Friday, April 14, 2017

Natural Cancer Bullets A - Z

There are many silver bullets that you can use to fight cancer. I will post some of these bullets (alphabetically) along with sources and brief explanations over the next several months.

Acai Berries

Source: Fruits from the Açaí Palm.

Brazilian berry destroys cancer cells in lab, UF study shows
Published today in the Journal of Agricultural and Food Chemistry, the study showed extracts from acai (ah-SAH’-ee) berries triggered a self-destruct response in up to 86 percent of leukemia cells tested, said Stephen Talcott, an assistant professor with UF’s Institute of Food and Agricultural Sciences. “Acai berries are already considered one of the richest fruit sources of antioxidants,” Talcott said. “This study was an important step toward learning what people may gain from using beverages, dietary supplements or other products made with the berries.”


Sources: Aloe Vera Plant, Aloe Vera Juice

Aloe-Emodin Induces Apoptosis in T24 Human Bladder Cancer Cells

AE inhibited cell viability, and induced G2/M arrest and apoptosis in T24 cells. AE increased the levels of Wee1 and cdc25c, and may have led to inhibition of the levels of cyclin-dependent kinase 1 and cyclin B1, which cause G2/M arrest. AE induced p53 expression and was accompanied by the induction of p21 and caspase-3 activation, which was associated with apoptosis. In addition, AE was associated with a marked increase in Fas/APO1 receptor and Bax expression but it inhibited Bcl-2 expression.

Anticancer effect of aloe-emodin on cervical cancer cells involves G2/M arrest and induction of differentiation.
Aloe-emodin inhibited the growth of HeLa cells in a dose-dependent manner at concentrations ranging between 2.5 and 40 micromol/L. The flow cytometric analysis showed that HeLa cells were arrested at the G2/M phase. This effect was associated with the decrease in cyclin A and CDK2, and the increase in cyclin B1 and CDK1. More importantly, the ALP activity was found to be increased by aloe-emodin treatment, and accompanied by the inhibition of PCNA expression. In addition, aloe-emodin suppressed the expression of PKCalpha and c-myc.

Aloe-emodin suppresses prostate cancer by targeting the mTOR complex 2
Our results herein are noteworthy in that prostate cancer cell growth is suppressed by aloe-emodin in vivo. Moreover, the low in vivo toxicity and tumor inhibitory activity of aloe-emodin observed in nude mice suggest that aloe-emodin is an effective chemopreventive agent against prostate cancer (Figure 6A and B). In conclusion, we showed here that mTORC2 is closely associated with prostate cancer cell growth. We also provided clear evidence showing that aloe-emodin effectively suppresses anchorage-independent cell growth and in vivo tumor growth in PC3 cancer cell-bearing nude mice by inhibiting Akt activity. Collectively, these findings support the anticancer efficacy of aloe-emodin through its targeting of mTORC2 for the inhibition of prostate cancer progression.
Protein kinase C involvement in aloe-emodin- and emodin-induced apoptosis in lung carcinoma cell
This study demonstrated aloe-emodin- and emodin-induced apoptosis in lung carcinoma cell lines CH27 (human lung squamous carcinoma cell) and H460 (human lung non-small cell carcinoma cell). Aloe-emodin- and emodin-induced apoptosis was characterized by nuclear morphological changes and DNA fragmentation.

The antiproliferative activity of aloe-emodin is through p53-dependent and p21-dependent apoptotic pathway in human hepatoma cell lines

The aim of this study is to investigate the anticancer effect of aloe-emodin in two human liver cancer cell lines, Hep G2 and Hep 3B. We observed that aloe-emodin inhibited cell proliferation and induced apoptosis in both examined cell lines, but with different the antiproliferative mechanisms.
Aloe-emodin Is a New Type of Anticancer Agent with Selective Activity against Neuroectodermal Tumors
Here we report that aloe-emodin (AE), a hydroxyanthraquinone present in Aloe vera leaves, has a specific in vitro and in vivo antineuroectodermal tumor activity. The growth of human neuroectodermal tumors is inhibited in mice with severe combined immunodeficiency without any appreciable toxic effects on the animals. The compound does not inhibit the proliferation of normal fibroblasts nor that of hemopoietic progenitor cells. The cytotoxicity mechanism consists of the induction of apoptosis, whereas the selectivity against neuroectodermal tumor cells is founded on a specific energy-dependent pathway of drug incorporation. Taking into account its unique cytotoxicity profile and mode of action, AE might represent a conceptually new lead antitumor drug.
Aloe-emodin induced in vitro G2/M arrest of cell cycle in human promyelocytic leukemia HL-60 cells.
Aloe-emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation of the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with aloe-emodin in HL-60 cells. Investigation of the levels of cyclin-dependent kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of Cdk2 were not effected with aloe-emodin in HL-60 cells. The levels of p27 were increased after HL-60 cells were cotreated with various concentrations of aloe-emodin.
Aloe-emodin-induced apoptosis in human gastric carcinoma cells
The purpose of this study was to investigate the anticancer effect of aloe-emodin, an anthraquinone compound present in the leaves of Aloe vera, on two distinct human gastric carcinoma cell lines, AGS and NCI-N87. We demonstrate that aloe-emodin induced cell death in a dose- and time-dependent manner. Noteworthy is that the AGS cells were generally more sensitive than the NCI-N87 cells. Aloe-emodin caused the release of apoptosis-inducing factor and cytochrome c from mitochondria, followed by the activation of caspase-3, leading to nuclear shrinkage and apoptosis.

Aloe-emodin induces in vitro G2/M arrest and alkaline phosphatase activation in human oral cancer KB cells
Aloe-emodin is a natural anthraquinone compound from the root and rhizome of Rheum palmatum. In this study, KB cells were treated with 2.5, 5, 10, 20, and 40 microM aloe-emodin for 1 to 5 days. The results showed that aloe-emodin inhibited cancer cells in a dose-dependent manner. Treatment with aloe-emodin at 10 to 40 microM resulted in cell cycle arrest at G2/M phase. The alkaline phosphatase (ALP) activity in KB cells increased upon treatment with aloe-emodin when compared to controls. This is one of the first studies to focus on the expression of ALP in human oral carcinomas cells treated with aloe-emodin. These results indicate that aloe-emodin has anti-cancer effect on oral cancer, which may lead to its use in chemotherapy and chemo preventment of oral cancer.


Source: Cannabis

Anandamide May Fight Aggressive Skin Cancer
According to the study’s results, anandamide may be involved in a complex mechanism that includes the CB1 receptor, and possibly GPR55 – a cannabinoid receptor in its own right. Although not much is known about GPR55, it is sometimes referred to as the CB3 receptor, because it responds to both endogenous and plant-derived cannabinoids.
The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation
Anandamide was the first brain metabolite shown to act as a ligand of “central” CB1 cannabinoid receptors. Here we report that the endogenous cannabinoid potently and selectively inhibits the proliferation of human breast cancer cells in vitro. Anandamide dose-dependently inhibited the proliferation of MCF-7 and EFM-19 cells with IC50 values between 0.5 and 1.5 μM and 83–92% maximal inhibition at 5–10 μM. The proliferation of several other nonmammary tumoral cell lines was not affected by 10 μM anandamide. The anti-proliferative effect of anandamide was not due to toxicity or to apoptosis of cells but was accompanied by a reduction of cells in the S phase of the cell cycle. ...These data suggest that anandamide blocks human breast cancer cell proliferation through CB1-like receptor-mediated inhibition of endogenous prolactin action at the level of prolactin receptor.

Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines
ANA induced a decrease of EGFR levels on LNCaP, DU145, and PC3 prostatic cancer cells by acting through cannabinoid CB1 receptor subtype and this leaded to an inhibition of the EGF-stimulated growth of these cells. Moreover, the G1 arrest of metastatic DU145 and PC3 growth was accompanied by a massive cell death by apoptosis and/or necrosis while LNCaP cells were less sensitive to cytotoxic effects of ANA. The apoptotic/necrotic responses induced by ANA on these prostatic cancer cells were also potentiated by the acidic ceramidase inhibitor, N-oleoylethanolamine and partially inhibited by the specific ceramide synthetase inhibitor, fumonisin B1 indicating that these cytotoxic actions of ANA might be induced via the cellular ceramide production. The potent anti-proliferative and cytotoxic effects of ANA on metastatic prostatic cancer cells might provide basis for the design of new therapeutic agents for effective treatment of recurrent and invasive prostatic cancers.
Cannabinoids, Endocannabinoids and Cancer
Cannabinoids exert a number of interesting effects that are dependent on the cell line or tumor type. Synthetic cannabinoids and the endocannabinoid system are implicated in inhibiting cancer cell proliferation and angiogenesis, reducing tumor growth and metastases, and inducing apoptosis.
Anandamide is an endogenous inhibitor for the migration of tumor cells and T lymphocytes
Cell migration is of paramount importance in physiological processes such as immune surveillance, but also in the pathological processes of tumor cell migration and metastasis development. The factors that regulate this tumor cell migration, most prominently neurotransmitters, have thus been the focus of intense investigation. While the majority of neurotransmitters have a stimulatory effect on cell migration, we herein report the inhibitory effect of the endogenous substance anandamide on both tumor cell and lymphocyte migration. ...Using the specific agonist docosatetraenoylethanolamide (DEA), we have observed that the norepinephrine-induced migration of colon carcinoma cells is inhibited by the CB1-R. The SDF-1–induced migration of CD8+ T lymphocytes was, however, inhibited via the CB2-R, as shown by using the specific agonist JWH 133. Therefore, specific inhibition of tumor cell migration via CB1-R engagement might be a selective tool to prevent metastasis formation without depreciatory effects on the immune system of cancer patients.
The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells
These findings suggest anandamide may be a useful chemopreventive/therapeutic agent for colorectal cancer as it targets cells that are high expressors of COX-2, and may also be used in the eradication of tumour cells that have become resistant to apoptosis.


Sources: Parsley, Celery, Coriander, Licorice, Majoram, Oregano, Rosemary, Tarragon, Citrus, Tea and Wheat.

Breast cancer effectively treated with chemical found in celery, parsley, mouse study suggests
Apigenin, a natural substance found in grocery store produce aisles, shows promise as a non-toxic treatment for an aggressive form of human breast cancer, following a new study. Researchers found apigenin shrank a type of breast cancer tumor that is stimulated by progestin, a synthetic hormone given to women to ease symptoms related to menopause.
Apigenin induces breast cancer cells
Apigenin is a low toxicity and non-mutagenic phytopolyphenol and protein kinase inhibitor. It exhibits anti-proliferating effects on human breast cancer cells. Here we examined several human breast cancer cell lines having different levels of HER2/neu expression and found that apigenin exhibited potent growth-inhibitory activity in HER2/neu-over expressing breast cancer cells but was much less effective for those cells expressing basal levels of HER2/neu
Selective growth-inhibitory, cell-cycle deregulatory and apoptotic response of apigenin in normal versus human prostate carcinoma cells
The growth-inhibitory and apoptotic potential of apigenin was also observed in a variety of prostate carcinoma cells representing different stage and androgen responsiveness. Apigenin may be developed as a promising chemopreventive and/or chemotherapeutic agent against prostate cancer.
Signal pathways involved in apigenin inhibition of growth and induction of apoptosis of human anaplastic thyroid cancer cells
Recently we demonstrated that several flavonoids can inhibit the proliferation of certain human thyroid cancer cell lines. Among the flavonoids tested, apigenin and luteolin are the most effective inhibitors of these tumor cell lines. In the present study, we investigated the signal transduction mechanism associated with the growth inhibitory effect of apigenin, using a human anaplastic thyroid carcinoma cell line, ARO.

5,6-Dichloro-ribifuranosylbenzimidazole- and apigenin-induced sensitization of colon cancer cells to TNF--mediated apoptosis

Here we report that inhibition of CK2 in HCT-116 and HT-29 cells with the use of two specific CK2 inhibitors, 5,6-dichloro-ribifuranosylbenzimidazole (DRB) and apigenin, effected a synergistic reduction in cell survival when used in conjunction with TNF-. Furthermore, there was a demonstrable synergistic reduction in colony formation in soft agar with the use of the same combinations.

Induction of apoptosis by apigenin in leukaemia HL-60 cells
The potency of these flavonoids on these features of apoptosis were in the order of: apigenin>quercetin>myricetin>kaempferol in HL-60 cells treated with 60μM flavonoids. These results suggest that flavonoid-induced apoptosis is stimulated by the release of cytochrome c to the cytosol, by procaspase-9 processing, and through a caspase-3-dependent mechanism. The induction of apoptosis by flavonoids may be attributed to their cancer chemopreventive activity. Furthermore, the potency of flavonoids for inducing apoptosis may be dependent on the numbers of hydroxyl groups in the 2-phenyl group and on the absence of the 3-hydroxyl group. This provides new information on the structure–activity relationship of flavonoids.
Arachidonyl Ethanolamide

Source: Cannabis

Arachidonyl ethanolamide induces apoptosis of uterine cervix cancer cells via aberrantly expressed vanilloid receptor-1
The major finding was that AEA induced apoptosis of CxCa cell lines via aberrantly expressed vanilloid receptor-1, whereas AEA binding to the classical CB1 and CB2 cannabinoid receptors mediated a protective effect. Furthermore, unexpectedly, a strong expression of the three forms of AEA receptors was observed in ex vivo CxCa biopsies.

Sources: wormwood plant

Artemisinin Induces Apoptosis in Human Cancer Cells
Artemisinin is a chemical compound extracted from the wormwood plant, Artemisia annua L. It has been shown to selectively kill cancer cells in vitro and retard the growth of implanted fibrosarcoma tumors in rats. In the present research, we investigated its mechanism of cytotoxicity to cancer cells. ...This rapid induction of apoptosis in cancer cells after treatment with DHA indicates that artemisinin and its analogs may be inexpensive and effective cancer agents.
Effects of artemisinin and its derivatives on growth inhibition and apoptosis of oral cancer cells
Artemisinin is of special biological interest because of its outstanding antimalarial activity. Recently, it was reported that artemisinin has antitumor activity. Its derivatives, artesunate, arteether, and artemeter, also have antitumor activity against melanoma, breast, ovarian, prostate, CNS, and renal cancer cell lines. Recently, monomer, dimer, and trimer derivatives were synthesized from deoxoartemisinin, and the dimers and the trimers were found to have much more potent antitumor activity than the monomers. ...The deoxoartemisinin trimer was found to have greater antitumor effect on tumor cells than other commonly used chemotherapeutic drugs, such as 5-FU, cisplatin, and paclitaxel. Furthermore, the ability of artemisinin and its derivatives to induce apoptosis highlights their potential as chemotherapeutic agents, for many anticancer drugs achieve their antitumor effects by inducing apoptosis in tumor cells.
Transferrin overcomes drug resistance to artemisinin in human small-cell lung carcinoma cells
Multiple drug resistance is a significant problem in small-cell lung cancer (SCLC). Artemisinin (ART) is a natural product used to treat drug-resistant malaria. The drug is effective because the Fe2+ present in infected erythrocytes acts non-enzymatically to convert ART to toxic products. We tested the effects of ART on drug-sensitive (H69) and multi-drug-resistant (H69VP) SCLC cells, pretreated with transferrin (TF) to increase the intracellular Fe2+ level. ...These data indicate the potential use of ART and TF in drug-resistant SCLC.
Dihydroartemisinin induces apoptosis and sensitizes human ovarian cancer cells to carboplatin therapy
The present study was designed to determine the effects of artemisinin (ARS) and its derivatives on human ovarian cancer cells, to evaluate their potential as novel chemotherapeutic agents used alone or in combination with a conventional cancer chemotherapeutic agent, and to investigate their underlying mechanisms of action. Human ovarian cancer cells (A2780 and OVCAR-3), and immortalized non-tumourigenic human ovarian surface epithelial cells (IOSE144), were exposed to four ARS compounds for cytotoxicity testing. The in vitro and in vivo antitumour effects and possible underlying mechanisms of action of dihydroartemisinin (DHA), the most effective compound, were further determined in ovarian cancer cells. ...These effects were also observed in in vivo ovarian A2780 and OVCAR-3 xenograft tumour models. In conclusion, ARS derivatives, particularly DHA, exhibit significant anticancer activity against ovarian cancer cells in vitro and in vivo, with minimal toxicity to non-tumourigenic human OSE cells, indicating that they may be promising therapeutic agents for ovarian cancer, either used alone or in combination with conventional chemotherapy.


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