Melatonin reduces lung cancer stemness through inhibiting of PLC, ERK, p38, ß-catenin, and Twist pathways - Yang - - Environmental Toxicology - Wiley Online Library
Lung cancer is one of the most common cancer in cancer-related deaths worldwide, which is characterized by its strong metastatic potential. The melatonin hormone secreted by the pineal grand has an a...
Cancer spread is increased by a high fat diet, ground-breaking evidence shows Researchers discover new cancer spreading protein -- ScienceDaily
New research shows that the metastatic process (cancer spread) is enhanced by fat intake. Mice given a high fat diet, including palmitic acid (a major component of palm oil which is found in lots of household products) developed the most aggressive cancer spread. The study identifies for the first time a protein called CD36 which has an essential role in cancer spreading.
Melatonin treatment induces apoptosis through regulating the nuclear f (...)
Melatonin, which is synthesized by the pineal gland and released into the blood, exhibits antitumor properties. However, the mechanisms underlying these effects, particularly in stomach cancer, remain unknown. In the present study, the effect of melatonin on the nuclear factor (NF)‑κB signaling pathway and the mitogen‑activated protein kinase signaling pathway, involving p38 and c‑Jun‑N‑terminal kinase (JNK), were investigated in SGC7901 gastric cancer cells. In addition, the effect of melatonin on the survival, migration and apoptosis of these cells was investigated in vitro in order to evaluate the use of melatonin for the treatment of gastric cancer. The results of the present study revealed that melatonin decreased the viability and migration of SGC7901 cells. Furthermore, melatonin induced apoptosis. Melatonin was identified to elevate the expression levels of phosphorylated (p)‑p38 and p‑JNK protein, and decrease the expression level of nucleic p‑p65. These results suggest that the protein levels of p65, p38 and JNK are associated with the survival of SGC7901 cells following treatment with melatonin. The optimal concentration of melatonin was demonstrated to be 2 mM, which significantly induced apoptosis following a 24 h treatment period. These findings suggest that conflicting growth signals in cells may inhibit the efficacy of melatonin in the treatment of gastric cancer. Therefore, adjunct therapy would be required to improve the efficacy of melatonin in the treatment of cancer.
Melatonin, a Full Service Anti-Cancer Agent Inhibition of Initiation, (...)
There is highly credible evidence that melatonin mitigates cancer at the initiation, progression and metastasis phases. In many cases, the molecular mechanisms underpinning these inhibitory actions have been proposed. What is rather perplexing, however, is the large number of processes by which mela …
Melatonin, mitochondria, and the cancer cell SpringerLink
The long-recognized fact that oxidative stress within mitochondria is a hallmark of mitochondrial dysfunction has stimulated the development of mitochondria-targeted antioxidant therapies. Melatonin should be included among the pharmacological agents able to modulate mitochondrial functions in cancer, given that a number of relevant melatonin-dependent effects are triggered by targeting mitochondrial functions. Indeed, melatonin may modulate the mitochondrial respiratory chain, thus antagonizing the cancer highly glycolytic bioenergetic pathway of cancer cells. Modulation of the mitochondrial respiratory chain, together with Ca2+ release and mitochondrial apoptotic effectors, may enhance the spontaneous or drug-induced apoptotic processes. Given that melatonin may efficiently counteract the Warburg effect while stimulating mitochondrial differentiation and mitochondrial-based apoptosis, it is argued that the pineal neurohormone could represent a promising new perspective in cancer treatment strategy.
Metformin Protects Against Breast Cancer Metastasis Natural Medicine (...)
ReferenceEl-Haggar SM, El-Shitany NA, Mostafa MF, El-Bassiouny NA. Metformin may protect nondiabetic breast cancer women from metastasis. Clin Exp Metastasis. 2016;33(4):339-357. ObjectiveTo investigate the impact of adding metformin to breast cancer adjuvant therapy in nondiabetic womenStudy Design and ParticipantsParticipants included women aged 40 to 65 from Damanhour Oncology Center (Damanhour, Egypt) with newly diagnosed breast cancer.
Mode of pP38 and Nf-kß Signalling Pathway on Induction of Apoptosis in Response to Flavonoids of Aloe Vera in Glioblastoma
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Epithelia are protected from adverse conditions by a mucous barrier. The secreted and transmembrane mucins that constitute the mucous barrier are largely unrecognized as effectors of carcinogenesis. However, both types of mucins are intimately involved ...
Cancer Treatment & Cancer Research City of Hope Comprehensive Cancer Center Los Angeles, CA
City of Hope has been deemed one of the nation's elite cancer hospitals by U.S. News & World Report and is recognized as a leading cancer hospital in the West. City of Hope also pioneers cancer and diabetes research, including clinical trials, and compassionate patient care.
Mucosal microbiome dysbiosis in gastric carcinogenesis Gut
Objectives We aimed to characterise the microbial changes associated with histological stages of gastric tumourigenesis. Design We performed 16S rRNA gene analysis of gastric mucosal samples from 81 cases including superficial gastritis (SG), atrophic gastritis (AG), intestinal metaplasia (IM) and gastric cancer (GC) from Xi’an, China, to determine mucosal microbiome dysbiosis across stages of GC. We validated the results in mucosal samples of 126 cases from Inner Mongolia, China. Results We observed significant mucosa microbial dysbiosis in IM and GC subjects, with significant enrichment of 21 and depletion of 10 bacterial taxa in GC compared with SG (q
Cancer treatment Therapeutic approach gives hope for the treatment of (...)
A new therapeutic approach gives promising results for the treatment of multiple myeloma, a cancer of the bone marrow currently considered incurable with conventional chemotherapy. The study resulted in a total cure rate of 41 percent, a record level using this strategy. Moreover, patients in complete remission six months after the allograft had a relapse-free survival rate of 60 percent.
Naltrexone at low doses upregulates a unique gene expression not seen (...)
Study of colorectal, lung cancer cells treated with low-dose naltrexone (LDN) and chemotherapy. LDN had anticancer activity during treatment schedules.
Nanoparticle therapy that uses LDL and fish oil kills liver cancer cel (...)
An experimental nanoparticle therapy that combines low-density lipoproteins (LDL) and fish oil preferentially kills primary liver cancer cells without harming healthy cells, researchers report.
Natural Substances that Fight Malignant Melanoma GreenMedInfo
Conventional medicine offers little hope in the fight against deadly malignant melanoma, but there are multiple foods, botanicals, and vitamins with proven anti-melanoma activity within nature’s pharmacopeia
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New mechanisms of gene inactivation may prevent aging and cancer -- Sc (...)
Every cell in our body contains the complete DNA library. So-called methyl groups regulate that in body tissues only the genetic information is expressed that is indeed needed in this tissue. Now, for the first time, researchers verified that a lack of methyl groups in the gene body leads to an incorrect gene activation and, as a consequence, may lead to the emergence of cancer.
Abstract 874 Circadianmelatonin disruption by dim light at night drive (...)
Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA Resistance to chemotherapy is a significant impediment to the treatment of breast cancer. More than 30% of breast cancer patients present with intrinsic resistance to chemotherapy; almost all who initially respond will develop acquired resistance. Resistant tumors frequently exhibit constitutive activation of numerous survival signaling pathways, including ERK, AKT, NF-kB, and STAT3. We have reported that the circadian hormone melatonin inhibits the growth of both ERá+/ERá- breast cancers and, as well as the daytime induced phospho-activation of ERK1/2, AKT and NF-kB in breast tumor xenografts. We also demonstrated that dim light at night (dLAN), by decreasing nocturnal melatonin, resulted in constitutive phospho-activation of ERK1/2, CREB, NF-kB, and STAT3, promoting resistance to tamoxifen and doxorubicin therapy. Here we tested the hypothesis that dLAN, via phospho-activation of ERK1/2 and STAT3, promotes resistance to paclitaxel (Pax). Female nude rats with “tissue-isolated” MCF-7 breast cancer xenografts were housed in photoperiodic conditions of either LD 12:12, 12:12dLAN (0.2 lux), or 12:12dLAN supplemented with nighttime melatonin (0.05 õg/ml) in the drinking water, with lights on at 0600 hrs and off at 1800 hrs. When estimated tumor weights reached 2.5 g, animals were treated daily with either diluent or Pax i.p. (4õã/kg) 2 h prior to onset of dLAN or dLAN with nighttime melatonin supplementation. Blood samples collected during the mid-dark phase (2400 hrs) showed elevated nocturnal melatonin in the LD 12:12 group, but significantly suppressed melatonin in the dLAN group. Tumor xenografts from rats housed in dLAN showed a 3-fold decrease in latency-to-onset and a 2.8-fold increased growth rates vs. those from rats receiving melatonin supplementation. Tumor cAMP levels, linoleic acid, and tumor metabolism (Warburg effect) were significantly elevated in dLAN tumors. Numerous signaling pathways including ERK1/2, RSK2, and STAT3, were phospho-activated and others including AKT and HER2/3 were elevated at 2400 hrs by dLAN but repressed in dLAN melatonin supplemented tumors. Tumors from dLAN rats showed intrinsic resistance to Pax, whereas those in LD 12:12 or dLAN and supplemented with nighttime melatonin rapidly regressed. These findings show that temporally coordinated and integrated metabolic and signal transduction mechanisms, particularly the STAT3 pathway, underlying human breast cancer growth, can be activated by the host's exposure to LAN with profound effects culminating in rapid tumor progression and the development of resistance to chemotherapy. Citation Format: Steven M. Hill, Shulin Xiang, Robert T. Dauchy, Lulu mao, Lin Yuan, Adam Hauch, Victoria P. Belancio, Melissa A. Wren-Dail, David Pointer, Peter W. Lundberg, Whitney M. Summers, David E. Blask. Circadian/melatonin disruption by dim light at night drives paclitaxel resistance in breast cancer via activation of stat3. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 874.
Case Report A Non-small Cell Lung Cancer Patient Treated with GcMAF, S (...)
This case report suggests a new concept of cancer treatment using local destruction of cancer tissue, in this case conducted with SDT and TTF therapy, to be used in combination with serum GcMAF and colostrum MAF immunotherapy as a systemic treatment.
Normalizing tumor oxygen supply could be key factor in the fight again (...)
The lack of oxygen in tumor cells changes the cells' gene expression, thereby contributing to the growth of cancer, suggest researchers. The findings are far-reaching, as the study also proved that maintaining a proper oxygen supply in tumors inhibits these so-called 'epigenetic aberrations.'