Vitamin K and its analogs: Potential avenues for prostate cancer management

Abstract

Epidemiological studies have demonstrated a relationship between cancer incidence and dietary habits. Especially intake of certain essential nutrients like vitamins has been shown to be beneficial in experimental studies and some clinical trials. Vitamin K (VK) is an essential nutrient involved in the blood clotting cascade, and there are considerable experimental data demonstrating its potential anticancer activity in several cancer types including prostate cancer. Previous in vitro and in vivo studies have focused mainly on anti-oxidative effects as the underlying anticancer mechanism of VK. However, recent studies reveal that VK inhibits the growth of cancer cells through other mechanisms, including apoptosis, cell cycle arrest, autophagy, and modulation of various transcription factors such as Myc and Fos. In the present review, we focus on the anticancer effect of dietary VK and its analogs on prostate cancer, with an emphasis on the signaling pathways that are activated following exposure to these compounds. This review also highlights the potential of VK and its derivatives as an adjuvant treatment in combination with other vitamins or with chemotherapeutic drugs. Based on our recent results and a review of the existing literature, we present evidence that VK and its derivatives can potentially be explored as cancer therapy, especially for prostate cancer.

Dietary Nutrient Patterns and Prostate Cancer Risk: A Case-Control Study from Iran

“…It is possible that synergistic effect of other nutrients in this pattern, cause the significant effect of folate on reducing the risk of prostate cancer, that is completely in line with our hypothesis based on the effect of interactions between nutrients and the predominance of the effect of a higher consumption of nutrients that exhibit behavioural coexistence. Inverse association between green leafy and cruciferous vegetables (the main source of vitamin K1) and prostate cancer risk have been reported in several studies (Hardin et al, 2011;Dasari et al, 2017). Also, the protective effect of vitamin K2 (another form of vitamin K that found in animal product) reported in one cohort study (Nimptsch et al, 2008).…”

“…Similarly, the ''plant source" pattern (loaded heavily on potassium, Vitamin K, total folate, beta-carotene and lutein) was negatively associated with risk of prostate cancer. Numerous studies have shown the protective effects of vitamin K and carotenoids consumption on prostate cancer risk (Nimptsch et al, 2008;Nimptsch et al, 2015;Dasari et al, 2017), However there is conflicting evidence regarding folate intake and prostate cancer risk. Some Studies found no association between dietary and total folate intake and prostate cancer risk, while other studies reported that higher blood folate levels increased prostate cancer risk (Figueiredo et al, 2009;Wang et al, 2014).…”

p62 Suppressed VK3-induced Oxidative Damage Through Keap1/Nrf2 Pathway In Human Ovarian Cancer Cells

“…It's known that VK3 exhibits potent anticancer effects in various cancers such as breast, hepatic, bladder, pharyngeal, and blood cancers [34]. VK3 promoted the ROS production which disrupted the intracellular calcium homeostasis, depleted cellular thiol levels, increased lipid peroxidation and finally killed the cancer cells [35]. Early in 2003 it was reported that VK3 may have antitumor effect on ovarian cancer [36].…”

Аnti-inflammatory effects of vitamin K on women's health

“…Накоплены данные, свидетельствующие о противоопухолевых эффектах витамина K, его роли при некоторых онкологических заболеваниях, таких как гепатоцеллюлярная карцинома, рак поджелудочной и предстательной желез [27,28]. В работе 2017 г. s. Dahlberg et al описали ряд патогенетических механизмов действия витамина K на опухолевые клетки: связывание с рецептором sXR приводит к подавлению роста опухоли путем снижения экспрессии протоонкогена с-Мус4, что сопровождается замедлением клеточной пролиферации; уменьшение воспалительных сигналов, потенцирующих развитие опухолевого процесса за счет активирования ядерного фактора каппа B (NF-κB); подавление опухолевого роста путем воздействия на сигнальные пути митоген-активируемых протеинкиназ; блокирование клеточного цикла путем подавления циклина D1; индукция апоптоза путем воздействия на каспазу-3; синтез цитотоксических актив ных форм кислорода [29].…”