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Antisense Bcl2 oligonucleotide in cisplatin-resistant bladder cancer cell lines
Objective:
To determine the change of expression of Bcl2 in cisplatin-resistant bladder cancer cell lines and the reversibility of chemoresistance to cisplatin with antisense oligonucleotide against Bcl2, as higher expression of Bcl2 is associated with drug resistance in many different cancer cell lines.
Materials And Methods:
In the cisplatin-resistant bladder tumour cell lines T24R1 and T24R2, the expression of Bcl2 was determined by reverse transcription-polymerase chain reaction and Western blot assay, and antisense oligonucleotide targeting of the Bcl2 coding sequence was administered with lipofectin.
Results:
The expression of Bcl2 mRNA and protein was greater in T24R1 and T24R2 cells than in the parent T24 cells. Short-term exposure to cisplatin up-regulated Bcl2 mRNA and protein expression in parent T24 cells. Treatment with antisense oligonucleotide down-regulated Bcl2 protein expression and significantly enhanced the cytotoxicity of cisplatin.
Conclusions:
Up-regulation of Bcl2 protein expression might be one of the mechanisms of cisplatin resistance in bladder cancer cells, and antisense Bcl2 oligonucleotide may be helpful in chemotherapy for bladder cancer by reversing cisplatin resistance.
Insights
Higher Bcl2 protein expression contributes to cisplatin resistance in bladder cancer. Antisense Bcl2 oligonucleotide therapy may reverse this resistance, enhancing chemotherapy effectiveness for bladder cancer patients.
Area of Science:
- Molecular Biology
- Oncology
- Pharmacology
Background:
- Elevated Bcl2 expression is linked to drug resistance across various cancers.
- Understanding Bcl2's role in cisplatin resistance is crucial for bladder cancer treatment.
Purpose of the Study:
- To investigate Bcl2 expression changes in cisplatin-resistant bladder cancer cell lines.
- To evaluate the potential of antisense Bcl2 oligonucleotide to reverse cisplatin chemoresistance.
Main Methods:
- Bcl2 expression (mRNA and protein) was quantified in T24R1 and T24R2 cisplatin-resistant cell lines using RT-PCR and Western blot.
- Antisense oligonucleotide targeting Bcl2 was administered to bladder cancer cells via lipofection.
Main Results:
- Bcl2 mRNA and protein levels were significantly higher in resistant cell lines (T24R1, T24R2) compared to parent T24 cells.
- Cisplatin treatment increased Bcl2 expression in parent T24 cells.
- Antisense Bcl2 oligonucleotide reduced Bcl2 protein expression and markedly increased cisplatin's cytotoxicity.
Conclusions:
- Increased Bcl2 protein expression is a potential mechanism driving cisplatin resistance in bladder cancer.
- Antisense Bcl2 oligonucleotide demonstrates promise in overcoming cisplatin resistance, potentially improving bladder cancer chemotherapy outcomes.
