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Reduced Lipocalin 2 Expression Contributes to Vincristine Resistance in Human Colon Cancer Cells
Xiao Guo1,2, Qin Li1,3, Yan-Fang Wang1,2
1Henan Collaborative Innovation Canter of Molecular Diagnosis and Laboratory Medicine, Xinxiang, Henan 453003, China.
Background:
Vincristine (VCR) resistance can lead to cancer chemotherapy failure. Although changes in gene expression are responsible for drug resistance, the specific identities and roles of these genes remain unclear.
Objective:
In this study, we aimed to identify differentially expressed genes and mechanisms of VCR resistance in colorectal cancer (CRC) cells.
Methods:
A VCR-resistant CRC cell line (HCT-8/VCR) was established, and differentially expressed proteins between HCT-8 and HCT-8/VCR cells were screened using a human cytokine array; the results were confirmed by reverse transcription polymerase chain reaction and Western blotting. Furthermore, differentially expressed proteins were downregulated using siRNA, and cell proliferation and apoptosis were assessed by Cell Counting Kit-8 assay and flow cytometry, respectively.
Results:
Compared with HCT-8 CRC cells, HCT-8/VCR cells showed downregulation of lipocalin 2 (LCN2). We found that siRNA-mediated downregulation of LCN2 in HCT-8 cells significantly increased VCR resistance. Furthermore, when we downregulated LCN2, we observed significant decreases in apoptosis, but no significant effect on cell cycle.
Conclusion:
Overall, these results demonstrate that LCN2 plays an important role in VCR resistance and is a potential therapeutic target for this disease.
Insights
Lipocalin 2 (LCN2) downregulation increases vincristine (VCR) resistance in colorectal cancer. Reducing LCN2 also decreases apoptosis, suggesting LCN2 is a potential therapeutic target for VCR-resistant cancers.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Vincristine (VCR) resistance is a major cause of chemotherapy failure in cancer treatment.
- The specific genes and mechanisms underlying VCR resistance are not fully understood.
- Identifying these factors is crucial for developing effective cancer therapies.
Purpose of the Study:
- To identify differentially expressed genes involved in VCR resistance in colorectal cancer (CRC) cells.
- To elucidate the mechanisms by which these genes contribute to VCR resistance.
- To evaluate potential therapeutic targets for overcoming VCR resistance.
Main Methods:
- Established a VCR-resistant CRC cell line (HCT-8/VCR).
- Screened differentially expressed proteins using a human cytokine array, confirmed by RT-PCR and Western blotting.
- Utilized siRNA to downregulate target proteins and assessed effects on cell proliferation and apoptosis via CCK-8 assay and flow cytometry.
Main Results:
- Lipocalin 2 (LCN2) was found to be downregulated in VCR-resistant CRC cells (HCT-8/VCR) compared to sensitive cells (HCT-8).
- siRNA-mediated downregulation of LCN2 in HCT-8 cells significantly increased VCR resistance.
- LCN2 downregulation led to decreased apoptosis but did not significantly affect the cell cycle.
Conclusions:
- Lipocalin 2 (LCN2) plays a significant role in mediating VCR resistance in colorectal cancer.
- LCN2 represents a potential therapeutic target for overcoming VCR resistance.
- Further research into LCN2 modulation could lead to improved cancer treatment strategies.
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