aloe emodin/neoplasms

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Aloe emodin suppresses EGF‑induced neoplastic cell transformation by inhibiting the ERK/MSK1 and AKT/GSK3β signaling pathways.

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Natural compounds which can block cell transformation due to potential for chemoprevention have received increased attention. The present study aimed to investigate whether aloe emodin, which is present in aloe latex or the roots of the Rheum palmatum L. are able to block epidermal growth factor

Aloe-Emodin Induces Breast Tumor Cell Apoptosis through Upregulation of miR-15a/miR-16-1 That Suppresses BCL2.

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Aloe-emodin (AE) is a natural compound derived from aloe vera and palmatum rhubarb and shows anticancer activities in various cancers. Bcl-2 family is the main regulator of cell death or cell survival. This study describes the effects of AE on proliferation of breast tumor (BT)

Aloe emodin inhibits the cytotoxic action of tumor necrosis factor.

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We demonstrate the capacity of an herbal anthraquinone aloe emodin to reduce the cytotoxicity of the proinflammatory cytokine tumor necrosis factor (TNF) towards L929 mouse fibrosarcoma and U251 human glioma cell lines. Aloe emodin inhibited both TNF-induced cell necrosis and apoptosis, but it did

Aloe-Emodin Enhances Tamoxifen Cytotoxicity by Suppressing Ras/ERK and PI3K/mTOR in Breast Cancer Cells.

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Aloe-emodin (AE) is derived from Aloe vera and rhubarb (Rheum palmatum) and exhibits anticancer activities via multiple regulatory mechanisms in various cancers. AE can also enhance the anticancer efficacy of cisplatin, doxorubicin, docetaxel, and 5-fluorouracil; however, its effects remain poorly

Aloe-emodin induces autophagy and apoptotic cell death in non-small cell lung cancer cells via Akt/mTOR and MAPK signaling

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Lung cancer has a relatively poor prognosis, and the clinical efficacy of targeted drugs remains unsatisfactory. Therefore, the search for safe and efficient novel antitumor drugs has become an urgent problem in the treatment of lung cancer. Aloe-emodin (AE), a medicinal herb, has been demonstrated

The molecular effects of aloe-emodin (AE)/liposome-AE on human nonmelanoma skin cancer cells and skin permeation.

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In this study, aloe-emodin (AE) was less cytotoxic to human noncancerous skin cells (premalignant keratinocytic HaCaT and fibroblast Hs68) than to nonmelanoma cancer cells (epidermoid carcinoma A431 and head and neck squamous cell carcinoma SCC25). Notably, AE induced apoptosis by up-regulating

Aloe-emodin inhibits HER-2 expression through the downregulation of Y-box binding protein-1 in HER-2-overexpressing human breast cancer cells.

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Human epidermal growth factor receptor-2 (HER-2)-positive breast cancer tends to be aggressive, highly metastatic, and drug resistant and spreads rapidly. Studies have indicated that emodin inhibits HER-2 expression. This study compared the HER-2-inhibitory effects of two compounds extracted from

Aloe emodin inhibits telomerase activity in breast cancer cells: transcriptional and enzymological mechanism.

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Telomerase plays an essential role in cancer cell proliferation. In this study, we investigated inhibition mechanism of aloe emodin (AE) on three different types of breast cancer cell lines, MDA-MB-453, MDA-MB-231 and MCF-7.The cells were treated with

Suppression of C-myc expression associates with anti-proliferation of aloe-emodin on gastric cancer cells.

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Aloe-emodin is a hydroxyanthraquinone found in Aloe vera, as well as in leaves and roots of other plants. The mechanisms of its anticancer effect are largely unknown. The present study investigated its molecular mechanisms. Crystal violet assay showed that aloe-emodin had a long-term

[Effect of Aloe emodin on invasion and metastasis of high metastatic breast cancer MDA-MB-231 cells].

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OBJECTIVE To investigate the effect of Aloe emodin (AE) on the invasive and metastatic abilities of human high metastatic breast cancer MDA-MB-231 cells. METHODS MTT assay was used to evaluate the viability of MDA-MB-231 cells after treated with AE for 6 h and 24 h. The adhesive potential of

The effect of aloe-emodin-induced photodynamic activity on the apoptosis of human gastric cancer cells: A pilot study.

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The aim of the present study was to explore the effect of aloe-emodin (AE)-induced photodynamic activity in human gastric cancer cells. AE was used as a photosensitizer to explore the effect of photodynamic therapy (PDT) in human gastric cancer cells (SGC-7901). An MTT assay was used to detect the

Aloe-emodin induces cell death through S-phase arrest and caspase-dependent pathways in human tongue squamous cancer SCC-4 cells.

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Aloe-emodin, one of the anthraquinones, has been shown to have anticancer activity in different kinds of human cancer cell lines. Therefore, the purpose of this study was to investigate the anti-cancer effect of aloe-emodin on human tongue squamous carcinoma SCC-4 cells. The results indicated that

Exploring a Novel Target Treatment on Breast Cancer: Aloe-emodin Mediated Photodynamic Therapy Induced Cell Apoptosis and Inhibited Cell Metastasis.

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Photodynamic therapy (PDT) as a clinical cancer therapy, is a mild therapy, which involves application of photosensitizers (PSs) located in target cells and then irradiated by corresponding wavelength. The activation of PSs generates radical oxygen species (ROS) to exert a selective cytotoxic

Aloe emodin inhibits colon cancer cell migration/angiogenesis by downregulating MMP-2/9, RhoB and VEGF via reduced DNA binding activity of NF-κB.

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Aloe emodin (AE), a natural anthraquinone, is reported to have antiproliferative activity in various cancer cell lines. In this study we analyzed molecular mechanisms involved in the antimigratory and antiangiogenic activity of this hydroxy anthraquinone in colon cancer cell, WiDr. Our results show

Emodin, aloe-emodin and rhein induced DNA damage and inhibited DNA repair gene expression in SCC-4 human tongue cancer cells.

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In our primary studies, we have shown that emodin, aloe-emodin and rhein induced cytotoxic effects, including cell cycle arrest and apoptosis in SCC-4 human tongue cancer cells. However, details regarding their effects on DNA damage and repair gene expression in SCC-4 cells are not clear. We

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