A Preliminary Studies About The Biological Functions Of MiR-569 On Lung Cancer Cells And Its Expression In The Serum Of Lung Cancer Patients

Objective:Lung cancer is one of the most prolific malignant tumors with the highest mortality in the world.Over the decades,the comprehensive treatment based on surgery,radiation and chemotherapy has made great progress,however,the overall treatment effect is still poor.It is mainly because most of the clinical diagnosis of lung cancer patients have been period,and tumor metastasis and multiple drug resistance.Therefore,there is an urgent need to find a reliable early diagnosis and effective treatment strategy.As the new darling of oncology researchers,micro RNAs(mi RNA)is expected to become the new anti-cancer weapons.Mi R-569 at 3q26.2,as part of 3q26.2 amplification,can participate in regulating the proliferation of breast and ovarian cancer cells.Furthermore,3q26.2 Amplification is one of the most common chromosomal aberrations in lung cancer.While,the expression and function mechanism of the mi R-569 in lung cancer has not yet reported.In this study,we tend to investigate the expression of mi R-569 in lung cancer cells,and made further study on its biological characteristics and the possible mechanism for the first time.Then,we wanted to make its expression in lung cancer serum clear.Methods:1.We evaluated the expression of mi R-569 in lung cancer cells(A549 ? HCC827?H1299?95D)and normal pulmonary bronchial epithelial cells(HBE)by quantitative real-time polymerase chain reaction.2.In order to define the biological characteristics of mi R-569 on lung cancer,wetransfected lung adenocarcinoma A549 cells with mi R-569 mimics.Proliferation,apotosis and migration of lung adenocarcinoma cells were assessed by CCK-8,flow cytometry and wound healing experiment,respectively.3.To make further study on the possible mechanism of mi R-569 in lung cancer,we filtered the potential target genes through bioinformatics analysis.And then verified the correlation between mi R-569 and c-FOS/HMGA2 by q RT-PCR and Western Blot.4.To test mi R-569 expression level in lung cancer serum,we collected 78 serum samples of lung cancer patients and healthy controls from the clinical laboratory of the first hospital affiliated to Dalian Medical Colleage.Through the q RT-PCR,we detected the expression level of lung cancer patients compared with the normal control.Results:1.Mi R-569 expression in lung cancer cells(A549?HCC827?H1299? 95D)was lower than that in normal lung epithelial cells(HBE).2.Mi R-569 mimic could inhibited cell proliferation,migration and induce apoptosis.3.48 hours after transfection,mi R-569 expression significantly elevated showed by q RT-PCR.Mi R-569 mimics could suppress m RNA and protein expression level of cFOS and HMGA2 notably showed by q RT-PCR and Western blot,respectively.4.The expression of mi R-569 in serum from lung cancer patients serum compared with normal controls was not statistically different.Conclusion: Mi R-569 expression in lung cancer cells was significantly lower compared with the normal pulmonary bronchial epithelial cells.And the possible mechanisms were that mi R-569 could act as a tumor suppressor gene by negatively regulating the expression of c-FOS and HMGA2.Mi R-569 is expected to become a new target for lung cancer treatment..However,the expression of mi R-569 in serum from lung cancer patients serum compared with normal controls was not statistically different.Mi R-569 can't be lung cancer biomarkers for early diagnosis.