Samuel Cos

ORCID: 0000-0003-4900-8516
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About
Contact & Profiles
Research Areas
  • Circadian rhythm and melatonin
  • Estrogen and related hormone effects
  • Spaceflight effects on biology
  • Dietary Effects on Health
  • Angiogenesis and VEGF in Cancer
  • Nutrition, Genetics, and Disease
  • Heavy Metal Exposure and Toxicity
  • Epigenetics and DNA Methylation
  • Radiation Therapy and Dosimetry
  • Glutathione Transferases and Polymorphisms
  • Chemical Reactions and Isotopes
  • DNA Repair Mechanisms
  • Cancer Cells and Metastasis
  • Genetics, Aging, and Longevity in Model Organisms
  • Cancer, Stress, Anesthesia, and Immune Response
  • Effects of Radiation Exposure
  • Antioxidant Activity and Oxidative Stress
  • Advanced Radiotherapy Techniques
  • Eicosanoids and Hypertension Pharmacology
  • Light effects on plants
  • Olfactory and Sensory Function Studies
  • Photoreceptor and optogenetics research
  • Neuroendocrine regulation and behavior
  • Effects and risks of endocrine disrupting chemicals
  • Free Radicals and Antioxidants

Instituto de Investigación Marqués de Valdecilla
2013-2024

Universidad de Cantabria
2012-2024

Hospital Universitari Sant Joan de Reus
2020

Marqués de Valdecilla University Hospital
1989-2017

Fundación Marques de Valdecilla
2013

University of Arizona
1990-1991

The epithelial-to-mesenchymal transition (EMT) is a cell-biological program that occurs during the progression of several physiological processes and can also take place pathological situations such as carcinogenesis. EMT consists sequential activation number intracellular signaling pathways aimed at driving epithelial cells toward acquisition series intermediate phenotypic states arrayed along epithelial–mesenchymal axis. These features include changes in motility, conformation, polarity...

10.3390/cancers16050956 article EN Cancers 2024-02-27

Melatonin has been shown to have a direct inhibitory action on the proliferation of estrogen-responsive MCF-7 human breast cancer cells in culture. In present study, we examined by flow cytometry whether this effect might be exerted G1 phase cell cycle, thus causing transition delay into S phase. order further verify hypothesis tested ability estradiol "rescue" from melatonin inhibition, and potential indoleamine block rescue tamoxifen inhibition. Following five days incubation, (10(-9)M)...

10.1111/j.1600-079x.1991.tb00007.x article EN Journal of Pineal Research 1991-01-01

Melatonin exerts oncostatic effects on breast cancer by interfering with the estrogen-signaling pathways. reduces estrogen biosynthesis in human cells, surrounding fibroblasts and peritumoral endothelial cells regulating cytokines that influence tumor microenvironment. This hormone also antiangiogenic activity tumoral tissue. In this work, our objective was to study role of melatonin regulation vascular growth factor (VEGF) cells. To accomplish this, we cocultured (MCF-7) umbilical vein...

10.1111/jpi.12007 article EN Journal of Pineal Research 2012-08-16

Abstract: Most of the current knowledge about mechanisms by which melatonin inhibits growth breast cancer cells point to an interaction with estrogen‐responsive pathways, thus behaving as antiestrogenic hormone. However, a possible effect on local synthesis estrogens had not been examined. The objective this work was study whether may modify aromatase activity in MCF‐7 modulating estrogen biosynthesis. In cultured testosterone estradiol‐free media, (1 n m ) counteracts testosterone‐induced...

10.1111/j.1600-079x.2004.00186.x article EN Journal of Pineal Research 2004-10-27

Melatonin inhibits proliferation of the estrogen‐responsive MCF‐7 human breast cancer cells. The objective this work was to assess whether melatonin not only regulates cell but also induces apoptosis. In experiment we used 1,25‐dihydroxycholecalciferol (D 3 ) as a positive control because it and cells were cultured with either 1 n M melatonin, 100 D or its diluent determine their effects on proliferation, viability, cell‐cycle phase distribution, population apoptotic cells, expression p53,...

10.1034/j.1600-079x.2002.1821.x article EN Journal of Pineal Research 2002-03-01

Melatonin inhibits the growth of breast cancer cells by interacting with estrogen-responsive pathways, thus behaving as an antiestrogenic hormone. Recently, we described that melatonin reduces aromatase expression and activity in MCF-7 human cells, modulating local estrogen biosynthesis. To investigate vivo aromatase-inhibitory properties our current study, this indoleamine was administered to rats bearing DMBA-induced mammary tumors, ovariectomized (ovx) treated testosterone. In these...

10.1002/ijc.21401 article EN International Journal of Cancer 2005-08-03

Cadmium (Cd) is a heavy metal affecting human health both through environmental and occupational exposure. There evidence that Cd accumulates in several organs carcinogenic to humans. In vivo, mimics the effect of estrogens uterus mammary gland. estrogen-responsive breast cancer cell lines, stimulates proliferation can also activate estrogen receptor independent estradiol. The ability this metalloestrogen increase gene expression MCF7 cells blocked by anti-estrogens suggesting activity these...

10.1111/j.1600-079x.2006.00315.x article EN Journal of Pineal Research 2006-01-25

Melatonin reduces the development of breast cancer interfering with oestrogen-signalling pathways, and also inhibits aromatase activity expression. Our objective was to study promoters through which melatonin modifies expression, evaluate ability regulate cyclooxygenases assess whether effects are related its on intracellular cAMP, in MCF-7 cells.Total mRNA, mRNA promoter regions expression were determined by real-time RT-PCR. PGE(2) cAMP measured kits.Melatonin downregulated gene two major...

10.1038/sj.bjc.6605336 article EN cc-by-nc-sa British Journal of Cancer 2009-09-22

Radiation and adjuvant endocrine therapy are nowadays considered a standard treatment option after surgery in breast cancer. Melatonin exerts oncostatic actions on human cancer cells. In the current study, we investigated effects of combination radiotherapy melatonin (1 mm, 10 μm 1 nm) significantly inhibited proliferation MCF-7 alone cell dose-dependent manner. Pretreatment cells with wk before radiation led to greater decrease compared alone. pretreatment also decreased G2 -M phase arrest...

10.1111/jpi.12205 article EN Journal of Pineal Research 2015-01-09

Results from clinical trials and multiple in vivo vitro studies point to melatonin as a promising adjuvant molecule with many beneficial effects when concomitantly administered chemotherapy. Melatonin palliates side‑effects enhances the efficacy of chemotherapeutic agents. However, mechanisms through which regulates molecular changes induced by agents remain largely unknown. In this study, we demonstrated that enhanced anti-proliferative apoptotic responses low doses docetaxel breast cancer...

10.3892/ijo.2017.4213 article EN International Journal of Oncology 2017-11-28

Melatonin mitigates cancer initiation, progression and metastasis through inhibition of both the synthesis estrogens transcriptional activity estradiol-ER (Estrogen receptor) complex in estrogen-dependent breast cell line MCF-7. Moreover, melatonin improves sensitivity MCF-7 to chemotherapeutic agents protects against their side effects. It has been described that potentiates anti-proliferative effects doxorubicin; however, molecular changes involving gene expression activation/inhibition...

10.3390/cancers11071011 article EN Cancers 2019-07-19

Cos S, Blask DE. Melatonin modulates growth factor activity in MCF‐7 human breast cancer cells. J. Pineal Res. 1994: 17: 25–32. Abstract has been shown to have direct oncostatic actions on estrogen‐responsive, cells culture. In the present study, we examined whether these inhibitory cell may be mediated through bioassayable activity. order test this hypothesis, estimated of conditioned medium (CM) from estradiol (E 2 ), or melatonin‐treated cells, presence absence melatonin growth. We also...

10.1111/j.1600-079x.1994.tb00110.x article EN Journal of Pineal Research 1994-08-01
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