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It was concluded that omega-3 fatty acid could inhibit the proliferation of pancreatic cancer cell line SW1990 cells and promote their apoptosis. The down-regulation of the cyclin E expression by omega-3 fatty acid might be one of the mechanisms for its anti-tumor effect on pancreatic cancer. Modulatory effects of EPA and DHA on proliferation and apoptosis of pancreatic cancer cells. Zhang W, Long Y, Zhang J, Wang C. J Huazhong Univ Sci Technolog Med Sci. 2007 Oct;27(5):547-50. PMID: 18060632

Egg yolk proteins suppress azoxymethane-induced aberrant crypt foci formation and cell proliferation in the colon of rats. Ishikawa S, Asano T, Takenoshita S, Nozawa Y, Arihara K, Itoh M. Nutr Res. 2009 Jan;29(1):64-9. PMID: 19185779 These results indicate that dietary egg yolk proteins have a preventive effect on AOM-induced large bowel carcinogenesis in rats; it exerts this effect by altering cell proliferation through SCFA production. This study suggests that the consumption of egg yolk proteins might be protective against colon carcinogenesis.

In the field of molecular biology, the peroxisome proliferator-activated receptors (PPARs) are a group of nuclear receptor proteins that function as transcription factors regulating the expression of genes.[1] PPARs play essential roles in the regulation of cellular differentiation, development, and metabolism (carbohydrate, lipid, protein), and tumorigenesis[2] of higher organism.

Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells. Mantena SK, Sharma SD, Katiyar SK. Mol Cancer Ther. 2006 Feb;5(2):296-308. PMID: 16505103 doi: 10.1158/1535-7163.MCT-05-0448 The effectiveness of berberine in checking the growth of androgen-insensitive, as well as androgen-sensitive, prostate cancer cells without affecting the growth of normal prostate epithelial cells indicates that it may be a promising candidate for prostate cancer therapy. The evaluation of ancient herbal medicines may indicate novel strategies for the treatment of prostate cancer, which remains the leading cause of cancer-related deaths in American men (1). In our present investigation, we show that a naturally occurring isoquinoline alkaloid, berberine, significantly inhibits the proliferation and reduces the viability of DU145 and PC-3 as well as LNCaP cells (Fig. 1), which suggests that berberine may be an effective chemotherapeutic agent against both androgen-sensitive and androgen-insensitive prostate cancer cells. Importantly, we found that berberine did not exhibit toxicity to nonneoplastic human prostate epithelial cells under the conditions used, except for a moderate reduction in cell viability at higher concentrations when cells were treated in vitro for an extended period of time. In conclusion, the results of the present study indicate that berberine inhibits proliferation and induces G1-phase arrest and apoptosis in human prostate cancer cells but not in normal human prostate epithelial cells. In addition, we provide mechanistic evidence that berberine-induced apoptosis in prostate carcinoma cells, particularly hormone-refractory prostate carcinoma cells, is mediated through enhanced expression of Bax, disruption of the mitochondrial membrane potential, and activation of caspase-3.

Effect of yerba mate (Ilex paraguariensis) tea on topoisomerase inhibition and oral carcinoma cell proliferation. Gonzalez de Mejia E, Song YS, Ramirez-Mares MV, Kobayashi H. J Agric Food Chem. 2005 Mar 23;53(6):1966-73. PMID: 15769122

White button mushroom phytochemicals inhibit aromatase activity and breast cancer cell proliferation. Grube BJ, Eng ET, Kao YC, Kwon A, Chen S. J Nutr. 2001 Dec;131(12):3288-93. PMID: 11739882

These results suggest that combination chemotherapy (FO+Cur or Lim) may favorably modulate CD4+ T-cell-mediated inflammation.D ietary curcumin and limonin suppress CD4+ T-cell proliferation and interleukin-2 production in mice. Kim W, Fan YY, Smith R, Patil B, Jayaprakasha GK, McMurray DN, Chapkin RS. J Nutr. 2009 May;139(5):1042-8. Epub 2009 Mar 25. PMID: 19321585 doi:10.3945/jn.108.102772

Docosahexaenoic acid suppresses arachidonic acid-induced proliferation of LS-174T human colon carcinoma cells. Habbel P, Weylandt KH, Lichopoj K, Nowak J, Purschke M, Wang JD, He CW, Baumgart DC, Kang JX. World J Gastroenterol. 2009 Mar 7;15(9):1079-84. PMID: 19266600 doi: 10.3748/wjg.15.1079.

Docosahexaenoic acid inhibits superoxide dismutase 1 gene transcription in human cancer cells: the involvement of peroxisome proliferator-activated receptor alpha and hypoxia-inducible factor-2alpha signaling. Tuller ER, Beavers CT, Lou JR, Ihnat MA, Benbrook DM, Ding WQ. Mol Pharmacol. 2009 Sep;76(3):588-95. Epub 2009 Jun 15. PMID: 19528198

"PPAR modulators are drugs which act upon the peroxisome proliferator-activated receptor."

Th1/Th2 balance: the hypothesis, its limitations, and implications for health and disease. Kidd P. Altern Med Rev. 2003 Aug;8(3):223-46. Review. PMID: 12946237 Th1 pathways typically produce activation of cytotoxic T lymphocytes (Tc), NK cells, macrophages, and monocytes, all of which can attack cancer cells and generally defend against tumors. 55 IFN-gamma and other Th1 cytokines are typically lower in advanced cancer patients, while the Th2 marker IL-4 can be higher or unchanged.56 Nodules of non-small cell lung cancer freshly removed from patients expressed a marked imbalance toward Th2, as did biopsy samples from basal cell carcinoma.57 In prostate cancer patients IL-2 was low (Th1) and IL-10 high.58 IL-10 is a confirmed Th1-suppressive cytokine, and heightened IL-10 is a common factor in cancer.55 IL-10 has a variety of suppressive effects that include inhibiting Th1 cytokine production, down-regulating APC and NK cell function, and lowering overall T-cell proliferation.57 Especially under the influence of IL-4 (Th2), tumor cells apparently up-regulate IL-10 that suppresses nearby killer cells. Tumor-derived IL-10 has been documented in lymphoma, ovarian carcinoma, melanoma, neuroblastoma, and renal cell and colon carcinoma.57 IL-12 is another cytokine that can be up-regulated by Th1 activity and inhibited by Th2.59 A low IL-12/IL-10 ratio was found in cervical cancer patients.55 Recent clinical studies suggest elevated IL-10 is predictive of a poor prognosis. 57 With both IL-4 and IL-10 being proven inhibitors of Th1 and promoters of Th2 activity, the recognized capability of cancerous tissue to suppress immunity is readily rationalized.

DURHAM, N.C. -- Restricting carbohydrates, regardless of weight loss, appears to slow the growth of prostate tumors, according to an animal study being published this week by researchers in the Duke Prostate Center. "Previous work here and elsewhere has shown that a diet light in carbohydrates could slow tumor growth, but the animals in those studies also lost weight, and because we know that weight loss can restrict the amount of energy feeding tumors, we weren't able to tell just how big an impact the pure carbohydrate restriction was having, until now," said Stephen Freedland, M.D., a urologist in the Duke Prostate Center and lead investigator on this study. The researchers believe that insulin and insulin-like growth factor contribute to the growth and proliferation of prostate cancer, and that a diet devoid of carbohydrates lowers serum insulin levels in the bodies of the mice, thereby slowing tumor growth, Freedland said.

Scientists in Japan recently studied some of the glyconutrients from spinach and found they inhibited destruction of DNA, cancer cell growth, and tumor growth. They used the nutrients to suppress the growth of colon adenocarcinoma in mice. After a two week period of ingesting the nutrients, a 56.1% decrease in solid tumor volume occurred without any side effects. And the nutrients reduced the ability of tumors to supply themselves with blood which they need to fuel their growth. Markers of cell proliferation were drastically reduced. (Lipids, August, 2008)

Vitamin D: the alternative hypothesis. Albert PJ, Proal AD, Marshall TG. Autoimmun Rev. 2009 Jul;8(8):639-44. Epub 2009 Feb 12. Review. PMID: 19393200 Emerging molecular evidence suggests that symptomatic improvements among those administered vitamin D is the result of 25-D's ability to temper bacterial-induced inflammation by slowing VDR activity. While this results in short-term palliation, persistent pathogens that may influence disease progression, proliferate over the long-term.

Vitamin D and breast cancer. Bertone-Johnson ER. Ann Epidemiol. 2009 Jul;19(7):462-7. Epub 2009 Feb 20. Review. PMID: 19230714 Though the relationship between vitamin D and breast cancer remains unclear, a growing body of evidence suggests that vitamin D may modestly reduce risk. A large number of in vitro studies indicate that vitamin D can inhibit cell proliferation and promote apoptosis and cell differentiation in breast tumor tissue. Results from analytic studies of sunlight exposure and dietary intake have been inconsistent but together generally support a modestly protective role of vitamin D, at least in some population subgroups. Studies using blood vitamin D metabolites to assess vitamin D status may be less prone to misclassification than those of diet and sunlight exposure. Overall, the two prospective and four case-control studies of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D tend to support a protective effect in older women. The relationship between common vitamin D receptor polymorphisms and risk remains unclear. Many questions about this relationship clearly remain, including the utility of assessing vitamin D through diet and sunlight exposure, the relationship between plasma metabolites, and the potential modifying effects of age, menopausal status and tumor characteristics. Given that vitamin D status is modifiable, additional prospective studies are necessary to determine if vitamin D may have important potential for breast cancer prevention.

Scientists have known that cruciferous vegetables contain a host of chemopreventive agents that act in many different ways to block cancer development.2 Key among these products are indole-3-carbinol (I3C) and sulforaphane.1,3 Cancer cells need a brisk blood supply to support their rampant growth and reproduction. Preliminary studies in vitro and in vivo have found that apigenin inhibits blood vessel growth (angiogenesis) in human ovarian cancer cells, blocking production of two main signaling molecules required to stimulate vessel growth.20,21 Scientists confirmed this effect in ovarian cancer cells, also finding that apigenin strongly inhibits cell proliferation.22 Apigenin and BITC: Complementary Cancer Protection Cancer cells also need energy to support their frenetic reproductive activity. Researchers applied apigenin to human pancreatic cancer cells in culture and studied the cells' uptake of glucose.14 Astonishingly, they found that apigenin deprived energy-hungry cancer cells of glucose to support their voracious appetites and aggressive growth. It did this by down-regulating vital glucose-transporting proteins in cancer cells. This approach could effectively starve deadly cancer cells and stop them in their tracks. Another cruciferous vegetable component receiving rave reviews is the sulfur-containing molecule benzyl isothiocyanate, or BITC (pronounced "bitsy"). As with apigenin, population studies have shown that higher intakes of BITC correlate with reduced risk of cancers of the lung, breast, and colon30 while blocking cancer development in a host of different ways. BITC induces breast cancer cell death by apoptosis (programmed cell death), interfering with cancer cells' energy utilization and causing them to die off before they can contribute to tumor growth.31,32 In human ovarian cancer cells, BITC induces apoptosis by a different mechanism. It stimulates "signaling" molecules that tell cancer cells it's time to close up shop.

Vitamin D and calcium insufficiency-related chronic diseases: molecular and cellular pathophysiology. Peterlik M, Cross HS. Eur J Clin Nutr. 2009 Dec;63(12):1377-86. Epub 2009 Sep 2. PMID: 19724293 doi:10.1038/ejcn.2009.105 A compromised vitamin D status, characterized by low 25-hydroxyvitamin D (25-(OH)D) serum levels, and a nutritional calcium deficit are widely encountered in European and North American countries, independent of age or gender. Both conditions are linked to the pathogenesis of many degenerative, malignant, inflammatory and metabolic diseases. Studies on tissue-specific expression and activity of vitamin D metabolizing enzymes, 25-(OH)D-1alpha-hydroxylase and 25-(OH)D-24-hydroxylase, and of the extracellular calcium-sensing receptor (CaR) have led to the understanding of how, in non-renal tissues and cellular systems, locally produced 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) and extracellular Ca2+ act jointly as key regulators of cellular proliferation, differentiation and function. Impairment of cooperative signalling from the 1,25-(OH)2D3-activated vitamin D receptor (VDR) and from the CaR in vitamin D and calcium insufficiency causes cellular dysfunction in many organs and biological systems, and, therefore, increases the risk of diseases, particularly of osteoporosis, colorectal and breast cancer, inflammatory bowel disease, insulin-dependent diabetes mellitus type I, metabolic syndrome, diabetes mellitus type II, hypertension and cardiovascular disease. Understanding the underlying molecular and cellular processes provides a rationale for advocating adequate intake of vitamin D and calcium in all populations, thereby preventing many chronic diseases worldwide.

n-3 fatty acids and gene expression. Deckelbaum RJ, Worgall TS, Seo T. Am J Clin Nutr. 2006 Jun;83(6 Suppl):1520S-1525S. Review. Erratum in: Am J Clin Nutr. 2006 Oct;84(4):949. PMID: 16841862 Accumulating evidence in both humans and animal models clearly indicates that a group of very-long-chain polyunsaturated fatty acids, the n-3 fatty acids (or omega-3), have distinct and important bioactive properties compared with other groups of fatty acids. n-3 Fatty acids are known to reduce many risk factors associated with several diseases, such as cardiovascular diseases, diabetes, and cancer. The mechanisms whereby n-3 fatty acids affect gene expression are complex and involve multiple processes. As examples, n-3 fatty acids regulate 2 groups of transcription factors, such as sterol-regulatory-element binding proteins and peroxisome proliferator-activated receptors, that are critical for modulating the expression of genes controlling both systemic and tissue-specific lipid homeostasis. Modulation of specific genes by n-3 fatty acids and cross-talk between these genes are responsible for many effects of n-3 fatty acids.

Apigenin inhibits growth and motility but increases gap junctional coupling intensity in rat prostate carcinoma (MAT-LyLu) cell populations. Czernik M, Sroka J, Madeja Z, Czyz J. Cell Mol Biol Lett. 2008;13(3):327-38. Epub 2008 Feb 21. PMID: 18292973 DOI: 10.2478/s11658-008-0003-z This in vitro data indicates that apigenin may affect cancer development in general, and prostate carcinogenesis in particular, via its influence on cellular activities decisive for both cancer promotion and progression, including cell proliferation, gap junctional coupling and cell motility and invasiveness.

"ScienceDaily (Nov. 30, 2009) - Universitat Autònoma de Barcelona (UAB) researchers have confirmed that a diet rich in polyphenols and polyunsaturated fatty acids, patented as an LMN diet, helps boost the production of the brain's stem cells -neurogenesis- and strengthens their differentiation in different types of neuron cells. The research revealed that mice fed an LMN diet, when compared to those fed a control diet, have more cell proliferation in the two areas of the brain where neurogenesis is produced, the olfactory bulb and the hippocampus, both of which are greatly damaged in patients with Alzheimer's disease. These results give support to the hypothesis that a diet made up of foods rich in these antioxidant substances could delay the onset of this disease or even slow down its evolution. The study will be published in the December issue of the Journal of Alzheimer's Disease and was directed by Mercedes Unzeta, professor of the UAB Department of Biochemistry and Molecular Biology"