The knockdown of Bmi-1 could effectively suppress cancer cell proliferation and tumourigenicity in several cancers. This study aims to investigate whether or not Bmi-1 plays a causative role in the proliferation of ovarian epithelial cancer cells and telomerase activity. The messenger RNA (mRNA) and protein expression levels of Bmi-1 in the human ovarian carcinoma cell line OVCAR-3 were downregulated by Bmi-1 siRNA, as confirmed by real-time polymerase chain reaction (PCR) and Western blot. Cell viability was analysed by MTT assay, and telomerase activity was analysed by a modified telomeric repeat amplification protocol. Targeting Bmi-1 with siRNA inhibited Bmi-1 mRNA over five-fold compared with the control cells, and inhibited Bmi-1 protein expression over three-fold compared with control cells. The viability of the OVCAR-3 ovarian cancer cell line was reduced by Bmi-1 mRNA compared to control cells. Telomerase activity was decreased 22.73% (from 0.33 to 0.255) by Bmi-1 siRNA treatment compared to control cells. As Bmi-1 siRNA depressed telomerase activity, cell immortalisation may be prevented; thus, silencing Bmi-1 may be a potential therapy to manage ovarian cancer.
Background: To explore the expression of TS, RRM, ERCC1, TUBB3 and STMN1 genes in the tissues of patients with non-small cell lung cancer (NSCLC) and its significance in guiding the postoperative adjuvant chemotherapy. Materials and Methods: Real time polymerase chain reaction (PCR) was applied to detect the expression of TS, RRM, ERCC1, TUBB3 and STMN1 genes in the tissues of NSCLC patients so as to analyze the relationship between the expression of each gene and the clinical characteristics and to guide the postoperative individualized chemotherapy according to the detection results of NSCLC patients. Results: Expression of TS gene was evidently higher in patients with adenocarcinoma than those with non-adenocarcinoma (P=0.013) and so was the expression of ERCC1 (P=0.003). The expression of TUBB3 gene was obviously higher in NSCLC patients in phases Ⅰ/Ⅱ and Ⅳ than those in phase Ⅲ (P 1 =0.021; P 2 =0.004), and it was also markedly higher in patients without lymph node metastasis than those with (P=0.008). The expression of STMN1 gene was apparently higher in patients in phase Ⅰ/Ⅱ than those in phase Ⅳ (P=0.002). There was no significant difference between the rest gene expression and the clinical characteristics of NSCLC patients (P>0.05). Additionally, the diseasefree survival (DFS) was significantly longer in patients receiving gene detections than those without (P=0.021). Conclusions: The selection of chemotherapeutic protocols based singly on patients' clinical characteristics has certain blindness. However, the detection of tumor-susceptible genes can guide the postoperative adjuvant chemotherapy and prolong the DFS of NSCLC patients.
Lung cancer is one of the most common and serious types of cancer, and is characterized by uncontrolled cell growth and metastasis from lung tissues to other body parts. The programmed cell death 5 (Pdcd5) protein is known to accelerate apoptosis in different cell types of tumor. The aim of the present study was to explore the role of Pdcd5 in lung carcinoma and to identify the mechanisms underlying the antitumorigenic properties of Pdcd5 in lung cancer. First, we detected and compared the expression of Pdcd5 in healthy and highly differentiated adenocarcinoma lung tissues. The results of histochemical staining and western blot analysis demonstrated that Pdcd5 expression is markedly decreased in highly differentiated lung adenocarcinoma. Next, we used the lung adenocarcinoma cell line A549 to study the effects of Pdc5 expression on proliferation and colony formation. The results revealed that the expression of Pdcd5 significantly inhibits cell proliferation and colony formation in A549 cells. Importantly, Pdcd5 expression induced tumor cell apoptosis, and the apoptotic proteins caspase-3 and -9 were activated. The expression of B-cell lymphoma 2 (Bcl-2) was reduced and that of Bcl2‑associated X protein (Bax) was increased, overall suggesting that the intrinsic apoptotic pathway is activated. Furthermore, using a mice xenograft model and vectors for stable expression or silencing of Pdcd5, we showed that stable expression of the protein significantly increases the survival rate of mice in vivo (P<0.01 compared to control). In conclusion, both in vitro and in vivo experiments demonstrated that Pdcd5 expression inhibits proliferation and induces apoptosis in the A549 cell line, indicating that the Pdcd5 protein may play an important role in the progression of lung cancer. Therefore, Pdcd5 may be a promising target for the therapy of lung carcinoma.
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