scholarly journals Anticancer Effect of COX-2 Inhibitor DuP-697 Alone and in Combination with Tyrosine Kinase Inhibitor (E7080) on Colon Cancer Cell Lines

2014 ◽  
Vol 15 (7) ◽  
pp. 3113-3121 ◽  
Author(s):  
Ahmet Altun ◽  
Nergiz Hacer Turgut ◽  
Tijen Temiz Kaya
Keyword(s):  
Colon Cancer ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Cell Lines ◽  
Cancer Cell ◽  
Kinase Inhibitor ◽  
Colon Cancer Cell ◽  
Anticancer Effect ◽  
Colon Cancer Cell Lines ◽  
Cox 2

scholarly journals G-749 Promotes Receptor Tyrosine Kinase TYRO3 Degradation and Induces Apoptosis in Both Colon Cancer Cell Lines and Xenograft Mouse Models

2021 ◽  
Vol 12 ◽  
Author(s):  
Hae Dong Kim ◽  
Eun Jung Park ◽  
Eun Kyoung Choi ◽  
Seuk Young Song ◽  
Kwang-Lae Hoe ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Tyrosine Kinase ◽  
Mouse Models ◽  
Cell Lines ◽  
Cancer Cell ◽  
Receptor Tyrosine Kinase ◽  
Kinase Inhibitors ◽  
Kinase Inhibitor ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines

G-749 is an FLT3 kinase inhibitor that was originally developed as a treatment for acute myeloid leukemia. Some FLT3 kinase inhibitors are dual kinase inhibitors that inhibit the TAM (Tyro3, Axl, Mer) receptor tyrosine kinase family and are used to treat solid cancers such as non-small cell lung cancer (NSCLC) and triple-negative breast cancer (TNBC). AXL promotes metastasis, suppression of immune response, and drug resistance in NSCLC and TNBC. G-749, a potential TAM receptor tyrosine kinase inhibitor, and its derivative SKI-G-801, effectively inhibits the phosphorylation of AXL at nanomolar concentration (IC50 = 20 nM). This study aimed to investigate the anticancer effects of G-749 targeting the TAM receptor tyrosine kinase in colon cancer. Here, we demonstrate the potential of G-749 to effectively inhibit tumorigenesis by degrading TYRO3 via regulated intramembrane proteolysis both in vitro and in vivo. In addition, we demonstrated that G-749 inhibits the signaling pathway associated with cell proliferation in colon cancer cell lines HCT15 and SW620, as well as tumor xenograft mouse models. We propose G-749 as a new therapeutic agent for the treatment of colon cancer caused by abnormal TYRO3 expression or activity.

Folic acid inhibition of EGFR-mediated proliferation in human colon cancer cell lines

1999 ◽  
Vol 277 (6) ◽  
pp. C1142-C1148 ◽  
Author(s):  
Richard Jaszewski ◽  
Ahmed Khan ◽  
Fazlul H. Sarkar ◽  
Omer Kucuk ◽  
Martin Tobi ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Folic Acid ◽  
Tyrosine Kinase ◽  
Cell Lines ◽  
Cancer Cell ◽  
Kinase Activity ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines ◽  
Hct 116

Although accumulating evidence suggests a chemopreventive role for folic acid in colon cancer, the regulation of this process in unknown. We hypothesize that supplemental folic acid exerts its chemopreventive role by inhibiting mucosal hyperproliferation, an event considered to be central to the initiation of carcinogenesis in the gastrointestinal tract. The present investigation examines the effect of supplemental folic acid on proliferation of Caco-2 and HCT-116 colon cancer cell lines. Furthermore, because certain tyrosine kinases, particularly epidermal growth factor receptor (EGFR), play a role in regulating cell proliferation, we also examined the folic acid-induced changes in tyrosine kinase activity and expression of EGFR. In Caco-2 and HCT-116 cells, maintained in RPMI 1640 medium containing 1 μg/ml folic acid, we observed that the supplemental folic acid inhibited proliferation in a dose-dependent manner. Pretreatment of HCT-116 and Caco-2 cell lines with supplemental folic acid (1.25 μg/ml) completely abrogated transforming growth factor-α (TGF-α)-induced proliferation in both cell lines. Tyrosine kinase activity and the relative concentration of EGFR were markedly diminished in both cell lines following a 24-h exposure to supplemental folic acid. The folic acid-induced inhibition of EGFR tyrosine kinase activity in colon cancer cell lines was also associated with a concomitant reduction in the relative concentration of the 14-kDa membrane-bound precursor form of TGF-α. In conclusion, our data suggest that supplemental folic acid is effective in reducing proliferation in two unrelated colon cancer cell lines and that EGFR tyrosine kinase appears to be involved in regulating this process.

scholarly journals Celecoxib increases retinoid sensitivity in human colon cancer cell lines

2010 ◽  
Vol 15 (3) ◽  
Author(s):  
Jian-Pei Liu ◽  
Hong-Bo Wei ◽  
Zong-Heng Zheng ◽  
Wei-Ping Guo ◽  
Jia-Feng Fang
Keyword(s):  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Human Colon Cancer Cell ◽  
Human Colon Cancer ◽  
Colon Cancer Cell Lines ◽  
Cox 2 ◽  
Ht 29

AbstractRetinoid resistance has limited the clinical application of retinoids as differentiation-inducing and apoptosis-inducing drugs. This study was designed to investigate whether celecoxib, a selective COX-2 inhibitor, has effects on retinoid sensitivity in human colon cancer cell lines, and to determine the possible mechanism of said effects. Cell viability was measured using the MTT assay. Apoptosis was detected via Annexin-V/PI staining and the flow cytometry assay. PGE2 production was measured with the ELISA assay. The expression of RARβ was assayed via western blotting. The results showed that celecoxib enhanced the inhibitory effect of ATRA in both COX-2 high-expressing HT-29 and COX-2 low-expressing SW480 cell lines. Further study showed the ATRA and celecoxib combination induced greater apoptosis, but that the addition of PGE2 did not affect the enhanced growth-inhibitory and apoptosis-inducing effects of the combination. Moreover, NS398 (another selective COX-2 inhibitor) did not affect the inhibitory effects of ATRA in the two cell lines. Western blotting showed that the expression of RARβ in HT-29 cell lines was increased by celecoxib, but not by NS398, and that the addition of PGE2 did not affect the celecoxib-induced expression of the retinoic acid receptor beta. In conclusion, celecoxib increased the expression of RARβ and the level of cellular ATRA sensitivity through COX-2-independent mechanisms. This finding may provide a potential strategy for combination therapy.

Valdecoxib recovers the lipid composition, order and dynamics in colon cancer cell lines independent of COX-2 expression

2017 ◽  
Vol 280 ◽  
pp. S224
Author(s):  
Aysun Inan Genç ◽  
Seher Gok ◽  
Sreeparna Banerjee ◽  
Feride Severcan
Keyword(s):  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Lipid Composition ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines ◽  
Cox 2

scholarly journals Anticancer effect of SN-38 on colon cancer cell lines with different metastatic potential

2008 ◽  
Author(s):  
Xiao-Feng Sun ◽  
Lillianne Ferreud ◽  
Joar Svanvik ◽  
Birgitta Holmlund ◽  
Åsa Wallin
Keyword(s):  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Metastatic Potential ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Anticancer Effect ◽  
Colon Cancer Cell Lines

Valdecoxib Recovers the Lipid Composition, Order and Dynamics in Colon Cancer Cell Lines Independent of COX-2 Expression: An ATR-FTIR Spectroscopy Study

2016 ◽  
Vol 71 (1) ◽  
pp. 105-117 ◽  
Author(s):  
Aysun Inan Genç ◽  
Seher Gok ◽  
Sreeparna Banerjee ◽  
Feride Severcan
Keyword(s):  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Attenuated Total Reflection ◽  
Therapeutic Effects ◽  
Aberrant Expression ◽  
Colon Cancer Cell Lines ◽  
Cox 2

Prostanoids play an important role in a variety of physiological and pathophysiological processes including inflammation and cancer. The rate-limiting step in the prostanoid biosynthesis pathway is catalyzed by cyclooxygenases (COXs). Aberrant expression of the inducible isoform COX-2 plays a significant role in colon cancer initiation and progression. In this study, we have hypothesized that COX-2 specific inhibitors such as Valdecoxib (VLX), being highly hydrophobic, may alter biophysical properties of cellular lipids. In this study, COX-2 expressing (HT29) and COX-2 non-expressing (SW620) colon cancer cell lines were treated with VLX and examined using attenuated total reflection infrared spectroscopy. The results revealed that VLX treatment decreased lipid fluidity in the cells irrespective of COX-2 expression status and affected order parameters of the lipids in both cell lines. Cluster analysis also indicated that the spectral differences between the two cell lines are profound and could be successfully differentiated. Valdecoxib treatment could enhance the composition, order and dynamics of the lipids of colon cancer cells independently of its COX-2 inhibitory mechanism. Valdecoxib has therapeutic effects upon colon cancer, therefore it can be used as an adjuvant and/or chemopreventive agent for colon cancer.

scholarly journals Selenomethionine Inhibits Growth and Suppresses Cyclooxygenase-2 (COX-2) Protein Expression in Human Colon Cancer Cell Lines

2002 ◽  
Vol 1 (4) ◽  
pp. 369-373 ◽  
Author(s):  
Antonio Baines ◽  
Michele Taylor-Parker ◽  
Anne-Christine Christian Renaud ◽  
Eugene W. Gerner ◽  
Mark A. Nelson
Keyword(s):  
Colon Cancer ◽  
Protein Expression ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Human Colon Cancer Cell ◽  
Human Colon Cancer ◽  
Colon Cancer Cell Lines ◽  
Cox 2
Sign in / Sign up

Export Citation Format

Share Document