ABSTRACT
[This retracts the article DOI: 10.3892/ol.2018.9512.].
ABSTRACT
BACKGROUND: To ascertain whether concurrent chemotherapy using liposomal paclitaxel and cisplatin could improve the outcomes of patients with locally advanced esophageal squamous cell carcinoma receiving intensity-modulated radiotherapy (IMRT). METHODS: A total of 72 patients with locally advanced esophageal squamous cell carcinoma, which were admitted to our hospital from October 2011 to December 2013, were retrospectively analyzed in this study. RESULTS: Thirty-six patients (50%) were treated with IMRT alone, while the other 36 patients (50%) were treated by IMRT combined with chemotherapy containing liposomal paclitaxel and cisplatin. Patients treated with chemoradiotherapy showed significantly superior overall survival (OS) and progression-free survival (PFS) compared to patients treated with IMRT alone (median OS: respectively, 29.7 vs. 12.9 months, P=0.0287; median PFS: respectively, 14.0 vs. 6.5 months, P=0.0186). Multivariate Cox analysis confirmed the inclusion of chemotherapy as an independent predictor of favorable OS and PFS. Both chemoradiotherapy and IMRT were well-tolerated in our cohort. CONCLUSIONS: Chemotherapy improved the prognosis of locally advanced esophageal squamous cell carcinoma treated with IMRT. Large prospective studies are needed to confirm the therapeutic value of IMRT combined with chemotherapy in locally advanced esophageal squamous cell carcinoma.
ABSTRACT
Early detection of nasopharyngeal carcinoma (NPC) is of vital importance for improving prognosis and survival rates. MicroRNA (miRNA) are a class of short and non-coding RNA molecules that are capable of inhibiting the translation of mRNA of target genes. Previous studies have revealed that miRNA are involved in tumorigenesis and cancer development. The RNase-resistance of circulating miRNA have made them valuable non-invasive biomarkers, and has therefore drawn particular attention to their therapeutic potential. The aim of the present study was to investigate the expression of the previously uncharacterized miR-639 in NPC. In a study population of 139 patients, higher expression of miR-639 was associated with metastasis, more advanced cancer stages, and lower disease-free survival rates. In vitro experiments involving transfection of human NPC C666-1 and NPC/HK1 cell lines with miR-639 mimics and antagomir indicated that overexpressing miR-639 promoted cell proliferation and migration, suppression of miR-639 inhibited proliferation and migration. The present study provides evidence that miR-639 is differentially expressed in NPC tissues of varying cancer stages, and suggests that quantifying circulating miR-639 may be of importance for non-invasive diagnosis and prognostic evaluation, and may have potential therapeutic utility.
ABSTRACT
BACKGROUND: The high mobility group A1 (HMGA1) proteins are architectural transcription factors found to be overexpressed in lung adenocarcinoma. Lentivirus-mediated RNA interference (RNAi) technology is a powerful tool for silencing endogenous or exogenous genes in human cancer cells. Our preliminary study shows that gemcitabine inhibits growth of the human lung cancer cell line SPCA-1 and induces apoptosis, and this effect might link with down-regulation of HMGA1 expression. This study aimed to investigate the chemosensitivity change of the lung adenocarcinoma cells SPCA-1 after HMGA1 inhibition by lentivirus-mediated RNAi. METHODS: We studied a highly malignant lung adenocarcinoma cell line (SPCA-1 cells). Lentiviral short-hairpin RNA (shHMGA1) expression vectors targeting HMGA1 were used for generation of lentiviral particles. After being transfected into the lung adenocarcinoma cell line SPCA-1, the expression of HMGA1 was determined by retrotranscriptase polymerase chain reaction (RT-PCR) and Western blotting. The effect of gemcitabine on proliferation of positive and negative cells was observed by methyl thiazolyl tetrazolium (MTT) assay and clonogenic survival assay. Apoptosis was observed by flow cytometery. Chemosensitivity to gemcitabine was determined by IC50 analysis. Caspase activity was quantitated by a caspase colorimetric protease assay kit. RESULTS: HMGA1-siRNA silenced its target mRNA specifically and effectively in SPCA-1 cells. The apoptotic rates of the scramble control group were (7.43 ± 0.21)%, (11.00 ± 0.20)%, and (14.93 ± 0.31)%, and the apoptotic rates in the silenced group were (9.53 ± 0.42)%, (16.67 ± 0.45)%, and (25.40 ± 0.79)% under exposure to 0.05, 0.5 and 5.0 µg/ml of gemcitabine (P < 0.05). The IC(50) of the silenced group was (0.309 ± 0.003) µg/ml which was significantly lower than in the scramble control group, (0.653 ± 0.003) µg/ml (P < 0.05). It reduced cancer cell proliferation and increased apoptotic cell death after being treated with gemcitabine compared with the scramble control group. HMGA1 silencing resulted in reduction in the phosphorylation of Akt, and promoted the activation of caspases 3, 8 and 9 upon exposure to gemcitabine. CONCLUSIONS: Lentivirus-mediated RNA interference of HMGA1 enhanced chemosensitivity to gemcitabine in lung adenocarcinoma cells. The mechanism may be associated with the PI-3K/Akt signal pathway. HMGA1 may represent a novel therapeutic target in lung cancer.
