2013Chinese Clinical OncologyRequires access

A experimental study of recombined human endostatin in combination with paclitaxel inducing apoptosis of esophageal cancer cell line Eca-109

Liu Yuan-yua

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Abstract

Objective To investigate the combining effect of the recombined human endostatin(endostar) and paclitaxel on the proliferation and apoptosis of human esophageal carcinoma Eca-109 cells. Methods MTT was used for detecting inhibitory rates of different concentrations of endostar and paclitaxel of monotherapy and combination therapy on the Eca-109 cells at 48h;the shape changes of those cells were observed under the optical microscope; flow cytometry method was used for the detection of apoptosis rates of different groups after stained with Annexin V/PI at 48h;RT-PCR was used to detect the different expression of mRNA for apoptosis related genes(Bcl-2, Bax, p21 and p53) among different groups at 48h. Results The half inhibitory concentration (IC50) at 48h of endostar and paclitaxel on the Eca-109 cells were 276.6627μg/ml and 3.8789μg/ml. Inhibition rates of the endostar group,paclitaxel group, the concurrently medicated group, the endostar followed by paclitaxel group and the paclitaxel followed by endostar group were (33.62±2.30)%, (49.14±1.45)%, (56.29±0.71)%, (41.88±1.23)% and (51.48±0.98)%. The cell inhibition rate of endostar and paclitaxel medicating concurrently was higher than other groups(P0.05). Under optical microscope, those medicated cells had typical apoptotic morphological changes. The apoptosis rates of endostar group, paclitaxel group, the concurrent group, endostar followed by paclitaxel group and the paclitaxel followed by endostar group were (8.78±0.19)%, (13.82±0.15)%, (18.88±0.29)%, (11.37±0.24)% and (14.88±0.34)%,respectively. The differences among the groups and compared with the negative control group were all statistically significant(P0.05). Compared with the control group,the endostar group and two sequential groups significantly decreased mRNA expression of Bcl-2,and the paclitaxel group also reduced the mRNA expression of Bcl-2. The three ways of drug combination all presented a decreasing mRNA expression of Bax. Every group could decrease the expression of p21. Sequential medication groups reduced the expression of p53. Conclusion Endostar in combination with paclitaxel can synergisticly induce apoptosis of the human esophageal carcinoma cell, and the mechanism may be related to the reduced expressions of antiapoptosis genes.

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Objective To investigate the combining effect of the recombined human endostatin(endostar) and paclitaxel on the proliferation and apoptosis of human esophageal carcinoma Eca-109 cells. Methods MTT was used for detecting inhibitory rates of different concentrations of endostar and paclitaxel of monotherapy and combination therapy on the Eca-109 cells at 48h;the shape changes of those cells were observed under the optical microscope; flow cytometry method was used for the detection of apoptosis rates of different groups after stained with Annexin V/PI at 48h;RT-PCR was used to detect the different expression of mRNA for apoptosis related genes(Bcl-2, Bax, p21 and p53) among different groups at 48h. Results The half inhibitory concentration (IC50) at 48h of endostar and paclitaxel on the Eca-109 cells were 276.6627μg/ml and 3.8789μg/ml. Inhibition rates of the endostar group,paclitaxel group, the concurrently medicated group, the endostar followed by paclitaxel group and the paclitaxel followed by endostar group were (33.62±2.30)%, (49.14±1.45)%, (56.29±0.71)%, (41.88±1.23)% and (51.48±0.98)%. The cell inhibition rate of endostar and paclitaxel medicating concurrently was higher than other groups(P0.05). Under optical microscope, those medicated cells had typical apoptotic morphological changes. The apoptosis rates of endostar group, paclitaxel group, the concurrent group, endostar followed by paclitaxel group and the paclitaxel followed by endostar group were (8.78±0.19)%, (13.82±0.15)%, (18.88±0.29)%, (11.37±0.24)% and (14.88±0.34)%,respectively. The differences among the groups and compared with the negative control group were all statistically significant(P0.05). Compared with the control group,the endostar group and two sequential groups significantly decreased mRNA expression of Bcl-2,and the paclitaxel group also reduced the mRNA expression of Bcl-2. The three ways of drug combination all presented a decreasing mRNA expression of Bax. Every group could decrease the expression of p21. Sequential medication groups reduced the expression of p53. Conclusion Endostar in combination with paclitaxel can synergisticly induce apoptosis of the human esophageal carcinoma cell, and the mechanism may be related to the reduced expressions of antiapoptosis genes.

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Available abstract

Objective To investigate the combining effect of the recombined human endostatin(endostar) and paclitaxel on the proliferation and apoptosis of human esophageal carcinoma Eca-109 cells. Methods MTT was used for detecting inhibitory rates of different concentrations of endostar and paclitaxel of monotherapy and combination therapy on the Eca-109 cells at 48h;the shape changes of those cells were observed under the optical microscope; flow cytometry method was used for the detection of apoptosis rates of different groups after stained with Annexin V/PI at 48h;RT-PCR was used to detect the different expression of mRNA for apoptosis related genes(Bcl-2, Bax, p21 and p53) among different groups at 48h. Results The half inhibitory concentration (IC50) at 48h of endostar and paclitaxel on the Eca-109 cells were 276.6627μg/ml and 3.8789μg/ml. Inhibition rates of the endostar group,paclitaxel group, the concurrently medicated group, the endostar followed by paclitaxel group and the paclitaxel followed by endostar group were (33.62±2.30)%, (49.14±1.45)%, (56.29±0.71)%, (41.88±1.23)% and (51.48±0.98)%. The cell inhibition rate of endostar and paclitaxel medicating concurrently was higher than other groups(P0.05). Under optical microscope, those medicated cells had typical apoptotic morphological changes. The apoptosis rates of endostar group, paclitaxel group, the concurrent group, endostar followed by paclitaxel group and the paclitaxel followed by endostar group were (8.78±0.19)%, (13.82±0.15)%, (18.88±0.29)%, (11.37±0.24)% and (14.88±0.34)%,respectively. The differences among the groups and compared with the negative control group were all statistically significant(P0.05). Compared with the control group,the endostar group and two sequential groups significantly decreased mRNA expression of Bcl-2,and the paclitaxel group also reduced the mRNA expression of Bcl-2. The three ways of drug combination all presented a decreasing mRNA expression of Bax. Every group could decrease the expression of p21. Sequential medication groups reduced the expression of p53. Conclusion Endostar in combination with paclitaxel can synergisticly induce apoptosis of the human esophageal carcinoma cell, and the mechanism may be related to the reduced expressions of antiapoptosis genes.

Key concepts: Paclitaxel, Apoptosis, Medicine, Flow cytometry, Annexin, Endostatin, MTT assay, Cancer research

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A experimental study of recombined human endostatin in combination with paclitaxel inducing apoptosis of esophageal cancer cell line Eca-109 — Research Paper | ScholarLens