Inhibition of cell proliferation and invasion in a human colon cancer cell line by 5-aminosalicylic acid

Kim, Y.-H.; Kim, M.H.; Kim, B.J.; Kim, J.J.; Chang, Dong Kyung; Son, Hee Jung; Rhee, Poong–Lyul; Rhee, Jong Chul

doi:10.1016/j.dld.2008.09.003

Cited by 14 publications

(5 citation statements)

References 40 publications

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“…Similar anti-proliferative effects have been reported with indomethacin after 72 hours [38], aspirin after 96 hours [38], NS398 after 72 hours [39], 5-aminosalicylic acid after 48 hours [40], and with sulindac sulfide after 24 hours [41]. However, Piazza and colleagues [42] were unable to inhibit growth in these same cell lines with aspirin, naproxen or salicylic acid [42], but found that ibuprofen and sulindac sulfoxide inhibited growth with a low potency in contrast to higher potency shown with indomethacin, sulindac sulfide and diclofenac.…”

Section: Nsaids Inhibit Colon Cancer Cell Proliferation In Vitrosupporting

confidence: 75%

NSAIDs and Cell Proliferation in Colorectal Cancer

2010

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Colon cancer is common worldwide and accounts for significant morbidity and mortality in patients. Fortunately, epidemiological studies have demonstrated that continuous therapy with NSAIDs offers real promise of chemoprevention and adjunct therapy for colon cancer patients. Tumour growth is the result of complex regulation that determines the balance between cell proliferation and cell death. How NSAIDs affect this balance is important for understanding and improving treatment strategies and drug effectiveness. NSAIDs inhibit proliferation and impair the growth of colon cancer cell lines when tested in culture in vitro and many NSAIDs also prevent tumorigenesis and reduce tumour growth in animal models and in patients, but the relationship to inhibition of tumour cell proliferation is less convincing, principally due to gaps in the available data. High concentrations of NSAIDs are required in vitro to achieve cancer cell inhibition and growth retardation at varying time-points following treatment. However, the results from studies with colon cancer cell xenografts are promising and, together with better comparative data on anti-proliferative NSAID concentrations and doses (for in vitro and in vivo administration), could provide more information to improve our understanding of the relationships between these agents, dose and dosing regimen, and cellular environment.

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Section: Nsaids Inhibit Colon Cancer Cell Proliferation In Vitrosupporting

confidence: 75%

NSAIDs and Cell Proliferation in Colorectal Cancer

2010

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“…Therefore, the decrease in MMP-2 and −9 level could be due to inhibition of COX-2 and the NF-κB and STAT3 signaling pathways. Several studies showed that metformin or 5-ASA can inhibit MMP’s expression [ 54 – 56 ].…”

Section: Discussionmentioning

confidence: 99%

Combination of metformin and 5-aminosalicylic acid cooperates to decrease proliferation and induce apoptosis in colorectal cancer cell lines

Saber¹,

Galal²,

Ain-Shoka³

et al. 2016

BMC Cancer

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BackgroundThe link between inflammation and cancer has been confirmed by the use of anti-inflammatory therapies in cancer prevention and treatment. 5-aminosalicylic acid (5-ASA) was shown to decrease the growth and survival of colorectal cancer (CRC) cells. Studies also revealed that metformin induced apoptosis in several cancer cell lines.MethodsWe investigated the combinatory effect of 5-ASA and metformin on HCT-116 and Caco-2 CRC cell lines. Apoptotic markers were determined using western blotting. Expression of pro-inflammatory cytokines was determined by RT-PCR. Inflammatory transcription factors and metastatic markers were measured by ELISA.ResultsMetformin enhanced CRC cell death induced by 5-ASA through significant increase in oxidative stress and activation of apoptotic machinery. Moreover, metformin enhanced the anti-inflammatory effect of 5-ASA by decreasing the gene expression of IL-1β, IL-6, COX-2 and TNF-α and its receptors; TNF-R1 and TNF-R2. Significant inhibition of activation of NF-κB and STAT3 transcription factors, and their downstream targets was also observed. Metformin also enhanced the inhibitory effect of 5-ASA on MMP-2 and MMP-9 enzyme activity, indicating a decrease in metastasis.ConclusionThe current data demonstrate that metformin potentiates the antitumor effect of 5-ASA on CRC cells suggesting their potential use as an adjuvant treatment in CRC.

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“…NF‐κB‐mediated expression of matrix metalloproteinases (MMPs) has a central role in tumorigenesis 59 . 5‐ASA inhibits MMPs expression via NF‐κB mediated cell signals and invasiveness 60 …”

Section: Methodsmentioning

confidence: 99%

“…59 5-ASA inhibits MMPs expression via NF-jB mediated cell signals and invasiveness. 60 Tumour necrosis factor-a seems to contribute to inflammation in IBD patients by initiation of intracellular signalling cascades resulting in release of transcriptional factor NF-jB and activation of COX-2 both of which have protumorigenic activity. 61 5-ASA blocks both COX-2-dependent and -independent cancer cell growth.…”

Section: Tnf-a Tgf-ß and Nf-jb Pathwaymentioning

confidence: 99%

Systematic review: molecular chemoprevention of colorectal malignancy by mesalazine

Lyakhovich

Gasché

2009

Aliment Pharmacol Ther

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SUMMARY BackgroundMesalazine (mesalamine) (5-ASA) is considered an anti-inflammatory drug for the treatment of inflammatory bowel disease. It is well tolerated by most patients and induces mucosal healing specifically in ulcerative colitis. Besides its anti-inflammatory properties, 5-ASA has been studied for cancer inhibitory activities as it seems to reduce colorectal cancer incidence in patients using this drug for long periods of time. However, detailed molecular mechanisms of drug action are vague.

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Inhibition of cell proliferation and invasion in a human colon cancer cell line by 5-aminosalicylic acid

Cited by 14 publications

References 40 publications

NSAIDs and Cell Proliferation in Colorectal Cancer

NSAIDs and Cell Proliferation in Colorectal Cancer

Combination of metformin and 5-aminosalicylic acid cooperates to decrease proliferation and induce apoptosis in colorectal cancer cell lines

Systematic review: molecular chemoprevention of colorectal malignancy by mesalazine

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