Catechins are present in a wide variety of plant products such as green tea, cacao, grape, grape juices, and wine. Catechins are polyphenolic compounds, such as epigallocatechin-3-gallate (EGCG), epigallocatechin, epicatechin-3-gallate and epicatechin, gallocatechins, and gallocatechin gallate. Catechins intake can reduce inflammatory events and platelet aggregation, and avoid cardiovascular dysfunctions, such as atherosclerosis, hypertension, endothelial dysfunction, cardiac ischemic diseases, cardiomyopathy, and cardiac hypertrophy (Khan and Mukhtar, 2018). Moreover, many studies have reported that catechins can present antitumor effect and increase chemotherapy response (Saiko et al., 2015; Mayr et al., 2015).
Saiko et al. (2015) described the antitumor action of EGCG by proapoptotic action in human cells of acute promyelocytic leukemia (HL-60). The results indicated that EGCG presented anticarcinogenic effect in HL-60 cells by inhibiting DNA synthesis, cell proliferation, increasing apoptosis, and arresting cell cycle. Also, Mayr et al. (2015) reported the synergism of catechin and cisplatin against biliary tract cancer. Different types of cell lines for this type of cancer were treated with EGCG alone and in combination with cisplatin. In addition, synergism increased apoptosis and cell cycle arrest. This association caused cell cycle arrest, decreased cell viability by increased apoptosis, and improved the chemotherapy response of biliary tract cancer treatment.
In addition, another investigation performed by Bimonte et al. (2015) indicated that catechin in combination with chemotherapeutic bleomycin generated an efficient antitumor synergism by inhibiting cell pancreatic cancer growth cell line (MiaPaCa-2). The combination of catechin and bleomycin was able to decrease cell proliferation by blocking S-phase of cell cycle and plasma membrane depolarization and activating apoptosis and DNA damage.
Saeed et al. (2015) reported that pretreatment with this molecule is able to attenuate the cardiotoxicity generated by doxorubicin in rats. Furthermore, EGCG is able to protect against neurotoxicity generated by cisplatin by inhibiting apoptosis in mice (Zou et al., 2014).
In addition, the potentiating synergistic effect of EGCG associated with doxorubicin was found in hepatocellular carcinoma cells (Hep3B), due to the increase in autophagy vesicles within tumor cells and, consequently, cell death increased (Chen et al., 2014).
Also, the antitumor action of EGCG was described by Shimizu et al. (2015). The results showed that this active molecule was able to inhibit cell growth and proliferation in human hepatocarcinoma cells by inducting apoptosis and inhibiting some molecules involved in cell proliferation and survival, such as AKT and extracellular signal-regulated kinase (ERK). Zhang et al. (2015) also found the same antitumor effect in hepatocellular carcinoma (LM6) cells and demonstrated that EGCG did not affect healthy liver cells.
Moreover, the antitumor effect of EGCG was also found in osteosarcoma (MG63 and U2OS) cell lines (Jiang et al., 2014), lung cancer (A549) (Sonoda et al., 2014; Ma et al., 2014), ovarian carcinoma (OVCAR-3) (Wang et al., 2014), and colorectal (HCT116) (Moseley et al., 2013).