Open Access
ARTICLE
Nicotinic acid induces apoptosis of glioma cells via the calcium-dependent endoplasmic reticulum stress pathway
XIANGCAI YANG1, JIAGUI QU2, JIEJING LI1,*
1 Department of R&D, Biotech & Science Company of UP, Guangzhou Branch, Guangzhou, 51000, China
2 State Key Laboratory of Brain and Cognitive Science, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, China
* Corresponding Author:JIEJING LI. Email:
BIOCELL 2022, 46(4), 1041-1051. https://doi.org/10.32604/biocell.2022.017383
Received 06 May 2021; Accepted 17 June 2021; Issue published 15 December 2021
Abstract
Malignant glioma is one of the most common and deadly tumors in the central nervous system while developing effective treatments for this devastating disease remains a challenge. Previously, we demonstrated that the vitamin nicotinic acid (NA) inhibits glioma invasion. Here, we show that high-dose NA induces apoptosis of malignant glioma cells
in vitro and
in vivo. In cultured U251 glioma cells treated with NA, we detected ER stress that was likely caused by elevated intracellular calcium levels. The elevated calcium can be attributed to the activation of TRPV1, a cation channel that has been implicated in cutaneous flushing caused by NA administration. Our data further suggested that NA-induced apoptosis is mediated by the calcium-dependent proteases called calpains, whose activities are drastically upregulated by NA. NA-induced apoptosis of U251 cells can be attenuated by blocking calpain activity or knocking down TRPV1. These results reveal a novel function of NA in regulating glioma cell apoptosis
via the calcium-dependent ER stress pathway and imply a potential application of NA for the treatment of malignant glioma.
Keywords
Cite This Article
YANG, X., QU, J., LI, J. (2022). Nicotinic acid induces apoptosis of glioma cells
via the calcium-dependent endoplasmic reticulum stress pathway.
BIOCELL, 46(4), 1041–1051. https://doi.org/10.32604/biocell.2022.017383