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Updated: May 17, 2026
The Influence of Liver Resection on Intrahepatic Tumor Growth
Published on: April 9, 2016
Ottelione A inhibited proliferation of Ehrlich ascites carcinoma cells in mice
M A El-Missiry1, A I Othman, M A Amer
1Zoology Department, Faculty of Science, Mansoura University, Egypt. maelmissiry@yahoo.com
Abstract:
While the main target of chemotherapy in cancer treatment is the induction of apoptosis and cell death, natural products provide a wealth to medicine and are considered great sources of new drugs for cancer treatment. We aimed to determine the antitumor effect of ottelione A (OTTE) on the growth and proliferation of Ehrlich ascites carcinoma cells (EACs) implanted i.p. in female mice. Animals were inoculated with EAC cells to serve as the control group. In the OTTE group, animals were implanted with EAC followed by i.p. administration of OTTE. Antitumor activity was evaluated 15days after tumor implantation. The administration of OTTE significantly reduced ascetic volume, viability of EAC cells and increased the survival of tumor-bearing animals. Flow cytometric analysis indicated that OTTE induced G(0)/G(1) cell cycle arrest and apoptosis. These findings were associated with an alteration of redox state of EAC cells, which might impact cascade effects leading to cell cycle arrest at G(0)/G(1) phase. These effects include a decreased expression of cyclin D1, increased p53 expression and down-regulation of rRNA level, stimulation of CD8+ infiltrating T-lymphocytes. In addition, OTTE normalized oxidative stress in the liver of mice-bearing EAC cells evidenced by increased the levels of glutathione, superoxide dismutase, and catalase. In conclusion, the differential expression of p53, cyclin D1, and rRNA in EAC cells as well as the infiltration of CD8+ after OTTE treatment may play critical roles in the G(0)/G(1) cell cycle arrest that blocks cell proliferation and induce apoptosis of cancer cells. The potent antitumor property of the ottelione A can be exploited further to develop therapeutic protocols for treatment of cancer.
Insights
Ottelione A (OTTE) exhibits potent antitumor effects against Ehrlich ascites carcinoma cells (EACs) in mice. This natural compound induces cancer cell cycle arrest and apoptosis, while also protecting the liver from oxidative stress.
Area of Science:
- Natural Product Chemistry
- Cancer Biology
- Immunology
Background:
- Natural products are vital sources for novel cancer therapeutics.
- Chemotherapy targets cancer cell death, but natural compounds offer alternative mechanisms.
- Ehrlich ascites carcinoma (EAC) is a model for studying antitumor agents.
Purpose of the Study:
- To evaluate the antitumor efficacy of ottelione A (OTTE) against EAC cells.
- To investigate the effects of OTTE on cancer cell proliferation, apoptosis, and host organ function.
- To elucidate the molecular mechanisms underlying OTTE's anticancer activity.
Main Methods:
- EAC cells were implanted intraperitoneally in female mice.
- Ottelione A was administered intraperitoneally to tumor-bearing mice.
- Antitumor activity was assessed by measuring tumor volume, cell viability, and animal survival.
- Flow cytometry was used to analyze cell cycle distribution and apoptosis.
- Molecular markers (p53, cyclin D1, rRNA) and immune cell infiltration (CD8+ T-lymphocytes) were evaluated.
- Liver oxidative stress markers (glutathione, SOD, catalase) were quantified.
Main Results:
- OTTE significantly reduced tumor volume and EAC cell viability.
- OTTE administration increased the survival rate of tumor-bearing mice.
- OTTE induced G(0)/G(1) cell cycle arrest and apoptosis in EAC cells.
- OTTE altered the redox state of EAC cells, decreasing cyclin D1 and increasing p53 expression.
- OTTE treatment stimulated CD8+ T-lymphocyte infiltration and normalized liver oxidative stress markers.
- OTTE treatment normalized liver oxidative stress by increasing glutathione, superoxide dismutase, and catalase levels.
Conclusions:
- Ottelione A demonstrates significant antitumor properties against EAC.
- OTTE-induced G(0)/G(1) cell cycle arrest and apoptosis are key mechanisms of its efficacy.
- Differential expression of p53, cyclin D1, and rRNA, along with CD8+ T-lymphocyte infiltration, contribute to OTTE's action.
- Ottelione A holds potential for developing new cancer therapeutic strategies.
