Expression of MMP2 and MMP9 (Gelatinases A and B) in Human Colon Cancer Cells

Damodharan, Umadevi; Ravikumar, Ganesan; Radhakrishnan, Uma C

doi:10.1007/s12010-011-9342-8

Cited by 37 publications

(27 citation statements)

References 12 publications

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“…CTMM promotes apoptosis, inhibits proliferation, reverses drug-resistance in chemotherapy and improves the effect of chemotherapy on cancer therapy (23). Emodin is one of these drugs which has been shown to play a therapeutic role in the gastrointestinal tract, and genitourinary cancer (5,(24)(25)(26). Our study showed that emodin suppressed tumor growth and induced tissue cell apoptosis.…”

Section: Discussionmentioning

confidence: 67%

“…A number of studies show that emodin has a good effect on treating prostate (4), colorectal (5) and pancreatic cancer (6). In this study, we found that the Panc-1 cells' MMP declined and apoptosis rate increased dose-dependently with emodin treatment and the cell proliferation of each group was inhibited in a dose-and time-dependent manner.…”

Section: Introductionmentioning

confidence: 99%

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Emodin induces Panc-1 cell apoptosis via declining the mitochondrial membrane potential

Liu

Zhang

et al. 2012

Oncology Reports

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Abstract. In this study, we investigated the apoptotic effect of emodin on human pancreatic cancer cell line Panc-1 in vitro and in vivo as well as the possible mechanisms involved. In vitro, human pancreatic cancer cell line Panc-1 was exposed to varying concentrations of emodin (0,10,20, 40 or 80 µmol/l). Then the mitochondrial membrane potential (MMP) was analyzed by JC-1 staining, cell apoptosis was analyzed by flow cytometry (FCM) and cell proliferation was analyzed by MTT. In vivo, nude mice orthotopically implanted were randomly divided into five groups to receive treatments by different doses of emodin: control group (normal saline 0.2 ml), E 10 group (emodin 10 mg/kg), E 20 group (emodin 20 mg/kg), E 40 group (emodin 40 mg/kg) and E 80 group (emodin 80 mg/kg). Each mouse was treated 5 times by intraperitoneal injection of emodin every 3 days. During the treatment, the feeding stuff was recorded. One week after the last treatment, we recorded the body weight and the maximum diameter of tumor in each group before the mice were sacrificed. Then the cell apoptosis of the tumor was tested by TUNEL assay. The results in vitro showed that the MMP of the cells declined and the apoptosis rate increased with the emodin concentration increasing and the cell proliferation of each group was inhibited in a dose-and time-dependent manner by emodin. The feeding stuff curve did not decline significantly in E 40 group and the apoptosis rate of the tumor cells in this group was higher than the lower-dose groups. Taken together, our results demonstrate that emodin may induce the pancreatic cancer cell apoptosis via declining the MMP and a moderate dose of emodin improved the living state of the model mice.

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Section: Discussionmentioning

confidence: 67%

Section: Introductionmentioning

confidence: 99%

Emodin induces Panc-1 cell apoptosis via declining the mitochondrial membrane potential

Liu

Zhang

et al. 2012

Oncology Reports

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“…Emodin also suppressed the NO-mediated up-regulation of MMP2 and MMP9 in the colon cancer cell line, WiDr. By reducing ECM degradation, these proteins promote tumor angiogenesis and metastasis [106]. It has been shown that emodin inhibited the invasiveness of human cancer cells by suppressing MMP9 expression and inhibiting AP-1 and NF-jB signaling pathways.…”

Section: Anti-angiogenic and Anti-metastatic Effects Of Emodinmentioning

confidence: 99%

Targeted abrogation of diverse signal transduction cascades by emodin for the treatment of inflammatory disorders and cancer

et al. 2013

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a b s t r a c tEmodin (1,3,8-trihydroxy-6-methylanthraquinone) is a natural occurring anthraquinone derivative isolated from roots and barks of numerous plants, molds, and lichens. It is found as an active ingredient in different Chinese herbs including Rheum palmatum and Polygonam multiflorum, and has diuretic, vasorelaxant, anti-bacterial, anti-viral, anti-ulcerogenic, anti-inflammatory, and anti-cancer effects. The anti-inflammatory effects of emodin have been exhibited in various in vitro as well as in vivo models of inflammation including pancreatitis, arthritis, asthma, atherosclerosis and glomerulonephritis. As an anti-cancer agent, emodin has been shown to suppress the growth of various tumor cell lines including hepatocellular carcinoma, pancreatic, breast, colorectal, leukemia, and lung cancers. Emodin is a pleiotropic molecule capable of interacting with several major molecular targets including NF-jB, casein kinase II, HER2/neu, HIF-1a, AKT/mTOR, STAT3, CXCR4, topoisomerase II, p53, p21, and androgen receptors which are involved in inflammation and cancer. This review summarizes reported anti-inflammatory and anti-cancer effects of emodin, and re-emphasizes its potential therapeutic role in the treatment of inflammatory diseases and cancer.

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“…The basic procedure consists in electrophoresis in polyacrylamide gels containing gelatin, inoculated with the media samples and revealed by an enzyme substrate buffer (50 mM Tris-HCl pH 8.0, 5 mM CaCl 2 , 0.02% NaN 3 ), followed by staining protocols. The noncolored areas are quantitative related to the degradation activity of MMP-2 and MMP-9, in both pro and active forms [18,70].…”

Section: The Role Of Matrix Metalloproteinases (Mmps)mentioning

confidence: 99%

Low Level Energy Photodynamic Therapy for Skin Processes and Regeneration

Tedesco¹,

Jesus²

2017

Photomedicine - Advances in Clinical Practice

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Skin is the largest human organ and displays multiple functions involving structure and protection against external agents that may affect the body. Solar radiation accelerates the normal aging process and may even cause great damage leading to many different cutaneous diseases and skin cancer. Moreover, a wound in the skin may be an open channel for the access of pathogens usually exposing blood vessels for infections and causing serious complications. For many reasons, regulatory skin processes are of great deal in different approaches: basic antiaging, wound healing, and skin cancer. In a good way, photoprocesses with specific wavelength at low energy levels associated with photoactive compounds are known to cause the opposite effect, promoting the healing of cutaneous diseases and leading to well-defined outcomes in rejuvenation and antiaging. This chapter will discuss the most relevant topics in photo skin regeneration using low energy levels associated with photodynamic therapy (PDT), which emerged as a combination to potentialize molecules with the already known effects of PDT and low level laser therapy (LLLT) in the treatment of skin pathologies, known as a photobiomodulation process.

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Expression of MMP2 and MMP9 (Gelatinases A and B) in Human Colon Cancer Cells

Cited by 37 publications

References 12 publications

Emodin induces Panc-1 cell apoptosis via declining the mitochondrial membrane potential

Emodin induces Panc-1 cell apoptosis via declining the mitochondrial membrane potential

Targeted abrogation of diverse signal transduction cascades by emodin for the treatment of inflammatory disorders and cancer

Low Level Energy Photodynamic Therapy for Skin Processes and Regeneration

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