RESUMEN
OBJECTIVE: To investigate the effect of EGFR-TKI targeted therapy in patients with advanced non-small cell lung cancer (NSCLC). METHODS: Eighty-four cases of NSCLC were retrospectively assigned into an observation group (OG, n=42) and a control group (CG, n=42) according to the treatment methods. The CG received conventional chemotherapy, and the OG received icotinib hydrochloride EGFR-TKI targeted therapy. The clinical efficacy, cellular immunity, humoral immunity, quality of life, adverse reactions and survival time were compared between the two groups. Cox regression analysis was used to analyze the factors influencing the prognosis of advanced NSCLC. RESULTS: The total response rate was substantially higher, and the incidence of adverse reactions was considerably lower in the OG than those in the CG (all P<0.05). The post-treatment SF-36 score was increased in both groups with significantly higher score in the OG than the CG (all P<0.001). The post-treatment CD4+ counts in both groups were notably lower than those of pre-treatment, and the count was lower in the CG than that in the OG (all P<0.001). The post-treatment CD8+ counts in both groups were notably higher after treatment than those of pre-treatment and was higher in the CG than that in the OG (all P<0.001). The post-treatment levels of IgM and IgA in both groups were declined compared with those of pre-treatment (P<0.001) with significantly lower levels in the OG than the CG (P<0.01). The 18-month mortality of the OG was significantly lower than that of the CG (P<0.05). Cox regression analysis showed that lesion diameter and differentiation degree of tumor cells were independent factors influencing the prognosis (P<0.05). CONCLUSION: EGFR-TKI targeted therapy can relieve clinical symptoms, and improve immune function and quality of life of patients with advanced NSCLC, which is worthy of clinical application.
RESUMEN
Stromal interaction molecule 1 (STIM1) is a calcium-sensing protein localized in the membrane of the endoplasmic reticulum. The expression of STIM1 has been shown to be closely associated with cell proliferation. The aim of the present study was to investigate the role of STIM1 in the regulation of cancer progression and its clinical relevance. The data demonstrated that the expression of the STIM1 was significantly higher in non-small-cell lung cancer (NSCLC) tissues than in benign lesions and was associated with advanced NSCLC T stage. Knockdown of STIM1 expression in NSCLC cell lines A549 and SK-MES-1 significantly inhibited cell proliferation and induces A549 and SK-MES-1 cell arrest at the G2/M and S phases of the cell cycle. Western blotting showed that the expression of cyclin-dependent kinase (CDK) 1 and CDK2 were reduced while knockdown of STIM1 expression. Furthermore, knockdown of STIM1 in NSCLC cells significantly reduced the levels of xenograft tumor growth in nude mice. These data indicate that aberrant expression of the STIM1 protein may contribute to NSCLC progression. Future studies should focus on targeting STIM1 as a novel strategy for NSCLC therapy.