Nicotinamide induces mitochondrial-mediated apoptosis through oxidative stress in human cervical cancer HeLa cells
Nicotinamide participates in energy metabolism and influences cellular redox status and modulates multiple pathways related with both cellular survival and death. Recent studies have shown that it induced proliferation inhibition and apoptosis in many cancer cells. However, little is known about the effects of nicotinamide on human cervical cancer cells. We aimed to evaluate the effects of the indicated concentrations nicotinamide on cell proliferation, apoptosis and redox-related parameters in HeLa cells and investigated the apoptotic mechanism.
Materials and methods
After the treatment of the indicated concentrations nicotinamide, HeLa cell proliferation was evaluated by the CCK-8 assay and the production of ROS (reactive oxygen species) was measured using 2′,7′-Dichlorofluorescin diacetate. The apoptotic effect was confirmed by observing the cellular and nuclear morphologies with fluorescence microscope and apoptotic rate of HeLa cell apoptosis was measured by flow cytometry using Annexin-V method. Moreover, we examined the mitochondrial membrane potential by JC-1 method and measured the expression of apoptosis related genes using qRT-PCR and immunoblotting.
Nicotinamide restrained the HeLa cell proliferation and significantly increased the accumulation of ROS and depletion of GSH at relatively high concentrations. Furthermore, nicotinamide promoted HeLa cell apoptosis via the intrinsic mitochondrial apoptotic pathway.
Our study revealed that nicotinamide induced the apoptosis through oxidative stress and intrinsic mitochondrial apoptotic pathways in HeLa cell. The results emerge that nicotinamide may be an inexpensive, safe and promising therapeutic agent or a neoadjuvant chemotherapy for cervical cancer patients, as well useful to find new drugs for cervical cancer therapy.
Previous article in issueNext article in issue
NicotinamideOxidative stressMitochondrial apoptotic pathwayCervical cancer
Volume 181, 15 July 2017, Pages 62-69
Author links open overlay panelYiFengYonghuaWangChengruiJiangZishuiFangZhiqiangZhangXiaoyingLinLiweiSunWeiyingJiang
https://doi.org/10.1016/j.lfs.2017.06.003Get rights and content
Nicotinamide induces mitochondrial-mediated apoptosis through oxidative stress in human cervical cancer HeLa cells - ScienceDirect https://www.sciencedirect.com/science/article/abs/pii/S0024320517302771
Flavonoid Apigenin Is an Inhibitor of the NAD+ase CD38 ...
Apr 01, 2013 · We confirmed that quercetin is a CD38 inhibitor in vitro and in cells. Importantly, we demonstrate that apigenin(芹菜素） is a novel inhibitor of CD38 in vitro and in vivo. Treatment of cells with apigenin or quercetin inhibits CD38 and promotes an increase in intracellular NAD + levels.
Cited by: 157
Publish Year: 2013
CST - CD38 Antibody
Since CD38 is the primary mammalian NAD + glycohydrolase responsible for NAD + metabolism, CD38 may be a valuable therapeutic target for treatment of metabolic diseases regulated by NAD +-dependent pathways (7,8). CD38 has also been considered a possible therapeutic target for antibody-mediated therapy for myeloma and chronic lymphocytic ...
Brand: Cell Signaling Technology
Category: Primary Antibodies