via a degradation
complex including GSK-3, CK1, Axin, APC, and
PP2A14,15. Previous studies have reported that the
Wnt/β-catenin signaling pathway is abnormally
active in hepatic carcinoma16. However, little is
known about the mechanism of Wnt/β-catenin
signaling in lung cancer cells.
In this study, we explored the effect of curcumin on proliferation in NSCLC A549 cells and
investigated its associated mechanism. Results
indicated that curcumin could inhibit NSCLC
proliferation induced by oxidative stress-mediated upregulation of the Wnt/β-catenin pathway.