Effects of estradiol, progestogens, and of tibolone on breast proliferation and apoptosis

Pompei, Luciano de Melo; Cunha, E P; Steiner, Marcelo Luis; Theodoro, Therésè Rachell; Mader, Ana Maria Amaral Antonio; Petri, Giuliana; Pinhal, Maria Aparecida da Silva; Fernandes, César Eduardo

doi:10.3109/13697137.2015.1020482

Cited by 6 publications

(4 citation statements)

References 14 publications

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“…Some limitations of our study can be mentioned, such as the fact that we have evaluated proliferation and apoptosis with only one marker for each one, PCNA and caspase-3 respectively, although these have shown results and have already been used in previous studies such as the one by Pompei et al 17 Another limiting factor was our relatively small number of animals in the different groups. A larger sample would probably show statistical significance in other parameters that in the graphic analysis seem to be different among groups.…”

Section: Discussionmentioning

confidence: 99%

Effect of Testosterone on Proliferation Markers and Apoptosis in Breasts of Ovariectomized Rats

Oliveira

Steiner

Theodoro

et al. 2019

Rev Bras Ginecol Obstet

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Objective To investigate the action of testosterone (T), isolated or associated with estradiol benzoate (EB), on the proliferation markers and apoptosis of breasts of ovariectomized rats. Methods A total of 48 castrated female Wistar rats were divided into 6 groups, and each of them were submitted to one of the following treatments for 5 weeks: 1) control; 2) EB 50 mcg/day + T 50 mcg/day; 3) T 50mcg/day; 4) EB 50 mcg + T 300 mcg/day; 5) T 300 mcg/day; and 6) EB 50 mcg/day. After the treatment, the mammary tissue was submitted to a histological analysis and immunoexpression evaluation of proliferation markers (proliferating cell nuclear antigen, PCNA) and apoptosis (caspase-3). Results There was a statistically significant difference among the groups regarding microcalcifications and secretory activity, with higher prevalence in the groups treated with EB. There was no difference among the groups regarding atrophy, but a higher prevalence of atrophy was found in the groups that received T versus those that received EB + T. There was a difference among the groups regarding the PCNA (p = 0.028), with higher expression in the group submitted to EB + T 300 mcg/day. Regarding caspase-3, there was no difference among the groups; however, in the group submitted to EB + T 300 mcg/day, the expression was higher than in the isolated T group. Conclusion Isolated T did not have a proliferative effect on the mammary tissue, contrary to EB. Testosterone in combination with EB may or may not decrease the proliferation, depending on the dose of T.

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Section: Discussionmentioning

confidence: 99%

Effect of Testosterone on Proliferation Markers and Apoptosis in Breasts of Ovariectomized Rats

Oliveira

Steiner

Theodoro

et al. 2019

Rev Bras Ginecol Obstet

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“…The roles of cortisol and testosterone in the induction of Bax-dependent apoptosis has been addressed in previous studies. In addition, progesterone has been shown to induce apoptosis in cervical, ovarian, and colon cancer cells through the Bax-dependent pathway (29,(38)(39)(40).…”

Section: Discussionmentioning

confidence: 99%

Cortisol and Testosterone Induce Bax and Bcl-2 Gene Expression and Caspases-8 and -9 Activity in Colon Cancer Cells (ht29) and Reduced the Cell Viability

Sarkhosh

Ahmadi

Khatami

et al. 2021

Preprint

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Cortisol and testosterone can inhibit the proliferation of colorectal cancer cells. Cortisol may augment the anti-cancer activity of testosterone in colorectal cancer cells. This research aimed to assess the impact of cortisol and testosterone on the viability of colon cancer cells (HTCs). The cytotoxic effects of cortisol and testosterone were evaluated using the MTT assay. Bax and Bcl-2 expression levels were determined using real-time PCR. The colorimetric method was used to assess the activity of caspase-8 and -9 enzymes. The expression levels of Bax and Bcl-2 genes significantly increased (p<0.001), as well as the activity levels of caspase-8 and -9, were elevated (p<0.001). Testosterone may exert cytotoxic activity in colon cancer cells in the presence of cortisol, and cortisol and testosterone cotreatment may contribute to the elevated Bax and Bcl-2 genes expression and caspase 8 and 9 activity enhancement in colorectal cancer cells.

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“…In particular, T inhibits the enzyme sulphatase, which reduces the desolfatation of estrone (E3) sulfate and blocks cell proliferation in the breast, stimulating apoptosis [16]. T was associated with the least breast epithelial proliferation (evaluated by proliferating cell nuclear antigen immunohistochemistry), but also the least apoptosis (by caspase-3 immunohistochemistry) in comparison to other EP treatments [17]. Several studies have also shown a reduction in breast density during T treatment, in contrast with 'typical' E-only or EP HTs [18,19].…”

Section: 'Progestin-free' Treatmentsmentioning

confidence: 99%

Postmenopausal hormone therapy in BRCA gene mutation carriers: to whom and which?

Grandi

Caroli

Cortesi

et al. 2020

Expert Opinion on Drug Safety

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Introduction: Risk-reducing-salpingo-oophorectomy (RRSO) inevitably leads BRCA mutation carriers to premature menopause. Areas covered: To evaluate the existing evidence for use of postmenopausal hormone therapy (HT) in BRCAmc, after RRSO or menopause occurring naturally, for both breast cancer (BC) survivors and those without BC. Expert opinion: All BC survivors are excluded from any HT treatment: in other BRCAmc, before 51 years of age the benefits of HT overcome the risks after RRSO and/or premature ovarian insufficiency (POF). After 51 years of age, it is important to treat only women with important vasomotor symptoms, after the failure of alternative therapies. Estrogens-only therapy plays a key role in hysterectomized women (HW). In the case of an intact uterus (UW), associations with the lowest dose of progestins/natural progesterone derivatives have to be preferred, as progestins has been shown to play an important role in BC transformation, especially in BRCA1mc. No studies have been performed in BRCAmc with regard to 'progestin-free' HT, in particular the old tibolone (both in HW and UW) and the new tissue-selective estrogen complex (in UW). However, preliminary data obtained from the general population are reassuring about the use of these 'progestin-free' preparations and BC safety.

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Effects of estradiol, progestogens, and of tibolone on breast proliferation and apoptosis

Cited by 6 publications

References 14 publications

Effect of Testosterone on Proliferation Markers and Apoptosis in Breasts of Ovariectomized Rats

Effect of Testosterone on Proliferation Markers and Apoptosis in Breasts of Ovariectomized Rats

Cortisol and Testosterone Induce Bax and Bcl-2 Gene Expression and Caspases-8 and -9 Activity in Colon Cancer Cells (ht29) and Reduced the Cell Viability

Postmenopausal hormone therapy in BRCA gene mutation carriers: to whom and which?

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