Background: Breast cancer remains a major cause of cancer mortality, with many tumors relying on progesterone receptor (PR) signaling for growth. Medroxyprogesterone acetate (MPA), a synthetic progestin, stimulates proliferation in PR-positive breast cancer cells, including T47D. RU486 (mifepristone), a PR antagonist, can counter MPA-induced effects and serves as a pharmacologic control. Crocin II, a carotenoid derived from Crocus sativus, has demonstrated anti-proliferative and apoptosis-inducing activity in several cancer models. As a phytochemical, it may offer a less toxic option for targeting hormone-driven breast cancer. This study evaluates whether Crocin II can attenuate MPA-induced proliferation in T47D cells using an MTT assay and explores its potential role in modulating hormone-mediated signaling. Methods: T47D breast cancer cells were cultured in DMEM/F12 supplemented with 10% FBS and 1% penicillin–streptomycin and maintained at 37°C with 5% CO 2 . Cells were seeded in 6-well plates and allowed to adhere for 24 hours prior to treatment. Experimental groups included an untreated control, MPA alone, MPA with RU486, MPA with Crocin II (10, 25, or 50 μM), and Crocin II alone. RU486 or Crocin II was added two hours before MPA. Treatments continued for 48 hours. After incubation, cells were washed with PBS, and viability was measured using the MTT assay. Formazan crystals were dissolved in DMSO, and absorbance was recorded at 570 nm with 620 nm correction. Viability was normalized to the untreated control. All conditions were run in duplicate with five biological replicates (n = 5). Results: MPA significantly increased T47D cell viability compared to control (p = 0.048). Co-treatment with 10 μM Crocin II significantly reduced MPA-induced viability (p = 0.0034). RU486, 25 μM Crocin II, and 50 μM Crocin II showed partial, but non-significant, reductions. Crocin II alone produced no significant change in viability. Data are presented as mean ± SEM. Conclusion: MPA promoted proliferation in PR-positive T47D cells, consistent with hormone-driven growth mechanisms. Crocin II attenuated MPA-induced viability in a dose related trend, with the strongest and only significant effect at 10 μM, while higher doses trended toward baseline. The lack of cytotoxicity with Crocin II alone suggests specificity toward hormone-mediated signaling. These findings support Crocin II as a potential modulator of PR-driven breast cancer growth. Planned VEGF ELISA and BCA assays will evaluate its effects on angiogenesis and further define its anti-tumor mechanism. References Jie H, Ma W, Huang C. Diagnosis, Prognosis, and Treatment of Triple-Negative Breast Cancer: A Review. Breast Cancer (Dove Med Press). 2025;17:265–274. Lambrianidou A, Koutsougianni F, Papapostolou I, Dimas K. Recent Advances on the Anticancer Properties of Saffron (Crocus sativus L.) and Its Major Constituents. Molecules. 2021;26(1):86. Mousavi SH, Tavakkol-Afshari J, Brook A, Jafari-Anarkooli I. Role of caspases and Bax protein in saffron-induced apoptosis in MCF-7 cells. Food Chem Toxicol. 2009;47:1909–1913. Shah D, Gupta A, Shah I, Hussain A. Potential of Benign Phytochemicals in the Management of Cancer. 2021. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Memon et al. (Fri,) studied this question.