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Nicotinic acid induces apoptosis of glioma cells via the calcium-dependent endoplasmic reticulum stress pathway

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.

Received 06 May 2021; Accepted 17 June 2021; Issue published 15 December 2021


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.


Nicotinic acid; Apoptosis; Calcium; Endoplasmic reticulum stress

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.

This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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