Proteome response in HT‐29 human colorectal cancer cells to two apoptosis‐inducing compounds with different mode of action

Winkelmann, I.; Näßl, Anna-Maria; Daniel, Hannelore; Wenzel, U.

doi:10.1002/ijc.23387

Cited by 10 publications

(6 citation statements)

References 40 publications

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“…Expression of the different protein spots was expressed as volume percentage (%vol). Tryptic digestion of regulated protein spots and peptide mass fingerprinting by matrix-assisted laser desorption/ ionization time-of-flight mass spectrometry (MALDI-TOF-MS) were performed as described previously (49).…”

Section: Methodsmentioning

confidence: 99%

Alterations in hepatic one-carbon metabolism and related pathways following a high-fat dietary intervention

Rubio‐Aliaga

Roos

Sailer

et al. 2011

Physiological Genomics

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Obesity frequently leads to insulin resistance and the development of hepatic steatosis. To characterize the molecular changes that promote hepatic steatosis, transcriptomics, proteomics, and metabolomics technologies were applied to liver samples from C57BL/6J mice obtained from two independent intervention trials. After 12 wk of high-fat feeding the animals became obese, hyperglycemic, and insulin resistant, had elevated levels of blood cholesterol and VLDL, and developed hepatic steatosis. Nutrigenomic analysis revealed alterations of key metabolites and enzyme transcript levels of hepatic one-carbon metabolism and related pathways. The hepatic oxidative capacity and the lipid milieu were significantly altered, which may play a key role in the development of insulin resistance. Additionally, high choline levels were observed after the high-fat diet. Previous studies have linked choline levels with insulin resistance and hepatic steatosis in conjunction with changes of certain metabolites and enzyme levels of one-carbon metabolism. The present results suggest that the coupling of high levels of choline and low levels of methionine plays an important role in the development of insulin resistance and liver steatosis. In conclusion, the complexities of the alterations induced by high-fat feeding are multifactorial, indicating that the interplay between several metabolic pathways is responsible for the pathological consequences.

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Section: Methodsmentioning

confidence: 99%

Alterations in hepatic one-carbon metabolism and related pathways following a high-fat dietary intervention

Rubio‐Aliaga

Roos

Sailer

et al. 2011

Physiological Genomics

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“…Stathmin is a microtubule regulating protein that prevents polymerization of alpha/beta heterodimers and also affects depolymerization of microtubules [27]. Partial loss of a Table 1 stathmin has been reported for Hela cells exposed to S-trityl-L-cysteine that inhibits a microtubule-associated kinesin [28] and also for HT-29 colorectal cancer cells exposed to the topoisomerase inhibitor camptothecin [29]. Over-expression of stathmin has been observed in a number of cancers, including breast and liver [30,31].…”

Section: Tubulins and Other Cytoskeletal Proteinsmentioning

confidence: 97%

Effects of the microtubule stabilizing agent peloruside A on the proteome of HL-60 cells

Wilmes¹,

Rawson²,

Peng³

et al. 2010

Invest New Drugs

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Peloruside A, isolated from the marine sponge Mycale hentscheli, has a similar mechanism of action to paclitaxel (Taxol®), a drug used clinically to treat tumors of the breast, ovary and lung. Paclitaxel and peloruside stabilize the polymerized form of tubulin and arrest cells in G₂/M of the cell cycle. We have therefore used two-dimensional electrophoresis of proteins to examine the effect of peloruside A on the human HL-60 promyeloid leukemic cell line. Our goals included investigation whether affected proteins could be mapped onto pathways that predicted the cellular effects of this compound. In response to 100 nM peloruside A treatment for 24 h, seventeen identified proteins showed significant change in abundance with fourteen increases and three decreases. Use of Ingenuity Pathways Analysis confirmed that peloruside A affected pathways consistent with the known effects on microtubules and apoptosis. Our results also indicate a potential role of c-Myc in the cellular actions of peloruside consistent with an induction of aneuploidy seen at low concentrations of peloruside.

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“…2,3 Specific to colorectal carcinogenesis, such findings are still accumulating. [4][5][6][7] Whether dietary intake of flavonoids is protective against colorectal cancer in humans cannot be easily extrapolated from cell line and animal findings. In this perspective, epidemiologic studies on the association of flavonoid intake with colorectal cancer risk are important, yet to date these have been limited.…”

mentioning

confidence: 99%

Dietary flavonol, flavone and catechin intake and risk of colorectal cancer in the Netherlands Cohort Study

Simons

Hughes

Arts

et al. 2009

Intl Journal of Cancer

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Dietary flavonoids are hypothesized to be protective against colorectal cancer, yet findings have been inconsistent. We examined the association of dietary flavonol, flavone and catechin intake with colorectal cancer endpoints within the Netherlands Cohort Study (NLCS). In addition, we explored whether body mass index (BMI) may be an effect modifier of this association. The NLCS includes 120,852 men and women who were 55-69 years and completed a self-administered questionnaire at baseline in 1986. A case-cohort approach was used for data processing and analysis. After 13.3 years, 1,444 male and 1,041 female colorectal cancer cases were available for estimation of hazard ratios and 95% confidence intervals for quintiles of flavonoid intake. After adjustment for potential confounders, no association of total flavonol and flavone intake and total catechin intake with colorectal cancer endpoints was observed. Analyses stratified for BMI showed significant inverse trends in the association of total catechin intake, (1)-catechin intake and (-)-epicatechin intake with rectal cancer in men with a BMI 25 kg/m 2 and in the association of total catechin intake and intake of kaempferol, myricetin and all individual catechins with colorectal cancer, in particular colon cancer, in women with a BMI < 25 kg/m 2 . In conclusion, our findings generally do not support an association of dietary flavonol, flavone and catechin intake with colorectal cancer endpoints. Dietary catechin intake may be associated with a decreased rectal cancer risk in overweight men. Dietary flavonol and catechin intake may be associated with a decreased colorectal cancer risk in normal weight women. ' UICCKey words: cohort studies; flavonoids; colonic neoplasms; rectal neoplasms Colorectal cancer is one of the most common forms of cancer in the Western world. Most colorectal cancers occur as sporadic (i.e., nonhereditary) forms for which main risk factors lie in diet and lifestyle. 1 The modifiable potential of dietary and lifestyle factors offers opportunities for prevention.Flavonoids are polyphenolic compounds present in foods and beverages from plant origin that are thought to possibly protect against cancer. In cell line and animal studies, flavonoids were shown to have an antioxidant effect, to interfere with or eliminate carcinogens, to inhibit cell proliferation, to induce apoptosis and to inhibit angiogenesis. 2,3 Specific to colorectal carcinogenesis, such findings are still accumulating. [4][5][6][7] Whether dietary intake of flavonoids is protective against colorectal cancer in humans cannot be easily extrapolated from cell line and animal findings. In this perspective, epidemiologic studies on the association of flavonoid intake with colorectal cancer risk are important, yet to date these have been limited. Those studies on flavonoid intake and colorectal cancer risk that were conducted yielded inconsistent results. [8][9][10][11][12][13][14][15][16][17] The most studied flavonoid subgroups are flavonols, flavones and catechins (also known...

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Proteome response in HT‐29 human colorectal cancer cells to two apoptosis‐inducing compounds with different mode of action

Cited by 10 publications

References 40 publications

Alterations in hepatic one-carbon metabolism and related pathways following a high-fat dietary intervention

Alterations in hepatic one-carbon metabolism and related pathways following a high-fat dietary intervention

Effects of the microtubule stabilizing agent peloruside A on the proteome of HL-60 cells

Dietary flavonol, flavone and catechin intake and risk of colorectal cancer in the Netherlands Cohort Study

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