Green tea (GT) has been shown to play an important role in cancer chemoprevention. However, the related molecular mechanisms need to be further explored, especially regarding the use of GT extract (GTE) from the food matrix. For this study, epigallocatechin gallate (EGCG) and epigallocatechin (EGC) were identified in GTE, representing 42 and 40% of the total polyphenols, respectively. MDA-MB-231 (p53-p.R280K mutant) and MCF-7 (wild-type p53) breast tumor cells and MCF-10A non-tumoral cells were exposed to GTE for 24–48 h and cell viability was assessed in the presence of p53 inhibitor pifithrin-α. GTE selectively targeted breast tumor cells without cytotoxic effect on non-tumoral cells and p53 inhibition led to an increase in viable cells, especially in MCF-7, suggesting the involvement of p53 in GTE-induced cytotoxicity. GTE was also effective in reducing MCF-7 and MDA-MD-231 cell migration by 30 and 50%, respectively. An increment in p53 and p21 expression stimulated by GTE was observed in MCF-7, and the opposite phenomenon was found in MDA-MB-231 cells, with a redistribution of mutant-p53 from the nucleus and no differences in p21 levels. All these findings provide insights into the action of GTE and support its anticarcinogenic potential on breast tumor cells.

Green tea is the second most consumed beverage following water, and the health benefits provided by its consumption have been well established from research in recent decades. The main bioactive compounds found in all Camellia sinensis-based teas are catechins, which have been reported to have antioxidant, anticancer, anti-inflammatory, and immunomodulatory properties. Although most of the health benefits are well established, studies show that the intact catechins as found in tea are poorly absorbed in the digestive tract. These compounds are degraded and undergo ring fission by the gut microbiota, increasing their absorption. In this review, we gather knowledge of the health benefits of green tea catechins and their metabolites, with a particular emphasis on the immunomodulatory effects in a cancer microenvironment scenario.

Introduction Type 2 diabetes remains a growing public health concern, and modifiable lifestyle behaviors represent a key target for prevention. Eating habits have been proposed to influence metabolic risk, yet evidence from large real-world cohorts with rigorous covariate control is limited. We hypothesized that habitual eating habits, especially eating speed, are a modifiable risk factor for incident type 2 diabetes in a Japanese adult population. Methods This retrospective observational study used lifestyle habit data from medical check-up records collected in Shizuoka, Japan (April 2008–March 2020). After applying exclusion criteria, 98,718 subjects aged 18–75 years were eligible for analysis. The analytic sample for each eating habit varied after propensity score matching. Cox proportional hazard regression was used to assess new-onset type 2 diabetes in relation to multiple eating behaviors, including eating speed, breakfast skipping, late dinners, post-dinner snacking and frequency of vegetable consumption. Covariate adjustment was performed using propensity score matching for sex, age, BMI, smoking and drinking status, blood pressure and LDL and HDL cholesterol levels. Results During the observation period, 4631 new cases of type 2 diabetes were identified. After full adjustment, fast eating was significantly associated with increased diabetes risk (HR: 1.12; 95% CI: 1.02–1.23; p = 0.01). Sex-stratified analysis showed that fast eating among women was associated with a 14% higher risk (HR: 1.14; 95% CI: 1.00–1.30; p = 0.03), while no statistically significant association was observed in men. Conclusion Habitual fast eating may represent a modifiable risk factor for type 2 diabetes, particularly among women, though the association was modest and warrants confirmation in future clinical studies.