Plant sterols (PS)/carbon steroid alcohols (Otaegui-Arrazola et al. 2010) are vital components of plant cell membranes and are key components of plant plasma membrane microdomains. Campesterol, stigmasterol, and β-sitosterol are most abundant PS in human diet (Roche et al. 2008). Biochemical and molecular effects of PS make them strong candidates for breast cancer therapy; there are compelling evidences for the same (Grattan Jr 2013). Estrogen is a well-recognized mediator of breast cells growth, and it also plays key role in etiology of breast cancer (Begg et al. 1987; Jordan 2000; Finlay-Schultz and Sartorius 2015). Increased amounts of estrogen are a potential risk factor for breast cancer (Gutendorf and Westendorf 2001; Rossouw et al. 2002; Hankinson et al. 2004; Touillaud et al. 2005). Touillaud et al. (2005) also stated that intake of β-sitosterol relates to greater occurrence of estrogen receptor-positive (ER+) than estrogen negative (ER-) breast cancer (OR 0.49; 95% CI 0.18–0.98). β-Sitosterol binds competitively to both α and β forms of ER. While, plant stanols and stanol esters failed to stimulate estrogen-responsive growth in MCF-7 lines (Baker et al. 1999). However, an evidence from reporter gene array studies in human breast cancer lines conforms PS as a weak selective estrogen receptor modulators (Gutendorf and Westendorf 2001).
