The melatonin action on stromal stem cells within pericryptal area in colon cancer model under constant light

Kannen, Vinicius; Marini, Tassiana; Zanette, Dalila Lucíola; Frajacomo, Fernando Tadeu Trevisan; Silva, Gyl E. B.; Silva, Wilson A.; Garcia, Sérgio Britto

doi:10.1016/j.bbrc.2011.01.074

Cited by 32 publications

(39 citation statements)

References 38 publications

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“…In CRC, melatonin reduced the CSC pool and the dysplastic injuries induced by constant light and carcinogen treatments in a model of rats [24]. According to this, we found that AA-NAT, MT1, and MT2 negatively correlate to CD44 and CD66c in CRC.…”

Section: Discussionmentioning

confidence: 53%

Section: Introductionmentioning

confidence: 99%

“…In CRC, melatonin inhibits cell growth and induces apoptosis in vitro [21,22,23] and in vivo [24]. Recently, it has been reported that melatonin decreases CSCs and dysplastic injuries in colon tissue [24]. To date, there are no data linking loss of p53 function and melatonin synthesis or signaling in cancer, however some findings emphasize that activation of the p53 tumor-suppressor pathway, mediated by MT1 and MT2, may be a critical mediator in the anticancer activity of melatonin in CRC and breast cancer in vitro [25,26].…”

Section: Introductionmentioning

confidence: 99%

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AA-NAT, MT1 and MT2 Correlates with Cancer Stem-Like Cell Markers in Colorectal Cancer: Study of the Influence of Stage and p53 Status of Tumors

Casado

Iñigo-Chaves

Jiménez-Ruiz

et al. 2017

IJMS

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The characterization of colon cancer stem cells (CSCs) may help to develop novel diagnostic and therapeutic procedures. p53 loss increases the pool of CSCs in colorectal cancer (CRC). Recent reports suggest that the oncostatic effects of melatonin could be related to its ability to kill CSCs. Although there are no data linking the loss of p53 function and melatonin synthesis or signaling in cancer, melatonin does activate the p53 tumor-suppressor pathway in this disease. In this work, we analyze whether the expression of melatonin synthesis and signaling genes are related to the expression of CSC markers and the implication of p53 status in samples from patients with CRC. Arylalkylamine N-acetyltransferase (AA-NAT), MT1, and MT2 expression decreased in tumor samples versus normal mucosa samples in mutated p53 (mtp53) tumors versus those with wild-type p53 (wtp53). Further, AA-NAT and MT2 expression were lower in advanced stages of the disease in wtp53 tumors. On the contrary, CD44 and CD66c expression was higher in tumor versus normal mucosa in wtp53 tumors. Additionally, CD44 expression was higher in advanced stages of the disease regardless of the p53 status. Patients with CD44highCD66chigh and wtp53 tumors in advanced stages showed low expression of AA-NAT and MT2 in wtp53 tumors. These results could indicate a possible interaction of these pathways in CRC.

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Section: Discussionmentioning

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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AA-NAT, MT1 and MT2 Correlates with Cancer Stem-Like Cell Markers in Colorectal Cancer: Study of the Influence of Stage and p53 Status of Tumors

Casado

Iñigo-Chaves

Jiménez-Ruiz

et al. 2017

IJMS

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“…Tumor stroma constitutes 60–90% of the colon tumor mass [14], and PCCS surrounding the cryptal bottom has been reported to initiate certain steps in colon tumor development, such as increased proliferation, microvessel formation, VEGF-synthesis, regulation of self-renewal and differentiation of intestinal cells [15]–[18]. ACFs are considered a suitable experimental model for studying early stages of colon cancer formation, mainly due to their close resemblance with the development of cancer in rodents and humans [17], [19].…”

Section: Introductionmentioning

confidence: 99%

Antiproliferative Effects of Fluoxetine on Colon Cancer Cells and in a Colonic Carcinogen Mouse Model

et al. 2012

Self Cite

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The antidepressant fluoxetine has been under discussion because of its potential influence on cancer risk. It was found to inhibit the development of carcinogen-induced preneoplastic lesions in colon tissue, but the mechanisms of action are not well understood. Therefore, we investigated anti-proliferative effects, and used HT29 colon tumor cells in vitro, as well as C57BL/6 mice exposed to intra-rectal treatment with the carcinogen N-methyl-N’-nitro-N-nitrosoguanidine (MNNG) as models. Fluoxetine increased the percentage of HT29 cells in the G0/G1 phase of cell-cycle, and the expression of p27 protein. This was not related to an induction of apoptosis, reactive oxygen species or DNA damage. In vivo, fluoxetine reduced the development of MNNG-induced dysplasia and vascularization-related dysplasia in colon tissue, which was analyzed by histopathological techniques. An anti-proliferative potential of fluoxetine was observed in epithelial and stromal areas. It was accompanied by a reduction of VEGF expression and of the number of cells with angiogenic potential, such as CD133, CD34, and CD31-positive cell clusters. Taken together, our findings suggest that fluoxetine treatment targets steps of early colon carcinogenesis. This confirms its protective potential, explaining at least partially the lower colon cancer risk under antidepressant therapy.

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“…In breast or colon cancer, evident experimental studies have confirmed a correlation between the disruption of the melatonin rhythm and cancer [164, 165]. Although the epidemiologic surveys suggest that men who worked at night at anytime have a higher risk for lung cancer, with excesses apparent across all main histologic subtypes [50], additional evidence for this from experimental studies is urgently needed.…”

Section: Potential Directionsmentioning

confidence: 99%

Melatonin as a potential anticarcinogen for non-small-cell lung cancer

Yang

Fan

et al. 2016

Oncotarget

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Non-small-cell lung cancer (NSCLC) is a leading cause of death from cancer worldwide. Melatonin, an indoleamine discovered in the pineal gland, exerts pleiotropic anticancer effects against a variety of cancer types. In particular, melatonin may be an important anticancer drug in the treatment of NSCLC. Herein, we review the correlation between the disruption of the melatonin rhythm and NSCLC incidence; we also evaluate the evidence related to the effects of melatonin in inhibiting lung carcinogenesis. Special focus is placed on the oncostatic effects of melatonin, including anti-proliferation, induction of apoptosis, inhibition of invasion and metastasis, and enhancement of immunomodulation. We suggest the drug synergy of melatonin with radio- or chemotherapy for NSCLC could prove to be useful. Taken together, the information complied herein may serve as a comprehensive reference for the anticancer mechanisms of melatonin against NSCLC, and may be helpful for the design of future experimental research and for advancing melatonin as a therapeutic agent for NSCLC.

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The melatonin action on stromal stem cells within pericryptal area in colon cancer model under constant light

Cited by 32 publications

References 38 publications

AA-NAT, MT1 and MT2 Correlates with Cancer Stem-Like Cell Markers in Colorectal Cancer: Study of the Influence of Stage and p53 Status of Tumors

AA-NAT, MT1 and MT2 Correlates with Cancer Stem-Like Cell Markers in Colorectal Cancer: Study of the Influence of Stage and p53 Status of Tumors

Antiproliferative Effects of Fluoxetine on Colon Cancer Cells and in a Colonic Carcinogen Mouse Model

Melatonin as a potential anticarcinogen for non-small-cell lung cancer

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