Table 1.

Epidemiological, in vivo and in vitro studies about the role of sex steroids in colorectal cancer development. Arrow up indicates stimulation and arrow down inhibition

SEX STEROIDS	EFFECT
Estrogens. Epidemiological studies [9–11, 18, 24]	⇩Incidence of CRC in women than men. ⇧E2, E1 and T/E2 concentration in postmenopausal women, but not in men. ⇩ERβ in tumor⇧cancer stages and tumor invasion. ⇧Aromatase in tumor ⇧Estrogens level ⇧Intratumoral E2 levels in men than healthy tissue.
In vivo studies [25–29]	⇧E2 ⇩Colon tumors in male and females. ⇧E2 ⇧⇩ Genes related with NF-kB, NRF2 and NLRP3. ⇩ERβ ⇧Inflammation and tumor growth.
In vitro studies [30–36]	⇧E2 ⇩Viability and migration ⇧E2 ⇧Apoptosis ⇧E2 ⇧⇩ Modulate P38/MAPK, JNK/PGE2, PI3K/AKT, MYC, MYB, RUNX2 and PROX1 pathways ⇧ ERβ Modulate the action of E2.
Androgens. Epidemiological studies [19–23]	⇧T in men ⇩ survival ⇩T in men ⇩CAG repeats in AR gene ⇩CAG in AR and CA in ER ⇧T levels ⇧AR in tumor tissue ⇧Tumor stage and metastasis
In vivo studies [26, 37–39]	⇧Androgens ⇧Number and size of tumors ⇧Androgens ⇧Inflammation (iNOS, COX2 and NRF2) ⇧Androgens ⇧Apoptosis in tumor cells
In vitro studies [39, 40]	⇧T ⇧Apoptosis and migration ⇧T⇧cytoskeleton reorganization PI3K/AKT/JNK pathway.