title: [Influence of interference of WIG-1 on the multi-drug resistance in small cell lung cancer].
abstract: 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.
authors.affiliation: Department of Oncology, Sichuan Provincial People's Hospital, Chengdu 610000, China.
authors.forename: Shuchun
authors.initials: S
authors.lastname: Luo
authors.affiliation: Department of Oncology, Sichuan Provincial People's Hospital, Chengdu 610000, China.
authors.forename: Yifeng
authors.initials: Y
authors.lastname: Bai
authors.affiliation: Department of Oncology, Sichuan Provincial People's Hospital, Chengdu 610000, China. Email: lanht@sina.com.
authors.forename: Haitao
authors.initials: H
authors.lastname: Lan
mesh_terms: D000970:Antineoplastic Agents; D017209:Apoptosis; D004268:DNA-Binding Proteins / Q000378:metabolism*; D015536:Down-Regulation; D018432:Drug Resistance, Multiple; D019008:Drug Resistance, Neoplasm / Q000502:physiology*; D005047:Etoposide; D006801:Humans; D008175:Lung Neoplasms / Q000378:metabolism*; D009687:Nuclear Proteins / Q000378:metabolism*; D034741:RNA, Small Interfering; D016601:RNA-Binding Proteins; D055752:Small Cell Lung Carcinoma / Q000378:metabolism*
chemical_list: D000970:Antineoplastic Agents; D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D034741:RNA, Small Interfering; D016601:RNA-Binding Proteins; C491518:Wig1 protein, mouse; D005047:Etoposide