In vitro differentiation of HT-29 M6 mucus-secreting colon cancer cells involves a trychostatin A and p27KIP1-inducible transcriptional program of gene expression

2007 ◽  
Vol 212 (1) ◽  
pp. 42-50 ◽  
Author(s):  
Clara Mayo ◽  
Josep Lloreta ◽  
Francisco X. Real ◽  
Xavier Mayol
2016 ◽  
Vol 65 (31) ◽  
pp. 6477-6487 ◽  
Author(s):  
María-Carmen López de las Hazas ◽  
Juana I. Mosele ◽  
Alba Macià ◽  
Iziar A. Ludwig ◽  
María-José Motilva

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Fatemeh Abedi ◽  
Soodabeh Davaran ◽  
Malak Hekmati ◽  
Abolfazl Akbarzadeh ◽  
Behzad Baradaran ◽  
...  

AbstractThe combination therapy which has been proposed as the strategy for the cancer treatment could achieve a synergistic effect for cancer therapies and reduce the dosage of the applied drugs. On account of the the unique properties as the high absorbed water content, biocompatibility, and flexibility, the targeting nanogels have been considred as a suitable platform. Herein, a non-toxic pH/thermo-responsive hydrogel P(NIPAAm-co-DMAEMA) was synthesized and characterized through the free-radical polymerization and expanded upon an easy process for the preparation of the smart responsive nanogels; that is, the nanogels were used for the efficient and controlled delivery of the anti-cancer drug doxorubicin (DOX) and chemosensitizer curcumin (CUR) simultaneously like a promising strategy for the cancer treatment. The size of the nanogels, which were made, was about 70 nm which is relatively optimal for the enhanced permeability and retention (EPR) effects. The DOX and CUR co-loaded nanocarriers were prepared by the high encapsulation efficiency (EE). It is important to mention that the controlled drug release behavior of the nanocarriers was also investigated. An enhanced ability of DOX and CUR-loaded nanoformulation to induce the cell apoptosis in the HT-29 colon cancer cells which represented the greater antitumor efficacy than the single-drug formulations or free drugs was resulted through the In vitro cytotoxicity. Overall, according to the data, the simultaneous delivery of the dual drugs through the fabricated nanogels could synergistically potentiate the antitumor effects on the colon cancer (CC).


2017 ◽  
Vol 39 (1) ◽  
pp. 17-24
Author(s):  
N Bezdieniezhnykh ◽  
O Kovalova ◽  
O Lykhova ◽  
R Kocherga ◽  
A Vorontsova ◽  
...  

Objective: To estimate the impact of the low-dose anticancer drugs (ACD) with the different mechanisms of action and human interferon (IFN) alpha 2b on the biological properties, immunophenotypic and cytogenetic characteristics of colon cancer cells in vitro. Materials and Methods: The study was performed on human colon cancer cell lines COLO 205, HT-29 and 3C-P treated with ACD and IFN in subtoxic concentrations. Expression of CD44, N-cadherin, vimentin, β-catenin, ERCC1 and Slug was assessed by immunocytochemical method. Using cytogenetic analysis, the numbers of mitoses, cells with micronuclei, apoptotic cells and cells with nuclear protrusions were studied. Results: The prolonged exposure (up to 30 days) of colon cancer cells to low-dose ACD (0.2–0.5 µg/ml cisplatin and 0.1–0.2 µg/ml irinotecan) in combination with IFN (500–1000 IU/ml) led to 37-fold decreased colony-forming activity of these cell and 10-fold reduction of the number of cells expressing mesenchymal protein markers (N-cadherin, vimentin). Also, in COLO 205 cells treated with ACD and IFN the number of SLUG- and CD44-positive cells decreased by 92 and by 85%, respectively. Long-term cultivation of HT-29 cells in the presence of cisplatin and IFN resulted in 5-fold suppression of ERCC1 expression. The cytogenetic analysis has shown that the ACD, IFN and their combinations in subtoxic concentrations caused significant genotoxic effect, suppression of cell proliferation and accumulation of cells with micronuclei. The sensitivity of colon cancer cells to ACD in standard cytotoxic concentrations did not change after prolonged low-dose exposure. Conclusion: The data showed that the prolonged action of the low doses of ACD on human colon cancer cells resulted in the suppression of cell proliferation, colony-forming activity in soft agar, expression of epithelialmesenchymal transition-associated markers and significant cytogenetic changes.


2011 ◽  
Vol 301 (2) ◽  
pp. G347-G355 ◽  
Author(s):  
Phil-Sun Oh ◽  
Vaishali B. Patel ◽  
Matthew A. Sanders ◽  
Shailender S. Kanwar ◽  
Yingjie Yu ◽  
...  

We have previously demonstrated that expression of the novel gene schlafen-3 (Slfn-3) correlates with intestinal epithelial cell differentiation (Patel VB, Yu Y, Das JK, Patel BB, Majumdar AP. Biochem Biophys Res Commun 388: 752–756, 2009). The present investigation was undertaken to examine whether Slfn-3 plays a role in regulating differentiation of FOLFOX-resistant (5-fluorouracil + oxaliplatin) colon cancer cells that are highly enriched in cancer stem cells (CSCs). Transfection of Slfn-3 in FOLFOX-resistant colon cancer HCT-116 cells resulted in increase of alkaline phosphatase activity, a marker of intestinal differentiation. Additionally, Slfn-3 transfection resulted in reduction of mRNA and protein levels of the CSC markers CD44, CD133, CD166, and aldehyde dehydrogenase 1 in both FOLFOX-resistant HCT-116 and HT-29 cells. This was accompanied by decreased formation of tumorosphere/colonosphere (an in vitro model of tumor growth) in stem cell medium and inhibition of expression of the chemotherapeutic drug transporter protein ABCG2. Additionally, Slfn-3 transfection of FOLFOX-resistant HCT-116 and HT-29 cells reduced Hoechst 33342 dye exclusion. Finally, Slfn-3 transfection inhibited the expression of transforming growth factor-α in both FOLFOX-resistant colon cancer cells, but stimulated apoptosis in response to additional FOLFOX treatment. In summary, our data demonstrate that Slfn-3 expression inhibits multiple characteristics of CSC-enriched, FOLFOX-resistant colon cancer cells, including induction of differentiation and reduction in tumorosphere/colonosphere formation, drug transporter activity, and autocrine stimulation of proliferation. Thus Slfn-3 expression may render colon CSCs more susceptible to cancer chemotherapeutics.


2020 ◽  
Vol 17 (3) ◽  
pp. 427-433
Author(s):  
Le Nhat Minh ◽  
Vo Trong Nhan ◽  
Nguyen Thi Nga ◽  
Tran Thu Huong ◽  
Phung Thi Kim Hue ◽  
...  

Nanotechnology is the key technology that brings many important applications in biomedical research.Nanolantanites present high stability, easy fabrication and functionalization. Tb3+ ion-containing nanomaterial, a specific type of nanolantanites, possess great prospects. In addition, cancer stem cells (CSCs) are directlyrelated to drug resistance, metastasis, recurrent cancer, etc. Therefore, CSCs are considered as the target forcancer researching and for discovery of more effective therapies. CD133, a trans-membrane glycoprotein, isone of the typical markers that are found to appear very commonly on the surface of many types of CSCs. Inthis study, CD133 monoclonal antibody (MAb) was cojugated with nanomaterials containing Tb3+. Thecoupling between fluorescented nanomaterials containing Tb3+ ions and CD133 MAb was then incubated withhuman colon cancer cells (HT-29) to evaluate its ability to label CSCs in vitro. The results showed thatnanorods containing rare-earth based Tb3+ ions which were fabricated by hydrothermal method, present thelength of about 300 - 800 nm and the diameter in range of 40 - 50 nm. The Tb3+ nanoparticals also havehexagonal structure of terbium phosphate monohydrate and green illuminant. Tb3+ nanorods were also furthersurface silica coated and amino-silane functionalized. This nanostructure was successfully combined withmonoclonal antibodies against CD133 which labelled the surface marker of HT-29 human colon cancer cells.As a result, the combination of CD133+TbPO4@Silica-NH2 (functionalized surface) showed strongerluminescence than the CD133+TbPO4 unfunctionalized combination.


RSC Advances ◽  
2016 ◽  
Vol 6 (74) ◽  
pp. 70099-70105 ◽  
Author(s):  
Xiaohui Zhang ◽  
Depeng Li ◽  
Jianzhong Qin ◽  
Yaozhong Xu ◽  
Kedong Ma

Antiproliferative effect of 4-thio-5-(2′′-thienyl)uridine on MC-38 cells, HT-29 cells and normal human fibroblasts cells.


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