Hypoxia and antioxidant signaling in human colon carcinoma HCT116 cells exposed in vitro to 64-Cu

2021 ◽  
Author(s):  
Gina Manda ◽  
Dana Niculae ◽  
Ionela-Victoria Neagoe ◽  
Radu Serban ◽  
Dragos-Andrei Niculae ◽  
...  
Keyword(s):  
Colon Carcinoma ◽  
Human Colon ◽  
Human Colon Carcinoma ◽  
Hct116 Cells

The influence of extracts from Rubus caesius leaves on human colon carcinoma cells cultured in vitro

Planta Medica ◽  
2014 ◽  
Vol 80 (16) ◽  
Author(s):  
R Paduch ◽  
M Tomczyk ◽  
A Wiater ◽  
A Dudek ◽  
M Pleszczynska ◽  
...  
Keyword(s):  
Colon Carcinoma ◽  
Human Colon ◽  
Carcinoma Cells ◽  
Colon Carcinoma Cells ◽  
Human Colon Carcinoma ◽  
Cells Cultured

scholarly journals Curcumin Downregulates Human GM3 Synthase (hST3Gal V) Gene Expression with Autophagy Induction in Human Colon Carcinoma HCT116 Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Miri Lee ◽  
Hyunju Choi ◽  
Kyoung-Sook Kim ◽  
Dong-Hyun Kim ◽  
Cheorl-Ho Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colon Carcinoma ◽  
Human Colon ◽  
Luciferase Reporter ◽  
Gm3 Synthase ◽  
Human Colon Carcinoma ◽  
Autophagy Induction ◽  
Promoter Deletion Analysis ◽  
V Gene ◽  
Hct116 Cells

Our recent report showed that curcumin, polyphenolic compound isolated from the herb Curcuma longa, upregulated the gene expression of human GD3 synthase (hST8Sia I) responsible for ganglioside GD3 synthesis with autophagy induction in human lung adenocarcinoma A549 cells. In this study, on the contrary to this finding, we demonstrated that curcumin downregulated the gene expression of human GM3 synthase (hST3Gal V) catalyzing ganglioside GM3 synthesis with autophagy induction in human colon carcinoma HCT116 cells. To clarify the mechanism leading to the downregulation of hST3Gal V gene expression in curcumin-treated HCT116 cells, we analyzed the curcumin-inducible promoter of the hST3Gal V gene by luciferase reporter assays. Promoter deletion analysis demonstrated that the -177 to -83 region, which includes putative binding sites for transcription factors NFY, CREB/ATF, SP1, EGR3, and MZF1, acts as the curcumin-responsive promoter of the hST3Gal V gene. Site-directed mutagenesis and chromatin immunoprecipitation analysis demonstrated that the CREB/ATF binding site at -143 is pivotal for curcumin-induced downregulation of hST3Gal V gene in HCT116 cells. The transcriptional activation of hST3Gal V in HCT116 cells was significantly repressed by an inhibitor of AMP-activated protein kinase (AMPK). These results suggest that AMPK signal pathway mediates hST3Gal V gene expression in HCT116 cells.

Cytotoxicity of New Ferulic-Acid Derivatives on Human Colon Carcinoma (HCT116) Cells

2019 ◽  
Vol 53 (6) ◽  
pp. 516-520
Author(s):  
L. A. Bakholdina ◽  
A. A. Markova ◽  
A. I. Khlebnikov ◽  
V. P. Sevodin
Keyword(s):  
Ferulic Acid ◽  
Colon Carcinoma ◽  
Human Colon ◽  
Human Colon Carcinoma ◽  
Hct116 Cells

Sensitizing human colon carcinoma HT-29 cells to cisplatin by cyclopentenylcytosine, in vitro and in vivo

Life Sciences ◽  
2000 ◽  
Vol 68 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Kamran Gharehbaghi ◽  
Thomas Szekeres ◽  
Joel A. Yalowitz ◽  
Monika Fritzer-Szekeres ◽  
Yves G. Pommier ◽  
...  
Keyword(s):  
Colon Carcinoma ◽  
Human Colon ◽  
Human Colon Carcinoma ◽  
Ht 29

scholarly journals TGF-beta 1 is an autocrine-negative growth regulator of human colon carcinoma FET cells in vivo as revealed by transfection of an antisense expression vector.

1992 ◽  
Vol 116 (1) ◽  
pp. 187-196 ◽  
Author(s):  
S P Wu ◽  
D Theodorescu ◽  
R S Kerbel ◽  
J K Willson ◽  
K M Mulder ◽  
...  
Keyword(s):  
Cell Growth ◽  
Colon Carcinoma ◽  
Growth Regulator ◽  
Human Colon ◽  
Tgf Beta ◽  
Transfected Cells ◽  
Colon Carcinoma Cells ◽  
Human Colon Carcinoma

Transforming growth factor-beta 1 (TGF-beta 1) has previously been implicated as a potential negative autocrine or paracrine growth regulator of certain cell types (Arteaga, C. L., R. J. Coffey, Jr., T. C. Dugger, C. M. McCutchen, H. L. Moses, and R. M. Lyons. 1990. Cell Growth & Differ. 1:367-374; Hafez, M. M., D. Infante, S. Winawer, and E. Friedman. 1990. Cell Growth & Differ. 1:617-626; Glick, A. B., K. C. Flanders, D. Danielpour, S. H. Yuspa, and M. B. Sporn. 1989. Cell Regulation. 1:87-97). This is based mainly on experiments assessing the effects of exogenous TGF-beta 1 or neutralizing antibodies to TGF-beta 1 on normal or tumor cell proliferation in vitro. However, direct evidence demonstrating such a negative regulation of tumor cell growth in vivo is still lacking. To overcome this problem we have constructed and used an antisense expression vector for TGF-beta 1 as a means of regulating endogenous TGF-beta 1 expression in tumor cells. Antisense-transfected FET human colon carcinoma cells showed a fivefold reduction in TGF-beta 1 mRNA and 15-fold reduction in TGF-beta 1 secretion. Antisense mRNA was detected in transfected cells by an RNase protection assay. Compared to control cells, cultured antisense-transfected cells showed a reduction in lag phase time rather than a change in doubling time. Cloning efficiencies of transfected cells were four times greater than control cells in anchorage-independent assays. Control cells did not form tumors at 5 x 10(5) in athymic nude mice. Antisense-transfected cells formed tumors in 40% of animals injected. At higher inocula (1 x 10(6) cells) antisense-transfected cells formed tumors in 100% of animals injected, but control cells still failed to form tumors. These results show that TGF-beta 1 acts as a negative growth regulator of human colon carcinoma cells in vivo as well as in vitro. Acquisition of partial or full resistance to such inhibitory effects may therefore contribute to tumor development and progression.

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