| Lung cancer(LC)is the most common cause of cancer-related death in the world,resulting in 1.8 million new cases and 1.6 million deaths every year.LC was divided into two subgroups:small cell lung cancer(SCLC,15%)and non-small cell lung cancer(NSCLC,85%).The overall 5-year survival rate of NSCLC is still as low as 23.6%.Only 19%of cases were diagnosed in the early stage of highly curable disease,and the 5-year survival rate is 59.5%.The diagnostic methods of NSCLC include sputum cytology,tissue biopsy and imaging examination,such as bronchoscopy,X-ray,nuclear magnetic resonance,positron emission tomography or computed tomography.Early diagnosis of non metastatic LC usually requires surgical resection,but advanced or metastatic LC needs chemotherapy alone or chemotherapy combined with radiotherapy.NSCLC usually reaches advanced stage when it is definitely diagnosed,which leads to poor prognosis.Although some innovative therapies,such as the third generation EGFR TKIs,more advanced radiotherapy technology,low toxicity and high efficiency chemotherapy drugs,immune checkpoint inhibitors PD-1 and PDL-1,have been used in the clinical treatment of NSCLC recently,due to the rapid drug resistance,radiotherapy resistance,and serious toxic and side effects after treatment The effect of prolonging overall survival rate(OS)is still limited.Advanced stage of tumor,heterogeneity of tumor histological subtypes,cognitive limitation of tumor biology,drug resistance and abnormal fluctuation of tumor gene expression profile are the key reasons for poor prognosis of NSCLC,and the treatment of NSCLC has entered a platform stage.Therefore,genomic medicine has become a new field of diagnosis and treatment of NSCLC,which will make up for the lack of cancer research of NSCLC.Accurate detection of biomarkers can accurately predict cancer in the early stage and improve OS of patients.More and more evidence shows that microRNA(miRNA)has been proposed as a potential biomarker to judge the prognosis and treatment sensitivity of NSCLCMiRNA is a class of small non coding endogenous RNA molecules(18-24 nucleotides),which is relatively stable,small size,and has obvious regulation of gene expression.So far,more than 2500 mature human miRNAs have been identified(http://www.mirbase.org/).MiRNAs regulate more than half of genes in human cells.For different miRNAs,the same messenger RNA(mRNA)may have different antisense sequence regions.Therefore,a single miRNA usually regulates multiple mRNAs at the same time,or a single mRNA is regulated by multiple miRNAs to form a complex network,which affects almost all biological processes,and is related to a variety of biological activities and the occurrence and development of a variety of diseases,including a variety of tumors,such as cell proliferation,cell differentiation,cell apoptosis,cell migration,tumor invasion,tumor metastasis and tumor resistance.Epithelial to mesenchymal transition(EMT)is a process in which epithelioid cells lose their attachment to the basement membrane,and show the interstitial characteristics of greater mobility and invasiveness.EMT makes cancer cells metastasize by migrating from primary tumor to blood and invading other organs.Some miRNAs affect the ability or possibility of EMT by regulating the expression of EMT related genes.Previous studies have revealed that miR-27b plays a complex role in many groups of cancer types,and regulates a series of processes,including cell proliferation and cell metastasis.However,there are still a few unsolved problems about the role and molecular mechanism of miR-27b in NSCLC.These questions include whether there is a relationship between the expression of miR-27b and tumorigenesis of NSCLC;what role the miRNA plays in EMT and tumor cell proliferation;the genes targeted by the miRNA in lung cancer and whether miR-27b plays a specific role in tumor;and the sensitization effect of cisplatin(CDDP)in NSCLC.The role of miRNAs in cells is mainly through complementary pairing with the 3’-UTR of the target mRNAs,thus inhibiting the translation of the target mRNAs and the expression of the target protein at the translation level.By synthesizing the information of miRNAs target protein database,it is found that there is a continuous binding site between the 3’-UTR region of Snail gene and the nucleotide sequence of miR-27b.We speculate that Snail may be the target protein of miR-27b.Therefore,we will study to verify whether Snail can bind to miR-27b and play a role in tumor EMT process and biological behaviors such as cancer cell migration and invasion.Therefore,in order to clarify the role of miR-27b in NSCLC and its possible molecular mechanism,we carried out the following five parts of research:part Ⅰ:we detected the expression level of miRNA-27b in tumor tissues of patients with NSCLC compared with adjacent control tissues,and analyzed the relationship between the miRNA-27b and the clinicopathological features of NSCLC patients.Part Ⅱ:to detect the effects of miR-27b overexpression on the biological characteristics of non-small cell lung cancer cells such as migration,proliferation and EMT in NSCLC cell lines H1299 and A549.Part Ⅲ:to explore whether Snail is a direct target gene of miR-27b by constructing Snai13’-UTR wild type and mutant reporter genes that complement miR-27b.Part Ⅳ:to explore the potential role of Snail in the sensitivity of non-small cell lung cancer cells to cisplatin by establishing H1299/miR-27b,H1299/miR-NC and H1299/miR-27b cell lines overexpressing miR-27b.Part Ⅴ:to explore the effect of miR-27b overexpression on the growth of subcutaneous NSCLC tumor in nude mice by constructing subcutaneous tumor model in nude mice.Part Ⅰ Expression and clinical significance of miR-27b in lung cancerBackground:Lung cancer is one of the most common causes of cancer-related death in the world.Most patients have reached advanced stage for the original diagnosis.The 5-year OS rate is23.6%.MicroRNAs are small non coding RNAs that bind to the 3’untranslated region of target messenger RNAto induce mRNA cleavage or translation inhibition.MiRNAs regulate multiple molecular biological processes,including cell development,cell differentiation,cell migration,cell invasion and cell apoptosis.By targeting at different targets,miRNAs play an oncogene or tumor suppressor role.Many miRNAs in NSCLC have abnormal changes and contribute to the growth and development.Studies have revealed that miR-27b is abnormally expressed in bladder cancer,gastric cancer,colorectal cancer,laryngeal squamous cell carcinoma、cervical cancer and other tumors,which may become a biomarker for the early diagnosis and comprehensive treatment of related tumors.At present,the research on the expression of miR-27b in NSCLC is relatively less.Objective:To explore the expression and clinical significance of miR-27b in non-small cell lung cancer.Methods:The samples were collected from 39 patients with NSCLC and corresponding adjacent tissues.After RNA was extracted in vitro,cDNA was synthesized by reverse transcription reaction,and then the expression of miR-27b was detected by QRT-PCR.Using U6 as internal reference,and the relative expression of miR-27b in the two samples were compared.The relationship between miR-27b expression level and TMN staging was analyzed.Results:(1)The expression of miR-27b was decreased in lung cancer tissues.Using U6 as internal reference,the expression level of miR-27b in cancer tissues was calculated and compared with that in corresponding control tissues.The results showed that the miR-27b in tumor tissues of NSCLC patients was much lower than that in adjacent control tissues.(2)Correlation between miR-27b expression and TNM stage in NSCLC patients.Based on the clinical TMN staging data of 39 NSCLC patients,the results showed that the down-regulation of miR-27b expression level was correlated with TNM staging of lung cancer patients.The higher the TMN stage(Ⅲ-Ⅳ),the lower the expression of miR-27b(P<0.05).Conclusion:The expression of miR-27b in tumor tissues of NSCLC patients is decreased.MiR-27b may participate in the occurrence and development of NSCLC as a tumor suppressor gene.The expression of miR-27b is not only low in NSCLC tissues,but also lower in the tissues with higher tumor stage.The lower expression level of miR-27b is likely to predict the deterioration of tumor.Part Ⅱ MiR-27b inhibits proliferation,migration and EMT of lung cancer cellsBackground:MiRNA is a kind of tiny non-coding endogenous RNA molecules(about 18-24 nucleotides in length),which widely exist in various eukaryotes and viruses and play a key role.MiRNA regulates cell transcription and protein translation by binding to the specific complementary sequence of the 3’UTR of the target mRNA.It has been confirmed that miRNA regulates nearly half of human genes,regulates gene activity at the post-transcriptional level by degrading or inhibiting mRNA translation,and plays an important role in many biological processes.EMT is a process in which epithelioid cells lose their attachment to the basement membrane,and show the interstitial characteristics of greater mobility and invasiveness.EMT makes cancer cells metastasize by migrating from primary tumor to blood and invading other organs.In NSCLC,the imbalance of miRNAs leads to greater EMT and more aggressive,migratory and potentially metastatic phenotypes.Previous studies have shown that miR-27b plays a complex role in many different cancer types,such as bladder cancer,cervical cancer,gastric cancer,colorectal cancer,laryngeal squamous cell carcinoma and other tumors,and regulates a series of processes,including cell proliferation and cell metastasis.At present,the biological mechanisms of miR-27b on NSCLC cell migration,cell proliferation and EMT are still unknown.Objective:Explore the molecular mechanism of miR-27b on the proliferation,migration and EMT of non-small cell lung cancer cells.Methods:In order to explore the biological function of miR-27b in lung cancer cells,we constructed H1299 and A549 cell lines stably expressing miR-27b and unrelated control miR-nc by lentivirus packaging.Lung cancer cell lines H1299 and A549 were infected with lentivirus carrying miR-27b and miR-nc,respectively,every 12 hours.After 3-4 days,they were screened with puromycin.After about 14 days,stable cell lines were obtained.Total RNAs were extracted and the expression levels of miR-27b and miR-nc in H1299 and A549 cell lines were detected by QRT PCR.In this experiment,we studied the influence of miR-27b on the migration of NSCLC cells.The cells stably expressing miR-27b and their control cells were inoculated into the upper chamber of Transwell chamber at a density of 50000 cells/well.After 16 hours,the medium in the chamber was sucked away,and the Transwell chamber was taken out.The residual lung cancer cells in the upper chamber were lightly wiped with cotton swabs,and the cells in the chamber were washed with PBS three times.Fix with 3%paraformaldehyde for 15 min,then dye with 0.1%crystal violet for 15 min.The cells were washed with PBS solution for three times and photographed under light microscope.Then the cells were washed with 33%acetic acid for 15 minutes.The eluent was collected and the absorbance OD value was read at 570 nm by enzyme reader.In addition,we also explored the effect of miR-27b on EMT of NSCLC cells.We inoculated the cells into six well plates,and transferred miR-27b and miR-nc to H1299 and A549 cell lines.After 2-3 days of culture,the morphological changes of cells were observed under light microscope and photographed.Under the light microscope,we found that compared with miR-nc group,the morphology of miR-27b group changed from spindle to cobblestone.We evaluated the expression of E-cadherin and vimentin by Western blotting.Compared with miR-nc,the expression of E-cadherin in miR-27b group was higher,while the expression of vimentin was lower.Results:(1)The expression level of miR-27b in lung cancer cells and its effect on cell proliferation:In this study,the effect of miR-27b on the proliferation of two cell lines was detected by CCK-8 experiment.The results showed that the proliferation level of H1299 and A549 cells in miR-27b group was significantly lower.The expression of miR-27b inhibited the proliferation of lung cancer cells in vitro.(2)Effect of miR-27b on migration of lung cancer cells:The migration of lung cancer cells is one of the main pathogenic factors of lung cancer.This study investigated the effect of miR-27b on the migration.The migration of miR-27b overexpressed H1299 and A549 stable cell lines was significantly weaker than that of control cells.(3)Effect of miR-27b on EMT:In this study,we tried to explore the effect of miR-27b on EMT of lung cancer cells.We evaluated the expression of E-cadherin and vimentin.Compared with miR-nc,the expression of E-cadherin in miR-27b group was higher,while the expression level of vimentin was lower.The results suggest that overexpression of miR-27b promotes EMT of lung cancer cells in vitro.Conclusion:In conclusion,this study found that miR-27b can inhibit the proliferation and migration of lung cancer cells,and inhibit the EMT effect of NSCLC cells by up regulating E-cadherin and down regulating vimentin.This study provides a certain research basis for exploring the relationship between miRNAs and the occurrence and development of EMT.Part Ⅲ Snail is the target gene of miR-27bBackground:Snail is a transcription inhibitor whose function has been extensively studied.It plays an important role in epithelial-mesenchymal transition(EMT)and the complementary morphogenesis program that controls normal development.However,its unregulated expression in cancer and disease progression related.Through the developmental process of co-selection,tumor cells mobilize Snail to promote EMT-like procedures and the related tissue invasion phenotype characteristics of aggressive cancer.Through the association between the increase of Snail expression and cancer progression,the possibility of promoting Snail-dependent EMT program to participate in tumorigenesis and development is still unclear.EMT and Snail are indispensable for embryonic development,but their effects on the migration of epithelial tumor cells are still controversial.Studies have shown that Snail is usually expressed in a small number of fibroblasts in the interstitium of breast and colon tumors;other studies have revealed that the correlation between Snail expression and patient survival in breast tumors is controversial,showing complex tumor suppressor Cancer-promoting effect.MiRNAs are endogenous non-coding RNAs with a length of 18-24 nucleotides,which regulate gene expression level after transcription;different miRNAs play different roles in cancer cell proliferation and EMT;the expression of Snail is similar to that of a series of events are related,from participating in the initiation of cancer-promoting EMT-like programs,tumor recurrence to the production of tumor stem cells.However,the potential cross-links between oncogenic processes,microRNA expression and Snail activity regulation have not yet been determined.Our previous studies have shown that the expression level of miR-27b in lung cancer cell lines and lung cancer tissues is significantly reduced,and the reduced expression of miR-27b is related to the later clinical stage of TNM.In addition,the repair of miR-27b inhibited the EMT of tumor cells in vitro and in vivo.In this study,we tried to reveal that miR-27b inhibits the upstream pathway of cancer cell EMT,and miR-27b plays an important role in regulating extracellular stimulation and cancer cell behavior.We try to explore how miR-27b mediates lung cancer EMT,and the functional connection between Snail and miR-27b,and reveal the role of these entities in lung cancer progression.Objective:Explore whether Snail is a target gene of miR-27b and its functional relationship.Methods:Many studies have reported the target genes of miR-27b.We integrated the information from the miRNAs target protein database and found that the 3’-UTR region of the Snail gene has a continuous binding site with the nucleotide sequence of miR-27b.The locus is highly conserved in many species.First,we constructed the Snail 3’-UTR wild-type and mutant reporter genes that contain complementary binding to miR-27b.PCR amplified the fragments of Snail 3’-UTR and miR-27b binding to each other and their mutants,inserted into the reporter gene luciferase vector,and identified by sequencing.Finally,Snail-WT(wild type)plasmid and Snail-MT(Mutant)plasmid.Transfect Snail-WT(wild type)plasmid or Snail-MT(mutant type)plasmid with miR-NC(control)or miR-27b and pRL-TK plasmids respectively into 293T cells,and test the intracellular luciferase activity after 48h,And use the luciferase activity of the pRL-TK plasmid as an internal reference for correction.Secondly,we used western blotting to detect the expression level of Snail in the cells to obtain the effect of miR-27b on the expression level of Snail protein.The two groups of NSCLC cell lines were transfected with 40nM miR-NC and miR-27b.After 72 hours,the protein was collected and the expression of Snail in the cells was detected by western blotting.Finally,the 39 pairs of NSCLC patient tumor tissues and their corresponding adjacent control tissues were collected to analyze the expression of Snail-mRNA by qRT-PCR,and calculate the expression level of Snail-mRNA in the cancer tissue and the corresponding control.Snail-mRNA expression in the tissues,and compare the relative expression levels of Snail-mRNA in the two specimens.Results:(1)The complementary binding region of Snail and miR-27b is conserved among species:By searching the miRNAs target protein database,it was found that there is a continuous binding site between the 3’-UTR region of the Snail gene and the nucleotide sequence of miR-27b,and this site is highly conserved in many organisms.(2)miR-27b targets and regulates Snail:First,compared with the miR-NC group co-transfected with Snail-WT,the luciferase activity of the miR-27b group co-transfected with Snail-WT was significantly reduced,a decrease of about 40%;compared with the co-transfected Snail Compared with the miR-NC group of-MT,there was no significant change in the luciferase activity of the miR-27b group co-transfected with Snail-MT(P>0.05).This result initially suggests that Snail may be the target of miR-27b.Secondly,compared with the miR-NC transfected group,the protein level of Snail in the miR-27b-transfected H1299 and A549 lung cancer cells was significantly inhibited(P<0.01).The above results all suggest that Snail is the target gene of miR-27b directly.(3)The expression level of Snail in NSCLC tumor tissue:Through comparison,it can be seen that the expression level of Snail in tumor tissues of NSCLC patients is much higher than its expression level in adjacent control tissues.The results of this study suggest that the expression level of Snail in the tumor tissues of NSCLC patients is elevated,which confirms that Snail is a direct target gene of miR-27b.Conclusion:In summary,this study found that there is a continuous binding site between the 3’-UTR region of Snail gene and the nucleotide sequence of miR-27b,and This site is highly conservative among many species;the results of the study suggest that Snail is the target gene of miR-27b directly acts;Snail is expressed in tumor tissues of NSCLC patients,which proves that Snail is the target gene of miR-27b directly.Part Ⅳ MiR-27b enhances CDDP sensitivity of lung cancer by targeting SnailBackground:Although the early diagnosis and comprehensive treatment of lung cancer have made great progress,an important part of the treatment of patients with lung cancer usually includes platinum-based chemotherapeutic drugs,cisplatin resistance is a major clinical challenge for patients with lung cancer,it is well known that continuous and/or multiple administration often leads to drug resistance,which often leads to treatment failure.Cisplatin is a well-known cytotoxic agent for DNA damage.Once CDDP enters the cell,cisplatin-DNA adducts will be formed,and these signals will activate the apoptotic pathway.Therefore,it is necessary to clarify the molecular mechanism of cisplatin resistance in order to overcome this resistance and develop a new and more effective treatment for lung cancer.More and more data show that cisplatin resistance is modified by miRNAs and plays a vital role.Experimental and clinical studies have shown that miRNAs can play a role as a tumor suppressor gene or oncogene in the occurrence and development of lung cancer.The molecular mechanism of CDDP resistance is not completely clear,involving many processes,such as cell cycle,cell apoptosis,drug transport,drug metabolism,DNA repair and so on.So far,it has been proved that miRNAs play an important role in the development of chemosensitivity and chemoresistance.A large number of studies suggest that miRNAs and its effect on cisplatin-based lung cancer cell chemosensitivity.Therefore,miRNAs regulates the sensitivity of tumor cells to chemotherapy through post-transcriptional regulation of multiple target genes,highlighting the potential of clinical manipulation of related miRNAs to overcome chemotherapy resistance.However,little is known about whether the expression of miR-27b affects the chemosensitivity of non-small cell lung cancer,and its potential molecular mechanism is not clear.The purpose of this study was to explore the potential role of miR-27b in the sensitivity of non-small cell lung cancer cells to cisplatin.Objective:Explore the potential role of miR-27b in the sensitivity of NSCLC cells to cisplatin and its possible molecular mechanism.Methods:In this study,H1299/miR-27b,H1299/miR-NC and H1299/miR-27b cells overexpressing Snail in logarithmic phase were inoculated into 96-well plates,different concentrations of cisplatin were added 24 hours after culture,and the cell viability was detected by CCK-8 reagent after 72 hours of culture.Then 5μM cisplatin was selected for follow-up experiment.H1299/miR-27b,H1299/miR-NC and H1299/miR-27b cells overexpressing Snail in logarithmic phase were inoculated into 96-well plate.After 24 hours of culture,5μM cisplatin was added respectively.At 24 hours,48 hours,72 hours,4 days and 5 days of culture,CCK-8 reagent was used to test the cell viability.Furthermore,the role of miR-27b and Snail in the apoptosis of lung cancer cells was explored by flow cytometry and caspase-3 activity detection kit.We inoculated H1299/miR-27b,H1299/miR-NC and H1299/miR-27b cells with overexpression of Snail in logarithmic phase into 6-well plates,and flow cytometry was used to test the apoptosis of cells treated with cisplatin and without cisplatin.Finally,H1299/miR-27b,H1299/miR-NC and H1299/miR-27b cells overexpressing Snail in logarithmic phase were inoculated into 6-well plates and treated with 5μM cisplatin and DMSO(control group)respectively.After collecting the cells,the 15min was lysed in an ice bath.After high-speed centrifugation 15min,the enzyme activity of caspase3 in the supernatant was determined by enzyme labeling instrument to reflect the level of apoptosis.Results:The results showed that H1299 cells overexpressing miR-27b were highly sensitive to CDDP,and the cell viability decreased gradually with the increase of cisplatin,while the viability of H1299 cells overexpressed by miR-27b decreased more significantly than that of H1299 cells expressed by miR-NC.It was also found that the growth rate of H1299/miR-27b cells treated with cisplatin was significantly slower,while the growth rate of H1299/miR-27b cells overexpressing Snail could be partially reversed,although the growth rate was slower than that of the control group,but faster than that of H1299/miR-27b cells group.There was no significant difference in the level of apoptosis among the three cell lines without cisplatin treatment,but the apoptosis level was significantly increased in H1299/miR-27b group after treatment with 5μM cisplatin for 48 hours,while that in H1299/miR-27b group with overexpression of Snail was significantly decreased.Caspase-3 is not only an enzyme in the family of proteases,but also a key enzyme in the process of apoptosis.Finally,the results showed that after 5μM cisplatin treatment,the caspase3 enzyme activity of H1299/miR27b group increased obviously,that is,the level of apoptosis increased significantly,while the H1299/miR-27b group with overexpression of Snail significantly decreased the level of apoptosis,which was accordant with the previous experimental results.Conclusion:The above studies show that miR-27b can increase the sensitivity of CDDP in H1299 cells,and this effect can be partially reversed by directly regulating Snail.It is concluded that miR-27b promotes the sensitivity of lung cancer cells to cisplatin through Snail.Part Ⅴ Animal level study on the effect of miR-27b on the growth of lung cancerBackground:MiRNA binds to the "seed sequence" of mRNA’s 3’-UTR,resulting in mRNA degradation or protein translation inhibition,which has been proved to be involved in a large number of molecular biological processes by regulating the expression of target genes.Previous studies have revealed that the expression level of miR-27b is related to many types of human malignant cancer,but there is still a lack of research on the mechanism of tumor inhibition and promotion in NSCLC,especially at the in vivo level.Our previous studies showed that:1)miR-27b can inhibit the proliferation and migration of lung cancer cells,and inhibit the EMT effect of lung cancer cells by up-regulating E-cadherin and down-regulating Vimentin,;2)Snail is the direct target gene of miR-27b.MiR-27b participates in the regulation of lung cancer cell invasion,EMT and cisplatin sensitivity through its target Snail,but it is not clear whether the level of miR-27b expression in vivo can be related to the occurrence and development of lung cancer.We will clarify whether in vivo level miR-27b can effectively inhibit the occurrence and development of lung cancer through subcutaneous tumorigenesis in nude mice.Objective:Investigate the effect of animal-level miR-27b on the occurrence and development of lung cancer.Methods:In this study,we studied whether the expression level of miR-27b in vivo can effectively inhibit the occurrence and development of lung cancer by subcutaneous tumorigenesis in nude mice and the expression level of Snail in tumor tissue.We selected 6-week-old BALB/c male nude mice and fed them without specific pathogen(SPF)for 5-7 days.The nude mice were randomly divided into two groups with 5 mice in each group.5 ×10～6 H1299/miR-27b stable cell lines or control cells were injected subcutaneously into the hind legs of nude mice.When the tumor was visible to the naked eye in 7-14 days,the length and width of the tumor were measured with Vernier caliper every 48 hours,and then the volume of the tumor was calculated:volume=0.5 × length × width 2,and the tumor volume growth curve was drawn.From the 14th day after inoculation,the tumor growth rate of the H1299/miR-27b group was significantly slower.On the 24th day,the tumor in the control group grew rapidly,resulting in insufficient blood supply to the tumor in nude mice,and ischemic necrotic tissue began to appear on the surface of the tumor.On the 24th day,the nude mice were killed,the tumor was stripped off,and the tumor was weighed and photographed.We further analyzed the expression of miR-27b target gene Snail in tumors.The necrotic part of the tumor was removed,and the total protein and RNA,were extracted and the expression of Snail was detected by westernblotting and qRT-PCR respectively.Results:The tumor weight in the miR-27b overexpression group was significantly lighter than control group,and the total amount of Snail protein in the tumors overexpressed by miR-27b was decreased.And the Snail of these tumors decreased by about 60%at the mRNA level.Conclusion:In summary,we found that the overexpression of miR-27b in the experimental model of subcutaneous tumorigenesis in nude mice inhibited the formation of subcutaneous tumor in nude mice,and the tumor growth rate was slow;at the molecular level,the expression of Snail,the target gene of miR27b,was also significantly inhibited in the tumor of miR-27b overexpression group,and the overexpression of miR-27b could significantly inhibit the growth of NSCLC tumor.General conclusion:(1)the expression of miR-27b in NSCLC tumor tissue and cell line is decreased,and it is involved in the occurrence and development of NSCLC as a tumor suppressor gene.(2)miR-27b inhibits tumor growth by directly binding to its 3’-UTR to inhibit the expression of Snail,thus inhibiting the proliferation,migration and EMT of NSCLC cells.(3)miR-27b increases the sensitivity of lung cancer to cisplatin by targeting Snail. |
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