Lysine‐specific demethylase 1 activation by vitamin B2 attenuates efficacy of apatinib for proliferation and migration of gastric cancer cell MGC‐803

Abstract

B vitamins play an essential role in the biosynthesis of nucleotides, replication of DNA, supply of methyl-groups, growth and repair of cells, aberrancies of which have all been implicated in carcinogenesis. Although the potential role of vitamin B in relation to the risk of cancer, including breast, and colorectal cancer, has been investigated in several observational studies, the mechanism of action is still unclear. In this study, vitamin B2 exhibited efficient activation of LSD1 by occupying the active sites where FAD stands. Interestingly, vitamin B2 significantly downregulated expression of CD86, a sensitive surrogate biomarker of LSD1 inhibition, and showed marked activation of gastric cancer cell migration and invasion. Meanwhile, vitamin B2 induced activation of LSD1 may attenuate the proliferation inhibition, and anti-migration effects of apatinib in gastric cancer cells. These findings suggested that vitamin B supplementation may interfere with the efficacy of apatinib in patients with gastric cancer.

Biochemical and Toxicological Evaluation of Atorvastatin and Riboflavin in Diethylnitrosamine Induced Hepatocellular Carcinoma

“…On the contrary, the excess of riboflavin may enhance the cell division of cancer cells as vitamins cause a manifold increase in the biosynthesis of nucleotides, replication of DNA, the supply of methyl-groups, growth and repair of the cells. Aberrant dysregulation in all these biological processes have been implicated in the development of carcinogenesis [43].…”

LINC00675 Suppresses Cell Proliferation and Migration via Downregulating the H3K4me2 Level at the SPRY4 Promoter in Gastric Cancer

“…Of note, a strong decrease was caused in SPRY4 protein level upon LINC00675 overexpression, consistent with the decrease in SPRY4 mRNA level (Figure S3). Since LSD1 has been proven to be an oncogene in GC in many studies, 38,39 we hypothesized that the overexpression of LINC00675 suppressed GC proliferation and metastasis through its competitive binding with LSD1, which partially inhibited the function of LSD1. To confirm the hypothesis, we designed the small interfering (si)-LSD1 plasmid and found that when LSD1 was efficiently decreased (Figure S4), the expression of SPRY4 was also downregulated, which was consistent with the results upon LINC00675 overexpression (Figure 4C).…”

Apatinib Promotes Ferroptosis in Colorectal Cancer Cells by Targeting ELOVL6/ACSL4 Signaling

“…Apatinib, also known as YN968D1, is a new oral smallmolecule agent with antiangiogenic effect for the treatment of multiple solid tumors, including gastric cancer, colorectal cancer and hepatocellular carcinoma. 11,12 It has been well reported that apatinib severs as an optional treatment in metastatic CRC. 13 Apatinib, used as third-line treatment, effectively improves the prognosis of patients with heavily treated metastatic CRC.…”