The Inhibition Of A Novel Type Peptide On Lewis Lung Tumor Cells In Vitro

Lung cancer is a malignant tumor that threatens human health.With the accelerated development of China’s industrialization, and the nat ional smoking rate increased year by year, leading to the rapid growt h of the incidence and mortality of lung cancer in cities and towns,a nd the mortality rate has been locatedin the head of the malignant tu mor in China.Lung cancer is not easy to bedetected in the early stage of the disease, the disease has often been developed to the late whe n come to see the doctor, So the patient have missed the best time fo r treatment.Current clinical treatment or more is still for the tradi tional treatment methods, such as surgery, radiotherapy and chemother apy.These traditional methods of treatment although can improve the c linical efficacy, prolong the survival time of patients, but these tr eatments face severe situation because of a lot of their side effects.So far, there are a lot of anti-tumor drugs developed at home and abr oad, but most of them have many adverse reactions, drug resistance an d high price. To this end, looking for high efficiency,low toxicity,l ow price, and can effectively improve the efficacy of drug treatment of lung cancer is still an urgent problem to be solved.Recent researc h shows that the novel type peptide drugs has anti-tumor effect, comp ared with other drugs,the novel type peptide drugs have the following advantages: due to its molecular weight, so it can more effectively penetrate the tumor; small molecular novel type peptide and radioacti ve material can combined with compound formation,which has higher sta bility; if a small molecular novel type peptide chain is composed of non natural amino acid, then this chain is not easy to be protease hydrolysis;the novel type peptide rarely be swallowed by reticuloendoth elial system;the novel type peptide can be synthesized in the large a mount, reducing the production cost, which is the novel type peptide value compared with other anti-tumor drugs.Because of the advantages of the novel type peptide, it has obvious advantages in the field of the treatment of tumor.Objective:To study the effect of novel type peptide on the proliferation and apoptosis of Lewis tumor cells Methods:The inhibition of the proliferation of Lewis tumor cells was observed by using MTT assay at different time(24h, 48 h and 72h).Transwell assay was used to detect the invasion of cells;We use AO/EB and mitochondrial membrane potential detection method to detect the apoptosis of cells with fluorescent microscopy in 48h;Using flow cytometry to detect cell cycle and apoptosis;Western blot method was used to detect the expression of Cyclin-D1 and Pro-caspase3 protein in Lewis tumor cells.Results:MTT results showed that novel type peptide has certain inhibitory effect on the proliferation of Lewis tumor cells at different time p oints, and 48 h is most obvious under the inverted microscope;cells sh owed the typical morphological features of apoptosis change in the gr oup of 2000μg·m L-1 novel type peptide;in the Transwell invasion cha mber experiment, the number of cells which can through the membrane d ecreased,shows the invasion of tumor cells reduced;the tumor cells ap optosis was observed by fluorescence microscopy,the morphological cha racteristics of cells has changed in the novel type peptide group,the mitochondrial membrane potentialdecreased significantly, indicating that the apoptosis of tumor cells happened.Cell cycle and apoptosis was detected by flow cytometry, G1/G0 cells increased, S phase cells de creased, the late apoptosis rate was increased; Western Blot results showed that with the increase of novel type peptide concentration, th e expression level of Cyclin-D1 protein and Pro-caspase3 protein were gradually reduced.Conclusion:The novel type peptide can inhibit the proliferation and invasion of lung cancer cells.The mechanism may be related to the decrease of Cyclin-D1 protein and Pro-caspase3 protein expression.Promote the apoptosis of lung cancer cells.