Boric Acid Exhibits Anticancer Properties in Human Endometrial Cancer Ishikawa Cells

Abstract

Objective This study aims to explore the potential anti-cancer properties of boric acid (BA) in human endometrial cancer Ishikawa cells by assessing its influence on cell viability, apoptosis, oxidative stress, and inflammatory responses. Methods The impact of BA at concentrations ranging from 2.5 to 100 mM on cell viability was assessed in Ishikawa cells and normal fibroblast L929 cells (used as the control) through the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Spectrophotometric measurements were performed to determine the total oxidant status (TOS) and total antioxidant status (TAS) in BA-treated cells, and the oxidative stress index (OSI) was calculated. The enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of cytochrome c and caspase 3, both of which are constituents of the extrinsic apoptotic pathway. Furthermore, changes in the concentrations of pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) in the cells were analyzed using ELISA and immunofluorescence staining. Results The exposure of Ishikawa cells to BA for 24 hours led to a dose-dependent decline in cell viability, with an IC 50 value of 40 mM. BA dose-dependently increased cytochrome c and caspase 3 levels in cancer cells. In Ishikawa cells, BA treatment led to a significant elevation in OSI. Moreover, the concentrations of TNF-α and IL-1β exhibited a dose-dependent decrease in BA-treated cells. On the other hand, in L929 cells, BA decreased OSI in a dose-dependent manner but did not change TNF-α and IL-1β levels. Concentrations up to 80 mM had no effect on cell viability and apoptosis, but BA at 80 mM concentration decreased viability and increased cytochrome c and caspase 3 levels in L929 cells. Conclusion BA inhibited cell viability, triggered apoptosis, induced oxidative stress, and suppressed inflammatory responses in endometrial cancer cells. Notably, at its IC 50 concentration, BA had no cytotoxic effect on normal fibroblasts. Given its favorable properties, BA may provide a valuable therapeutic option to impede the development and progression of endometrial cancer.

Borax affects cellular viability by inducing ER stress in hepatocellular carcinoma cells by targeting SLC12A5

“… 35 Moreover, in vitro experiments employing various cell lines, such as Ishikawa cells, illustrated a significant decline in cell proliferation at boric acid concentrations of 40 mM and above. 36 Additionally, our earlier research revealed that treatment with 10.77 mM boric acid in DU‐145 cells led to a noteworthy reduction in cell growth. 37 Collectively, extant literature delineates a trend wherein boron compounds impede cancer cell proliferation beyond a certain concentration threshold.…”

“…Prior studies have indicated that boric acid, another boron compound, augmented viability in HepG2 cells in a concentration‐dependent manner, exhibiting an IC50 value of approximately 24 mM 35 . Moreover, in vitro experiments employing various cell lines, such as Ishikawa cells, illustrated a significant decline in cell proliferation at boric acid concentrations of 40 mM and above 36 . Additionally, our earlier research revealed that treatment with 10.77 mM boric acid in DU‐145 cells led to a noteworthy reduction in cell growth 37 .…”

Borax induces ferroptosis of glioblastoma by targeting HSPA5/NRF2/GPx4/GSH pathways

“…In vivo and in vitro studies have provided evidence of the prophylactic and therapeutic effectiveness of boric acid in rats as well as highlighting its anti‐cancer properties in human endometrial cancer Ishikawa cells and DU‐145 prostate cancer cells. 17 , 22 , 23 Cancer cells are known for producing higher levels of reactive oxygen species (ROS) compared to normal cells, primarily due to disruptions in their redox balance. 24 This imbalance between antioxidant and oxidant molecules in cancer cells provides an opportunity for cancer therapy.…”