scholarly journals Pyruvate Treatment Restores the Effectiveness of Chemotherapeutic Agents in Human Colon Adenocarcinoma and Pleural Mesothelioma Cells

2018 ◽  
Vol 19 (11) ◽  
pp. 3550 ◽  
Author(s):  
Eleonora Mungo ◽  
Loredana Bergandi ◽  
Iris Salaroglio ◽  
Sophie Doublier
Keyword(s):  
Multidrug Resistance ◽  
Cancer Cells ◽  
Colon Adenocarcinoma ◽  
Glucose Consumption ◽  
Mitochondrial Respiratory Chain ◽  
Human Colon ◽  
Chemotherapeutic Agents ◽  
Cross Resistance ◽  
Ht29 Cells ◽  
Human Colon Adenocarcinoma

Emerging evidence supports the idea that a dysfunction in cell metabolism could sustain a resistant phenotype in cancer cells. As the success of chemotherapeutic agents is often questioned by the occurrence of multidrug resistance (MDR), a multiple cross-resistance towards different anti-cancer drugs represent a major obstacle to cancer treatment. The present study has clarified the involvement of the carbon metabolites in a more aggressive tumor colon adenocarcinoma phenotype and in a chemoresistant mesothelioma, and the role of pyruvate treatment in the reversion of the potentially related resistance. For the first time, we have shown that human colon adenocarcinoma cells (HT29) and its chemoresistant counterpart (HT29-dx) displayed different carbon metabolism: HT29-dx cells had a higher glucose consumption compared to HT29 cells, whereas human malignant mesothelioma (HMM) cells showed a lower glucose consumption compared to HT29 cells, accompanied by a lower pyruvate production and, consequently, a higher production of lactate. When treated with pyruvate, both HT29-dx and HMM cells exhibited a re-established accumulation of doxorubicin and a lower survival ability, a decreased activity of multidrug resistance protein 1 (MRP1) and a restored mitochondrial respiratory chain function, improving the effectiveness of the chemotherapeutic agents in these resistant cancer cells.

Stable differentiation of a human colon adenocarcinoma cell line by sodium butyrate is associated with multidrug resistance

1994 ◽  
Vol 160 (2) ◽  
pp. 213-226 ◽  
Author(s):  
Samuel B. Ho ◽  
Pei-Sha Yan ◽  
Rajvir Dahiya ◽  
Brent A. Neuschwander-Tetri ◽  
Carol Basbaum ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Cell Line ◽  
Sodium Butyrate ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Adenocarcinoma Cell Line ◽  
Adenocarcinoma Cell ◽  
Human Colon Adenocarcinoma

Induction of G2/M Arrest and Apoptosis by the Methanol Extract of Typha orientalis in Human Colon Adenocarcinoma HT29 Cells

2013 ◽  
Vol 41 (4) ◽  
pp. 425-432 ◽  
Author(s):  
Soojung Jin ◽  
Seung-Geun Yun ◽  
You Na Oh ◽  
Ji-Young Lee ◽  
Hyun-jin Park ◽  
...  
Keyword(s):  
Methanol Extract ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Ht29 Cells ◽  
Typha Orientalis ◽  
Human Colon Adenocarcinoma

scholarly journals Phosphofructokinase 2 and glycolysis in HT29 human colon adenocarcinoma cell line. Regulation by insulin and phorbol esters

1990 ◽  
Vol 268 (2) ◽  
pp. 465-470 ◽  
Author(s):  
C Denis-Pouxviel ◽  
T Gauthier ◽  
D Daviaud ◽  
J C Murat
Keyword(s):  
Phorbol Esters ◽  
Lactate Production ◽  
Colon Adenocarcinoma ◽  
Glucose Consumption ◽  
Human Colon ◽  
Kinetic Properties ◽  
Dependent Manner ◽  
Glycerol Phosphate ◽  
Ht29 Cells ◽  
Long Term Treatment

Kinetic properties of phosphofructokinase 2 (PFK2) and regulation of glycolysis by phorbol 12-myristate 13-acetate (PMA) and insulin were investigated in highly glycolytic HT29 colon cancer cells. PFK2 was found to be inhibited by citrate and, to a lesser extent, by phosphoenolpyruvate and ADP, but to be insensitive to inhibition by sn-glycerol phosphate. From these kinetic data, PFK2 from HT29 cells appears different from the liver form, but resembles somewhat the heart isoenzyme. Fructose 2,6-bisphosphate (Fru-2,6-P2) levels, glucose consumption and lactate production are increased in a dose-dependent manner in HT29 cells treated with PMA or insulin. The increase in Fru-2,6-P2 can be related to an increase in the Vmax. of PFK2, persisting after the enzyme has been precipitated with poly(ethylene glycol), without change in the Km for fructose 6-phosphate. The most striking effects of PMA and insulin on Fru-2,6-P2 production are observed after long-term treatment (24 h) and are abolished by actinomycin, cycloheximide and puromycin, suggesting that protein synthesis is involved. Furthermore, the effects of insulin and PMA on glucose consumption, lactate production, Fru-2,6-P2 levels and PFK2 activity are additive, and the effect of insulin on Fru-2,6-P2 production is not altered by pre-treatment of the cells with the phorbol ester. This suggests that these effects are exerted by separate mechanisms.

Epoxylathyrol Derivatives: Modulation of ABCB1-Mediated Multidrug Resistance in Human Colon Adenocarcinoma and Mouse T-Lymphoma Cells

2015 ◽  
Vol 78 (9) ◽  
pp. 2215-2228 ◽  
Author(s):  
Ana M. Matos ◽  
Mariana Reis ◽  
Noélia Duarte ◽  
Gabriella Spengler ◽  
Joseph Molnár ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Lymphoma Cells ◽  
T Lymphoma Cells ◽  
T Lymphoma ◽  
Human Colon Adenocarcinoma

scholarly journals Anti-oxidative and Anti-cancer Activities of Treculia africana Extract in Human Colon Adenocarcinoma HT29 Cells

2015 ◽  
Vol 25 (5) ◽  
pp. 515-522 ◽  
Author(s):  
You Na Oh ◽  
Soojung Jin ◽  
Hyun-jin Park ◽  
Byung Woo Kim ◽  
Hyun Ju Kwon
Keyword(s):  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Ht29 Cells ◽  
Anti Cancer ◽  
Treculia Africana ◽  
Human Colon Adenocarcinoma

scholarly journals STAT6 mRNA and protein knockdown using multiple siRNA sequences inhibits proliferation and induces apoptosis of the human colon adenocarcinoma cell line, HT-29

2018 ◽  
Author(s):  
C. Salguero-Aranda ◽  
D. Sancho-Mensat ◽  
S. Sultan ◽  
A. Reginald ◽  
L. Chapman
Keyword(s):  
Cancer Cells ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Colorectal Cancers ◽  
Colon Cancer Cells ◽  
Adenocarcinoma Cell Line ◽  
Adenocarcinoma Cell ◽  
Individual Sequences ◽  
Ht 29 ◽  
Human Colon Adenocarcinoma

AbstractThe transcription factor STAT6 is strongly expressed in various tumours and is most highly expressed in malignant lymphomas and pancreatic, colorectal, prostate and breast cancers. STAT6 expression in colorectal cancer is associated with an increased malignancy, poor prognosis and poor survival rates. Colorectal cancer has an incidence of approximately 1,361,000 patients per annum worldwide and approximately 60% of those cancers show STAT6 expression. Techniques aimed at reducing or blocking STAT6 expression may be useful in treating colorectal cancers. Celixir’s four proprietary STAT6 specific small interfering RNA (siRNA) sequences were tested in vitro using the human colon adenocarcinoma cell line, HT-29. The four sequences were introduced individually and in combination into HT-29 cells at different concentrations (10 to 200 nM). Decreases in STAT6 mRNA and protein levels were analysed to confirm the transfection was successful. STAT6 knockdown effects were measured by analysing cell proliferation and apoptosis. Results showed that 100nM siRNA concentration was the most effective and all four individual sequences knocked-down STAT6 mRNA and protein by more than 50%. Although all individual sequences were capable of significantly inhibiting cell proliferation, STAT6.1 and STAT6.4 were the best. STAT6 silencing also significantly induced late and total apoptotic events. In conclusion, these results demonstrate that STAT6 siRNA sequences are capable of inhibiting the proliferation, and inducing late apoptosis, of HT-29 colon cancer cells and, in some instances, halving the number of cancer cells. These experiments will be repeated using xenografts of STAT6-expressing colon cancer cells in immunocompromised mice and the STAT6 siRNA sequences will be tested in other cancers in which STAT6 is expressed. The STAT6 siRNA sequences therefore represent a potential treatment for the most serious colorectal cancers and a wide variety of STAT6-expressing cancers.

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