scholarly journals Protective role of p21(Waf1/Cip1) against prostaglandin A2-mediated apoptosis of human colorectal carcinoma cells.

1996 ◽  
Vol 16 (12) ◽  
pp. 6654-6660 ◽  
Author(s):  
M Gorospe ◽  
X Wang ◽  
K Z Guyton ◽  
N J Holbrook
Keyword(s):  
Cell Death ◽  
Colorectal Carcinoma ◽  
Expression System ◽  
Ectopic Expression ◽  
Growth Arrest ◽  
Protective Role ◽  
Cellular Growth ◽  
Human Colorectal Carcinoma ◽  
P21 Waf1 ◽  
Prostaglandin A2

Prostaglandin A2 (PGA2) suppresses tumor growth in vivo, is potently antiproliferative in vitro, and is a model drug for the study of the mammalian stress response. Our previous studies using breast carcinoma MCF-7 cells suggested that p21(Waf1/Cip1) induction enabled cells to survive PGA2 exposure. Indeed, the marked sensitivity of human colorectal carcinoma RKO cells to the cytotoxicity of PGA2 is known to be associated with a lack of a PGA2-mediated increase in p21(Waf1/Cip1) expression, inhibition of cyclin-dependent kinase activity, and growth arrest. To determine if cell death following exposure to PGA2 could be prevented by forcing the expression of p21(Waf1/Cip1) in RKO cells, we utilized an adenoviral vector-based expression system. We demonstrate that ectopic expression of p21(Waf1/Cip1) largely rescued RKO cells from PGA2-induced apoptotic cell death, directly implicating p21(Waf1/Cip1) as a determinant of the cellular outcome (survival versus death) following exposure to PGA2. To discern whether p21(Waf1/Cip1)-mediated protection operates through the implementation of cellular growth arrest, other growth-inhibitory treatments were studied for the ability to attenuate PGA2-induced cell death. Neither serum depletion nor suramin (a growth factor receptor antagonist) protected RKO cells against PGA2 cytotoxicity, and neither induced p21(Waf1/Cip1) expression. Mimosine, however, enhanced p21(Waf1/Cip1) expression, completely inhibited RKO cell proliferation, and exerted marked protection against a subsequent PGA2 challenge. Taken together, our results directly demonstrate a protective role for p21(Waf1/Cip1) during PGA2 cellular stress and provide strong evidence that the implementation of cellular growth arrest contributes to this protective influence.

scholarly journals Fluorescent magnetic submicronic polymer (FMSP) nanoparticles induce cell death in human colorectal carcinoma cells

2018 ◽  
Vol 46 (sup3) ◽  
pp. S247-S253 ◽  
Author(s):  
Firdos Alam Khan ◽  
Sultan Akhtar ◽  
Dana Almohazey ◽  
Munthar Alomari ◽  
Sarah Ameen Almofty ◽  
...  
Keyword(s):  
Cell Death ◽  
Colorectal Carcinoma ◽  
Carcinoma Cells ◽  
Induce Cell Death ◽  
Human Colorectal Carcinoma

scholarly journals Blockade of irradiation-induced autophagosome formation impairs proliferation but does not enhance cell death in HCT-116 human colorectal carcinoma cells

2012 ◽  
Vol 40 (4) ◽  
pp. 1267-1276 ◽  
Author(s):  
ANA CRISTINA DE ALBUQUERQUE-XAVIER ◽  
LILIAN GONÇALVES R. BASTOS ◽  
JULIO CESAR MADUREIRA DE FREITAS ◽  
FERNANDA LEVE ◽  
WALDEMIR FERNÁNDEZ DE SOUZA ◽  
...  
Keyword(s):  
Cell Death ◽  
Colorectal Carcinoma ◽  
Carcinoma Cells ◽  
Autophagosome Formation ◽  
Hct 116 ◽  
Human Colorectal Carcinoma

scholarly journals Ectopic Expression of a Self-Incompatibility Module Triggers Growth Arrest and Cell Death in Vegetative Cells

2020 ◽  
Vol 183 (4) ◽  
pp. 1765-1779 ◽  
Author(s):  
Zongcheng Lin ◽  
Fei Xie ◽  
Marina Triviño ◽  
Mansour Karimi ◽  
Maurice Bosch ◽  
...  
Keyword(s):  
Cell Death ◽  
Ectopic Expression ◽  
Growth Arrest ◽  
Self Incompatibility ◽  
Vegetative Cells

scholarly journals Molecular mechanisms responsible for programmed cell death-inducing attributes of terpenes from Mesua ferrea stem bark towards human colorectal carcinoma HCT 116 cells

2017 ◽  
Vol 15 (1) ◽  
pp. 71-80 ◽  
Author(s):  
Muhammad Asif ◽  
Majed Ahmed Al-Mansoub ◽  
Shamsuddin Sultan Khan ◽  
Ashwaq Hamid Salem Yehya ◽  
Mohammed Oday Ezzat ◽  
...  
Keyword(s):  
Cell Death ◽  
Colorectal Carcinoma ◽  
Programmed Cell Death ◽  
Molecular Mechanisms ◽  
Stem Bark ◽  
Hct 116 ◽  
Human Colorectal Carcinoma ◽  
Hct 116 Cells

scholarly journals Palbociclib Induces Senescence in Melanoma and Breast Cancer Cells and Leads to Additive Growth Arrest in Combination With Irradiation

2021 ◽  
Vol 11 ◽  
Author(s):  
Tina Jost ◽  
Lucie Heinzerling ◽  
Rainer Fietkau ◽  
Markus Hecht ◽  
Luitpold V. Distel
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Growth Arrest ◽  
Melanoma Cells ◽  
Cellular Growth ◽  
Cycle Arrest ◽  
Wide Range

IntroductionSeveral kinase inhibitors (KI) bear the potential to act as radiosensitizers. Little is known of the radiosensitizing effects of a wide range of other KI like palbociclib, which is approved in ER+/HER2- metastatic breast cancer.MethodIn our study, we used healthy donor fibroblasts and breast cancer and skin cancer cells to investigate the influence of a concomitant KI + radiation therapy. Cell death and cell cycle distribution were studied by flow cytometry after Annexin-V/7-AAD and Hoechst staining. Cellular growth arrest was studied in colony-forming assays. Furthermore, we used C12-FDG staining (senescence) and mRNA expression analysis (qPCR) to clarify cellular mechanisms.ResultsThe CDK4/6 inhibitor palbociclib induced a cell cycle arrest in the G0/G1 phase. Cellular toxicity (cell death) was only slightly increased by palbociclib and not enhanced by additional radiotherapy. As the main outcome of the colony formation assays, we found that cellular growth arrest was induced by palbociclib and improved by radiotherapy in an additive manner. Noticeably, palbociclib treatment clearly induced senescence not only in breast cancer and partly in melanoma cells, but also in healthy fibroblasts. According to these findings, the downregulation of senescence-related FOXM1 might be an involved mechanism of the senescence-induction potential of palbociclib.ConclusionThe effect on cellular growth arrest of palbociclib and radiotherapy is additive. Palbociclib induces permanent G0/G1 cell cycle arrest by inducing senescence in fibroblasts, breast cancer, and melanoma cells. Direct cell death induction is only a minor secondary mechanism of action. Concomitant KI and radiotherapy is a strategy worth studying in clinical trials.

miR-297 modulates multidrug resistance in human colorectal carcinoma by down-regulating MRP-2

2012 ◽  
Vol 446 (2) ◽  
pp. 291-300 ◽  
Author(s):  
Ke Xu ◽  
Xin Liang ◽  
Ke Shen ◽  
Daling Cui ◽  
Yuanhong Zheng ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Colorectal Carcinoma ◽  
Cell Line ◽  
Ectopic Expression ◽  
Carcinoma Cells ◽  
Transcriptional Level ◽  
Parent Cell ◽  
Platinum Drug ◽  
Expression Levels ◽  
Human Colorectal Carcinoma

Colorectal carcinoma is a frequent cause of cancer-related death in men and women. miRNAs (microRNAs) are endogenous small non-coding RNAs that regulate gene expression negatively at the post-transcriptional level. In the present study we investigated the possible role of microRNAs in the development of MDR (multidrug resistance) in colorectal carcinoma cells. We analysed miRNA expression levels between MDR colorectal carcinoma cell line HCT116/L-OHP cells and their parent cell line HCT116 using a miRNA microarray. miR-297 showed lower expression in HCT116/L-OHP cells compared with its parental cells. MRP-2 (MDR-associated protein 2) is an important MDR protein in platinum-drug-resistance cells and is a predicted target of miR-297. Additionally miR-297 was down-regulated in a panel of human colorectal carcinoma tissues and negatively correlated with expression levels of MRP-2. Furthermore, we found that ectopic expression of miR-297 in MDR colorectal carcinoma cells reduced MRP-2 protein level and sensitized these cells to anti-cancer drugs in vitro and in vivo. Taken together, our findings suggest that miR-297 could play a role in the development of MDR in colorectal carcinoma cells, at least in part by modulation of MRP-2.

scholarly journals p21/WAF1 expression in human colorectal carcinoma: association with p53, transcription factor AP-2 and prognosis

1999 ◽  
Vol 81 (1) ◽  
pp. 133-140 ◽  
Author(s):  
K M Ropponen ◽  
J K Kellokoski ◽  
P K Lipponen ◽  
T Pietiläinen ◽  
M J Eskelinen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Colorectal Carcinoma ◽  
Human Colorectal Carcinoma ◽  
P21 Waf1
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