Potential Chemotherapeutic Effect of Selenium for Improved Canceration of Esophageal Cancer

Abstract

Esophageal squamous cell carcinoma is the most common type of esophageal cancer and accounts for 5% of malignant tumor deaths. Recent research suggests that chronic inflammation and DNA damage may drive the onset of esophageal squamous cell carcinoma, implying that lowering chronic inflammation and DNA damage compounds may provide chemo-prevention. According to epidemiological and experimental evidence, selenium is linked to a lower risk of several malignancies, including esophageal squamous cell carcinoma. However, its exact mechanism is still unclear. In the present study, we used cell lines and a 4-NQO mice model to explore the anti-cancer mechanism of four types of selenium. Our findings indicated that selenium inhibited the proliferation, colony formation, and ROS level of ESCC cell lines in a time-dependent manner. Intriguingly, selenium treatment impeded 4-NQO-induced high-grade intraepithelial neoplasia and reduced the number of positive inflammatory cells by preserving DNA from oxidative damage. In addition, selenium significantly decreased the expression of Ki-67 and induced apoptosis. This study demonstrates that selenium has a significant chemo-preventive effect on ESCC by reducing high-grade dysplasia to low-grade dysplasia. For the first time, selenium was shown to slow down the progression of esophageal cancer by lowering inflammation and oxidative DNA damage.

Selenium suppressed growth of Ehrlich solid tumor and improved health of tumor‐bearing mice

“…Furthermore, it was shown that Se‐induced P53 activation may downregulate Bcl‐2 and upregulate Bax, which would induce Ehrlich cancer cells to undergo apoptosis (Ramakrishnan et al, 2009). These data agree with earlier research that Se promotes apoptosis in hematological malignancies, (Ehudin et al, 2022) leukemia and lymphoma cells (Wu et al, 2014) and esophageal cancer (Ahsan et al, 2022).…”

“…Furthermore, it was shown that Se-induced P53 activation may downregulate Bcl-2 and upregulate Bax, which would induce Ehrlich cancer cells to undergo apoptosis (Ramakrishnan et al, 2009). These data agree with earlier research that Se promotes apoptosis in hematological malignancies, (Ehudin et al, 2022) leukemia and lymphoma cells (Wu et al, 2014) and esophageal cancer (Ahsan et al, 2022). It has been reported that, glutathione and Se interacted to form hydrogen selenide, or selenodiglutathione, which causes cytotoxicity in the form of DNA damage, ROS generation and cell death (Kim et al, 2021;Lipinski, 2017).…”

Selenium-Containing Agents Acting on Cancer—A New Hope?

“…In the years, special attention has been devoted to the potential usefulness of Se-containing compounds in the battle against cancer, acting as anticancer and chemopreventive agents, inducing antioxidant and pro-oxidant effects at low and high doses, respectively [ 48 , 49 ]. Inorganic compounds, especially selenite 3 , showed chemopreventive properties higher than the organic ones, despite their higher toxicity [ 50 ].…”

Esophagus cancer and essential trace elements

“…Numerous studies have shown selenium to be related to the risk of EC. It was reported that selenium could slow down the development of ESCC by decreasing the expression of Ki-67, inducing apoptosis, and lowering inflammation and oxidative DNA damage, thus exerting an important chemopreventive effect on ESCC by reducing high-grade dysplasia to low-grade dysplasia ( 47 , 48 ). Zhang et al ( 49 ) found that β-catenin/TCF pathway played a vital role in selenium induced-growth inhibition and apoptosis in ESCC cells ( 49 ).…”