Brassinosteroids cause cell cycle arrest and apoptosis of human breast cancer cells

Steigerova, Jana; Oklešťková, Jana; Levková, Monika; Rárová, Lucie; Kolář, Zdeněk; Strnad, Miroslav

doi:10.1016/j.cbi.2010.09.006

Cited by 72 publications

(56 citation statements)

References 49 publications

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“…Both compounds were shown to inhibit cell growth of the cancer cells. BS treatment resulted in arrest of cell cycle in the G1 phase and an induction of apoptosis [104,110]. A range of techniques including flow cytometry, Western blotting, TUNEL, DNA ladder assays and immunofluorescence analyses was used for study of BS-induced apoptosis of human prostate cancer cell lines LNCaP and DU-145 [111].…”

Section: Anticancer Effectsmentioning

confidence: 99%

Steroid plant hormones: Effects outside plant kingdom

2015

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Section: Anticancer Effectsmentioning

confidence: 99%

Steroid plant hormones: Effects outside plant kingdom

2015

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“…In recent years, it was shown that BRs as the typical phytohormones have an impact not only on plants, but also on living organisms outside the plant kingdom [8]. Their ability to suppress growth and induce the death of cancer cells in animals is even more interesting [9,10]. It should be noted that not only BRs with the full set of functional groups are active, but also their analogues or biosynthetic precur sors, in particular, these containing the low polar groups in the cyclic moiety [11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Synthesis and biological activity of the probable biosynthetic precursors of 241-norbrassinolide

et al. 2012

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A number of 24-norbrassinolide biosynthetic precursors containing low polar functional groups (3beta3-OH, 3-keto-, delta2- or 2alpha,3alpha-epoxy-) in A-cycle and (22R,23R)-diol in the side chain has been prepared. Studies of these compounds as proliferation regulators in MCF-7 human breast cancer and LnCaP human prostate adenocarcinoma cells showed that most nonpolar (22R,23R)-derivatives effectively suppressed proliferation. Dependence of proliferation on concentration of studied compounds was found in human prostate carcinoma LnCaP cells (IC50 = 13-28 microM at 72 h of incubation in a medium containing 10% FBS; suppression of DNA biosynthesis). A number of compounds induced apoptosis (23-33%); arrested cell cycle in S- and G2/M-phases; and caused partial cells detachment during prolonged incubations.

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“…We have recently shown that strigolactone analogues induce growth arrest and apoptosis in breast cancer cell lines [3], thereby adding the SLs to the list of plant-derived effective anti-cancer agents that are being assessed for their ability to inhibit the growth and survival of human cancer cell lines [4-6] [7, 8] [9, 10]. …”

Section: Introductionmentioning

confidence: 99%

Strigolactone analogues induce apoptosis through activation of p38 and the stress response pathway in cancer cell lines and in conditionally reprogrammed primary prostate cancer cells.

et al. 2014

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Strigolactones are a novel class of plant hormones produced in roots and regulate shoot and root development. We have previously shown that synthetic strigolactone analogues potently inhibit growth of breast cancer cells and breast cancer stem cells. Here we show that strigolactone analogues inhibit the growth and survival of an array of cancer-derived cell lines representing solid and non-solid cancer cells including: prostate, colon, lung, melanoma, osteosarcoma and leukemic cell lines, while normal cells were minimally affected. Treatment of cancer cells with strigolactone analogues was hallmarked by activation of the stress-related MAPKs: p38 and JNK and induction of stress-related genes; cell cycle arrest and apoptosis evident by increased percentages of cells in the sub-G1 fraction and Annexin V staining. In addition, we tested the response of patient-matched conditionally reprogrammed primary prostate normal and cancer cells. The tumor cells exhibited significantly higher sensitivity to the two most potent SL analogues with increased apoptosis confirmed by PARP1 cleavage compared to their normal counterpart cells. Thus, Strigolactone analogues are promising candidates for anticancer therapy by their ability to specifically induce cell cycle arrest, cellular stress and apoptosis in tumor cells with minimal effects on growth and survival of normal cells.

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Brassinosteroids cause cell cycle arrest and apoptosis of human breast cancer cells

Cited by 72 publications

References 49 publications

Steroid plant hormones: Effects outside plant kingdom

Steroid plant hormones: Effects outside plant kingdom

Synthesis and biological activity of the probable biosynthetic precursors of 241-norbrassinolide

Strigolactone analogues induce apoptosis through activation of p38 and the stress response pathway in cancer cell lines and in conditionally reprogrammed primary prostate cancer cells.

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