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[Influence of interference of WIG-1 on the multi-drug resistance in small cell lung cancer]
Shuchun Luo1, Yifeng Bai1, Haitao Lan1
1Department of Oncology, Sichuan Provincial People's Hospital, Chengdu 610000, China.
Objective:
To investigate the role of wild-type p53-induced gene 1 (WIG-1) on the regulation of multi-drug resistance in small cell lung cancer.
Methods:
The expressions of WIG-1 protein and gene were detected by Western blot and real-time PCR (RT-PCR) in both the drug-sensitive H69 and drug-resistant H69AR cell lines, respectively. Meanwhile, the differential expression of WIG-1 was also detected in peripheral blood samples of responders and non-responder patients. Furthermore, the WIG-1 expression was inhibited by siRNA in H69AR cells, then the drug-sensitivities of H69AR cells to chemotherapy agents such as ADM, DDP, VP-16 were detected by CCK8 assay, and apoptosis rate was detected by flow cytometry. The possible association of WIG-1 with clinical parameters was evaluated.
Results:
The expression of WIG-1 was significantly increased in H69AR cells (5.965 ± 0.890) than that in the H69 cells (1.023 ± 0.127) (P = 0.007). The expression of WIG-1 was significantly increased in the non-responder patients (4.169 ± 0. 970) than in the H69 cells and responders (1.673 ± 0.127) (P < 0.001). The drug-sensitivities of H69AR cells to chemotherapeutic drugs were increased when the expression of the WIG-1 was down-regulated. The apoptosis rate was significantly decreased in the H69AR cells (1.037 ± 0.049)% compared with that in the H69 cells [(7.963 ± 0.097)%, (P < 0.01)]. The apoptosis rate was increased in the H69AR-Si-WIG-1 cells (20.915 ± 0.890)% than that of (1.037 ± 0.049)% in the H69AR and H69AR-NC group (2.025 ± 0.097)% (P < 0.01). The expression of WIG-1 was not significantly associated with gender, and age (P > 0.05), but significantly correlated with chemosensitivity, overall survival and clinical stage (P < 0.001 for all).
Conclusions:
Our results suggest that WIG-1 is involved in the regulation of the multidrug resistance mechanism in small cell lung cancer. Selective silencing of the WIG-1 gene may reverse the multidrug resistance of SCLC via increasing cell apoptosis.
Insights
Wild-type p53-induced gene 1 (WIG-1) is upregulated in multidrug-resistant small cell lung cancer (SCLC). Silencing WIG-1 can reverse drug resistance and increase apoptosis in SCLC cells.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Small cell lung cancer (SCLC) often develops multidrug resistance (MDR), limiting treatment efficacy.
- Wild-type p53-induced gene 1 (WIG-1) is a potential regulator of cellular responses to stress and drugs.
Purpose of the Study:
- To investigate the role of WIG-1 in the regulation of MDR in SCLC.
- To explore WIG-1 as a potential therapeutic target for overcoming SCLC drug resistance.
Main Methods:
- Western blot and RT-PCR were used to detect WIG-1 expression in SCLC cell lines and patient samples.
- WIG-1 was inhibited using siRNA in drug-resistant SCLC cells (H69AR).
- Drug sensitivity (CCK8 assay) and apoptosis rates (flow cytometry) were assessed after WIG-1 inhibition.
Main Results:
- WIG-1 expression was significantly higher in drug-resistant SCLC cells (H69AR) and non-responder patients compared to sensitive cells and responders.
- Down-regulating WIG-1 expression increased the sensitivity of H69AR cells to chemotherapy drugs.
- Inhibition of WIG-1 significantly increased apoptosis in H69AR cells.
Conclusions:
- WIG-1 plays a role in the MDR mechanism of SCLC.
- Selective silencing of WIG-1 can reverse MDR in SCLC by enhancing cancer cell apoptosis.
- WIG-1 expression correlates with chemosensitivity, overall survival, and clinical stage in SCLC patients.
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