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Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
Published on: February 6, 2015
[Effects of cyclooxygenase-2 antisense vector on proliferation and sensitivity to cisplatin of H1299 cells]
Zhiqiang Gao1, Liang Tang, Bo Su
1Department of Oncology, Shanghai Pneumology Hospital, Shanghai 200433, P.R.China.
Background:
At present, it has been known that cyclooxygenase-2 (COX-2) plays a crucial role in invasion, development and metastasis of non-small cell lung cancer (NSCLC). In order to explore whether the expression of COX-2 inhibits the occurrence and development of NSCLC, antisense vector of human COX-2 gene is transfected into COX-2 highly expressing NSCLC cell line H1299 and its effects on proliferation and sensitivity to cisplatin of H1299 are analysed.
Methods:
H1299 cells were transfected with antisense vector of human COX-2 gene using LipoVecTM transfecting technique. Transfected cells were selected with Geneticin (G418). The COX-2 mRNA level was examined by using reverse polymerase chain reaction (RT-PCR). The COX-2 protein level was examined by Western Blot. The proliferative status and sensitivity to cisplatin of cells was measured by methabenzthiazuron (MTT) assay.
Results:
RT-PCR showed a lower COX-2 mRNA level in transfected cells. The level of COX-2 protein was decreased apparently. The proliferative index of the transfected cells decreased significantly (P < 0.05). The IC50 value of cisplatin decreased remarkably in transfected cells (1.8mg/l) compared with that in H1299 cells without transfection (3.8mg/l) (P < 0.05).
Conclusions:
Transfection with antisense vector of human COX-2 gene can not only inhibit the proliferation of H1299 cells, but also increase the sensitivity to cisplatin of H1299 cells.
Insights
Inhibiting cyclooxygenase-2 (COX-2) in non-small cell lung cancer (NSCLC) cells with an antisense vector reduced proliferation. This approach also enhanced the cancer cells
Area of Science:
- Molecular Biology
- Cancer Research
- Genetics
Context:
- Cyclooxygenase-2 (COX-2) is implicated in the progression and metastasis of non-small cell lung cancer (NSCLC).
- Understanding the role of COX-2 in NSCLC is crucial for developing targeted therapies.
Purpose:
- To investigate the effect of inhibiting COX-2 expression on NSCLC cell proliferation and chemosensitivity.
- To analyze the impact of transfecting H1299 NSCLC cells with a human COX-2 antisense vector.
Summary:
- H1299 NSCLC cells were transfected with a COX-2 antisense vector, leading to reduced COX-2 mRNA and protein levels.
- Transfected cells exhibited significantly decreased proliferation rates.
- The sensitivity of H1299 cells to cisplatin was markedly increased post-transfection, indicated by a lower IC50 value.
Impact:
- Inhibition of COX-2 can suppress NSCLC cell growth.
- Targeting COX-2 may enhance the efficacy of chemotherapy drugs like cisplatin in NSCLC treatment.
- Provides a potential therapeutic strategy for managing NSCLC.
