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...

Full description

Saved in:
Bibliographic Details
Published in:Life sciences (1973) 2017-07, Vol.181, p.62-69
Main Authors: Feng, Yi, Wang, Yonghua, Jiang, Chengrui, Fang, Zishui, Zhang, Zhiqiang, Lin, Xiaoying, Sun, Liwei, Jiang, Weiying
Format: Article
Language:English
Subjects:
Antineoplastic Agents - administration & dosage
Antineoplastic Agents - pharmacology
Apoptosis
Apoptosis - drug effects
Cancer
Cancer therapies
Cell proliferation
Cell Proliferation - drug effects
Cervical cancer
Cervix
Chemical compounds
Chemotherapy
Cholecystokinin
Cytometry
Drugs
Energy metabolism
Female
Flow Cytometry
Fluorescence
Gene expression
HeLa Cells
Humans
Immunoblotting
Membrane potential
Membrane Potential, Mitochondrial - drug effects
Metabolism
Microscopy, Fluorescence
Mitochondria
Mitochondria - drug effects
Mitochondria - metabolism
Mitochondrial apoptotic pathway
Niacinamide - administration & dosage
Niacinamide - pharmacology
Nicotinamide
Oxidation-Reduction - drug effects
Oxidative stress
Oxidative Stress - drug effects
Pharmacology
Reactive oxygen species
Reactive Oxygen Species - metabolism
Studies
Uterine Cervical Neoplasms - drug therapy
Uterine Cervical Neoplasms - pathology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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. 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.
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2017.06.003