Abstract

<p class="Abstract">The main aim of the present research work was to demonstrate the antitumor and apoptotic activities of oxypeucedanin hydrate monoacetate isolated from <em>Angelica dahurica</em> against Caco-2 colon cancer cells. MTT cell viability assay along with clonogenic assays were used to study the effect of the compound on cell cytotoxicity and the colony forming tendency. Fluorescence microscopy using acridine orange/ethidium bromide was used to study the effects on apoptosis. <em>In vitro</em> wound healing assay and Western blotting were carried out to study effect on cell migration and PI3K-signalling pathway. The results revealed that oxypeucedanin hydrate monoacetate inhibited Caco-2 cell proliferation and decreased the number of cancer colony forming cells. This compound exerted anti-migratory effects in dose- and time-dependent manner. As compared to the untreated control, drug-treated cells showed significant inhibition of cancer cell migration. Oxypeucedanin hydrate monoacetate significantly down-regulated the expression of pAkt and pPI3K in Caco-2 cells.</p><p> </p>

Highlights

  • Malignant cancer disorders constitute one of the leading causes of death in most countries

  • MTT assay revealed that oxypeucedanin hydrate monoacetate showed a potent growth inhibitory effect on the proliferation of Caco-2 cancer cells with IC50 values 36.4, 42.1 and 46.3 μM at 72, 48 and 24 hours time intervals respectively

  • Clonogenic assay revealed that oxypeucedanin hydrate monoacetate leads to a significant reduction in the number of cancer colony forming cells which showed strong dose-dependence (Figure 1 and 2)

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Summary

Introduction

Malignant cancer disorders constitute one of the leading causes of death in most countries. There are various factors which give rise to colon cancer and these include mutations in adenomatous polyposis coli, loss in tumor suppressor gene p53, disruption in cell cycle and suppression in apoptosis (Kinzler and Vogelstein, 1996; Samowitz et al, 2002; Sebolt-Leopold et al, 1999; Torrance et al, 2000). It follows agents which can manage these above mentioned defects could as potential chemotherapeutic agents in controlling the growth of colon cancer cells

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