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Malignant tumor is a major disease affecting human health. The nano-delivery system itself has a unique size effect and it can achieve tumor-targeted distribution of drug molecules, improve the therapeutic effect, and reduce the toxic and side effects on normal tissues and cells after functional modification. Patient-derived xenografts (PDX) models can be established by transplanting patient-derived cancer cells or small tumor tissue into immunodeficient mice directly. Compared with the tumor cell line model, this model can preserve the key features of the primary tumor such as histomorphology, heterogeneity, and genetic abnormalities, and keep them stable between generations. PDX models are widely used in drug evaluation, target discovery and biomarker development, especially providing a reliable research platform for the diagnosis and treatment evaluation of nano-delivery systems. This review summarizes the application of several common cancer PDX models in the evaluation of nano-delivery systems, in order to provide references for researchers to perform related research.
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Objective:To establish the patient derived xenograft (PDX) model of liver malignant tumor, analyze the related factors affecting the carcinogenesis of PDX model, and analyze the differences of biological characteristics between the primary tumor and PDX model.Methods:Fresh liver malignant tumor tissue samples were collected from the patients who received the surgery from the Tianjin First Central Hospital and the samples were inoculated subcutaneously into BALB/c-nu mice. The correlations between clinicopathological information and tumor formation rate were analyzed, and the pathological morphology and specific protein expression of PDX model and primary tumor were compared.Results:Thirty-three PDX models were successfully established from 63 cases of liver malignant tumors. The overall tumor formation rate was 52.4% (33/63), including 46.3% (25/54) of primary liver cancer and 88.9% (8/9) of liver metastasis. The main factors affecting the tumor formation rate were tumor pathological type, distant metastasis and TNM stage (all P<0.05). The pathological morphology and specific protein expression of PDX model and primary tumor were similar. Conclusion:The PDX model of liver malignant tumor was successfully constructed, and the tumor formation rate was high, and can maintain the biological characteristics of the primary tumor.
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Objective:To investigate the effect of lncRNA UCA1 on the radiosensitivity of in vitro cultured glioma cell lines SHG-44, U87 and U251 by regulating the miR-873-5p expression. Methods:The survival of glioma cells SHG-44, U87 and U251 treated with different radiation intensities (0, 2, 4, 6 and 8 Gy) was detected by colony formation assay. The expression levels of UCA1 in glioma cells SHG-44, U87 and U251 were measured by qRT-PCR. The radiation-resistant glioma cells U87 and U251 were selected for subsequent study. After silencing UCA1 expression and/or over-expressing miR-873-5p, the cell survival rate was detected by colony formation assay, and the cell apoptosis rate was determined by flow cytometry. The dual luciferase reporter gene assay and qRT-PCR were employed to verify the targeting relationship between UCA1 and miR-873-5p.Results:UCA1 was up-regulated in the radiation-resistant U87 and U251 cells. Silencing UCA1 or over-expressing miR-873-5p inhibited the survival of U87 and U251 cells, and promoted the cell apoptosis induced by radiation exposure. miR-873-5p was a target gene of UCA1, and UCA1 negatively regulated the expression of miR-873-5p. The inhibition of miR-873-5p could reverse the effect of silencing UCA1 on the radiosensitivity of glioma cells. Silencing UCA1 increased the inhibitory effect of radiation on the glioma cell U251 xenografts.Conclusion:Silencing UCA1 inhibits the survival of glioma cells and promotes the cell apoptosis by up-regulating the expression of miR-873-5p, thereby increasing the radiosensitivity of glioma cells.
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Head and neck cancer is the seventh common cancer in the world, and various existing treatment strategies provide modest benefit for most patients with head and neck cancer. Meanwhile, therapeutic strategies lacking molecular typing significantly hinder the development of individualized treatment for head and neck cancer. In recent years, connected by preclinical models, the novel ideal has gradually reached a consensus in terms of facilitating inter-transformation of clinical problems and basic achievements. As a bridge between basic research and clinical transformation, patient-derived xenografts (PDX) models precisely replicate genetic characteristics and tumor evolution, which are displaying great vitality in elucidating the mechanism of tumorigenesis and progression. Moreover, cohorts composed of several PDX models highlight the unique advantages of mice for drug screening and biomarker analysis for patients. This ideal preclinical model explores potential treatment strategies suited the ethical standards as much as possible for patients.
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Animals , Humans , Mice , Disease Models, Animal , Head and Neck Neoplasms , Heterografts , Xenograft Model Antitumor AssaysABSTRACT
Non-small-cell lung cancer (NSCLC) is a complex disease which is influenced by multiple factors. Recentstudies demonstrated that long non-coding RNA (lncRNA) MIAT was involved in tumor metastasis. However,the underlying mechanism of MIAT in NSCLC remains largely unknown. In this study, MIAT, miR-139-5pand MMP2 expression were measured by quantitative reverse transcriptase PCR (QRT-PCR) or Westernblotting, respectively, and we found the expression of MIAT and MMP2 were elevated, while miR-139-5p wasdecreased in NSCLC tissues and cell lines. Transwell assay showed MIAT and MMP2 functioned as anoncogene to induce cell migration and invasion in NSCLC, but miR-139-5p served as a tumor suppressor inNSCLC to inhibit cell migration and invasion. Besides that, in vivo experiments also indicated MIAT deletioninhibited tumor growth. The relationship between miR-139-5p and MIAT or MMP2 was then confirmed byLuciferase reporter assay, and the results showed that MIAT directly interacted with miR-139-5p and miR-139-5p targetedly suppressed MMP2 in NSCLC cells. Furthermore, expression analysis showed that MIAT indirectly regulated MMP2 by sponging miR-139-5p. Finally, rescue assay suggested that miR-139-5p restorationreversed MIAT-overexpression-induced promotion on the migration and invasion of NSCLC cells. In conclusion, our results demonstrated that lncRNA MIAT modulated the migration and invasion of NSCLC byregulating miR-139-5p and MMP2.
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@#[Abstract] Objective: To investigate the effect and mechanism of sevoflurane on the proliferation and invasion of colon cancer SW480 cells and the growth of transplanted tumor in nude mice by regulating the phosphorylation of PI3K. Methods: Colon cancer SW480 cells were treated with sevoflurane and randomly divided into control group, 0.5% sevoflurane group, 1.0% sevoflurane group and 2.0% sevoflurane group for subsequent experiments. The proliferation ability of SW480 cells was detected by Clone formation assay, mRNA expression levels of MDM2 and survivin in cells were detected by RT-PCR, invasion ability of cells was detected by Transwell assay, and protein expression levels of MDM2, survivin, VEGF, PI3K, p-PI3K, AKT and p-AKT were detected by Western blotting. PI3K activator 740Y-P was added for verification. SW480 cell transplanted tumor model was constructed on nude mice, and the tumor mass was weighed. The positive expression rates of MDM2 and VEGF in the transplanted tumor tissues were detected by Immunohistochemistry. Results: As compared with the control group and the low-dose group, the clone formation rate of SW480 cells and the number of invaded cells in the 1.0% and 2.0% sevoflurane groups were significantly decreased (all P<0.01), the mRNA and protein levels of MDM2 in the cells were significantly increased (all P<0.01), while the mRNA and protein levels of survivin were significantly decreased (all P<0.01); and the protein levels of VEGF, p-PI3K/PI3K and p-AKT/AKT were significantly decreased (all P<0.01). 740Y-P could reverse the effect of sevoflurane on the proliferation, invasion and expression of proteins associated with the PI3K/AKT signaling pathway in SW480 cells. The mass of transplanted tumor in 2.0% sevoflurane group was significantly decreased (P<0.01), and the positive MDM2 expression rate in tumor tissues was significantly increased (P<0.01), while the positive VEGF expression rate was significantly decreased (P<0.01). Conclusion: Sevoflurane inhibits the proliferation and invasion of colon cancer SW480 cells and the growth of xenografts in nude mice possibly by inhibiting PI3K phosphorylation.
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OBJECTIVE@#To investigate the effect of β-arrestin1 overexpression on tumor progression in a NCG mouse model bearing T-cell acute lymphocytic leukemia (T-ALL) Molt-4 cell xenograft.@*METHODS@#Molt-4 cells were tagged with firefly-luciferase (F-Luc) by lentiviral infection, and fluorescence intensity of the cells was detected using a luminescence detector. Molt-4 cell lines with β-arrestin1 overexpression or knockdown were constructed by lentivirus infection and injected the tail vein in sub-lethal irradiated NCG mice. Body weight changes and survival time of the xenografted mice were observed, and the progression of T-ALL in the mice was evaluated using an fluorescence imaging system. Sixteen days after xenografting, the mice were euthanatized and tumor cell infiltration was observed in the slices of the liver and spleen.@*RESULTS@#We successfully tagged Molt-4 cells with F-Luc and overexpressed or knocked down β-arrestin1 in the tagged cells. Bioluminescent imaging showed obvious luminescence catalyzed by F-Luc in Molt-4 cells. After injection of Molt-4-Luc cells into irradiated NCG mice, a gradual enhancement of luminescence in the xenografted mice was observed over time, while the body weight of the mice decreased. Compared with the control mice, the mice xenografted with β-arrestin1-overexpressing Molt-4 cells had significantly prolonged survival time ( < 0.001), while the survival time of the mice xenografted with Molt-4 cells with β- arrestin1 knockdown was significantly shortened ( < 0.001). Histological examination revealed fewer infiltrating tumor cells in the liver and spleen of the mice xenografted with β-arrestin1-overexpressing Molt-4 cells in comparison with the mice bearing parental Molt-4 cell xenografts.@*CONCLUSIONS@#β-arrestin1 overexpression suppresses tumor progression in mice bearing Molt-4 cell xenograft.
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Animals , Humans , Mice , Disease Progression , Heterografts , T-Lymphocytes , Transplantation, Heterologous , beta-Arrestin 1ABSTRACT
Objective@#Pancreatic ductal adenocarcinoma cancer (PDAC) is one of the leading causes of cancer-related death worldwide. Hence, the development of effective anti-PDAC therapies is urgently required. Patient-derived xenograft (PDX) models are useful models for developing anti-cancer therapies and screening drugs for precision medicine. This review aimed to provide an updated summary of using PDX models in PDAC.@*Data sources@#The author retrieved information from the PubMed database up to June 2019 using various combinations of search terms, including PDAC, pancreatic carcinoma, pancreatic cancer, patient-derived xenografts or PDX, and patient-derived tumor xenografts or PDTX.@*Study selection@#Original articles and review articles relevant to the review’s theme were selected.@*Results@#PDX models are better than cell line-derived xenograft and other models. PDX models consistently demonstrate retained tumor morphology and genetic stability, are beneficial in cancer research, could enhance drug discovery and oncologic mechanism development of PDAC, allow an improved understanding of human cancer cell biology, and help guide personalized treatment.@*Conclusions@#In this review, we outline the status and application of PDX models in both basic and pre-clinical pancreatic cancer researches. PDX model is one of the most appropriate pre-clinical tools that can improve the prognosis of patients with pancreatic cancer in the future.
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PURPOSE: Recurrence and chemoresistance (CR) are the leading causes of death in patients with high-grade serous carcinoma (HGSC) of the ovary. The aim of this study was to identify genetic changes associated with CR mechanisms using a patient-derived xenograft (PDX) mouse model and genetic sequencing. MATERIALS AND METHODS: To generate a CR HGSC PDX tumor, mice bearing subcutaneously implanted HGSC PDX tumors were treated with paclitaxel and carboplatin. We compared gene expression and mutations between chemosensitive (CS) and CR PDX tumors with whole exome and RNA sequencing and selected candidate genes. Correlations between candidate gene expression and clinicopathological variables were explored using the Cancer Genome Atlas (TCGA) database and the Human Protein Atlas (THPA). RESULTS: Three CR and four CS HGSC PDX tumor models were successfully established. RNA sequencing analysis of the PDX tumors revealed that 146 genes were significantly up-regulated and 54 genes down-regulated in the CR group compared with the CS group. Whole exome sequencing analysis showed 39 mutation sites were identified which only occurred in CR group. Differential expression of SAP25,HLA-DPA1, AKT3, and PIK3R5 genes and mutation of TMEM205 and POLR2A may have important functions in the progression of ovarian cancer chemoresistance. According to TCGA data analysis, patients with high HLA-DPA1 expression were more resistant to initial chemotherapy (p=0.030; odds ratio, 1.845). CONCLUSION: We successfully established CR ovarian cancer PDX mouse models. PDX-based genetic profiling study could be used to select some candidate genes that could be targeted to overcome chemoresistance of ovarian cancer.
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Animals , Female , Humans , Mice , Carboplatin , Cause of Death , Drug Therapy , Exome , Gene Expression , Genome , Heterografts , Odds Ratio , Ovarian Neoplasms , Ovary , Paclitaxel , Recurrence , Sequence Analysis, RNA , Statistics as TopicABSTRACT
Objective To observe the effect of hypoxia on the expression of epithelial growth factor receptor (EGFR) and cell apoptosis of breast and cervical cancer xenografts in nude mouse models.Methods The nude mouse models with MCF-7 and HeLa xenografts were established.The degree of hypoxia and EGFR expression were observed by confocal microscopy.The influence of EGFR expression on cell apoptosis under hypoxia was observed by TUNEL assay.Results EGFR expression was either up-regulated or down-regulated in the MCF-7 and HeLa cells with high degree of hypoxia.Furthermore,the degree of apoptosis was reduced in tumor tissues with high EGFR expression compared with that in those with low expression of EGFR.Conclusion The hypoxia in MCF-7 and HeLa cells exerts heterogeneous effect on EGFR expression.Under hypoxic conditions,EGFR exoression is negatively correlated with cell apoptosis.
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Objective Study on the effect of isocorydine in human cervical cancer Siha cells xenografts in nude mice , to explore the inhibition mechanism of isocorydine in cervical carcinoma .Methods Establishment of human cervical cancer Siha cells subcutaneous xenografts model in BALB /c (nu/nu) nude mice.When the average diameter of the transplanted tumor≥0.5 cm, mice were randomly assigned into control group and experimental group .In experimental group, the model was administered by intraperitoneal injection of different doses of isocorydaline .After 4 weeks, the tumor tissues were removed , the histopathological changes of the tumor were observed by HE staining , and the ex-pression of proteins in the tumor tissue were observed by immunohistochemical staining and Western blot .Results Compared with the control group , the tumor volume of experimental group was significantly decreased ( P<0.05);the cell morphology transformed from stem cells to epithelioid cells , and the expression of E-cadherin was significantly in-creased while the expression of HPV 16E6 and vimentin was decreased .Conclusions Isocorydine may inhibit the de-velopment of cervical cancer by inhibiting the expression of E 6 protein and EMT-related signaling pathway .
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Objective To establish a rat xenograft model of human uterine leiomyoma using immunosuppressive a-gent and provide a useful tool for the study on uterine leiomyoma. Methods Intragastric administration with immunosup-pressive agent mycophenolate mofetil(MMF)(40 mg/kg)was given to rats for two weeks before the surgery until the end of the experiment. 20 SPF female Wistar rats were randomly divided into 4 groups after abdominal transplantation of human leiomyoma tissues:group A received femoston containing 0.4 mg/kg estradiol and 2 mg/kg dydrogesterone, group B re-ceived estadiol 0.4 mg/kg,group C received dydrogesterone 2 mg/kg,and group D served as the control group, received distilled water 1 mL/200 g. All rat received the corresponding drugs once per day for 2 days. Samples were taken at 4 weeks after the surgery to observe the pathology of the tumor tissues. Results The modeling success rates were 90% in the group A,40 % in the group B,and 0% in the groups C and D. Conclusions Rat xenograft model of human leiomyoma can be successfully established using an immunosuppressive agent femostone with a high modeling success rate and low cost. It can be used as a new animal model for the study of transplanted leiomyoma.
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<p><b>OBJECTIVE</b>Escape from the body's immune response is a basic characteristic of lung cancer, and indoleamine-2,3-dioxygenase (IDO) plays a key role in mediating immune escape of non-small-cell lung cancer, which leads to recurrence and metastasis. Feiji Recipe, a compound Chinese herbal medicine, has the effect of stabilizing lesions and prolonging survival in patients with lung cancer. The purpose of this study was to investigate the mechanisms underlying the anticancer properties of Feiji Recipe.</p><p><b>METHODS</b>An orthotopic transplant model of mouse Lewis lung cancer, with stable expression of IDO gene, was established in C57BL/6 mice. Optical imaging was used to observe the effects of Feiji Recipe in the treatment of lung cancer in vivo. The effects of Feiji Recipe on the proliferation of mouse Lewis lung cancer cell line 2LL, 2LL-enhanced green fluorescent protein (2LL-EGFP) and 2LL-EGFP-IDO were investigated, and the apoptosis of T-cells was examined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide using flow cytometry. Chemical composition of Feiji Recipe was validated by high-performance liquid chromatography.</p><p><b>RESULTS</b>Compared to the control group, the survival of animals treated with Feiji Recipe was significantly prolonged (P = 0.0074), and the IDO protein level decreased (P = 0.0072); moreover, the percentages of CD4CD25 T-cells and Foxp3 T-cells were significantly decreased (P < 0.05). The molecular mechanism of Feiji Recipe against lung cancer may relate to the regulation of immune cells, such as T-cells and regulatory T-cells.</p><p><b>CONCLUSION</b>The molecular mechanism of Feiji Recipe in treatment of lung cancer is to restore the function of T-cells in the cancer microenvironment through interfering with the IDO pathway.</p>
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Animals , Humans , Male , Mice , Apoptosis , Carcinoma, Lewis Lung , Drug Therapy , Allergy and Immunology , Cell Proliferation , Disease Models, Animal , Drugs, Chinese Herbal , Growth Inhibitors , Indoleamine-Pyrrole 2,3,-Dioxygenase , Genetics , Allergy and Immunology , Lung Neoplasms , Drug Therapy , Allergy and Immunology , Mice, Inbred C57BL , T-Lymphocytes, Regulatory , Allergy and ImmunologyABSTRACT
This study aimed to investigate the feasibility of the establishment of a human cancer xenograft model using samples from computed tomography (CT)-guided percutaneous biopsy. Fresh tumor tissues obtained from 10 cancer patients by CT-guided percutaneous biopsy were subcutaneously inoculated into NOD-Prkdcem26Il2rgem26Nju (NCG) mice to establish human patient-derived tumor xenograft (PDTX) models. The formation of first and second generation xenografts was observed, and tumor volume was recorded over time. Tumor tissue consistency between the PDTX model and primary tumors in patients was compared using H&E staining and immunohistochemistry. Pharmacodynamic tests of clinically used chemotherapeutic drugs were conducted on second generation xenografts, and their effects on tumor growth and body weight were observed. CT-guided percutaneous biopsy samples were successfully collected from 10 patients with advanced cancers. The PDTX model was established in mice using tumor samples obtained from 4 cancer patients, including one small cell carcinoma sample, two adenocarcinoma samples, and one squamous cell carcinoma sample. The success rate was 40%. The obtained PDTX model maintained a degree of differentiation, and morphological and structural characteristics were similar to primary tumors. The pharmacodynamic test of chemotherapeutic drugs in the PDTX model revealed a therapeutic effect on tumor growth, as expected. CT-guided percutaneous biopsy samples can be effectively used to establish a PDTX model, and test these chemotherapy regimens.
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Humans , Animals , Male , Female , Middle Aged , Aged , Adenocarcinoma/pathology , Disease Models, Animal , Liver Neoplasms/pathology , Lung Neoplasms/pathology , Xenograft Model Antitumor Assays/methods , Antineoplastic Agents/pharmacokinetics , Deoxycytidine/analogs & derivatives , Deoxycytidine/pharmacokinetics , Feasibility Studies , Image-Guided Biopsy/methods , Mice, Inbred Strains , Organoplatinum Compounds/pharmacokinetics , Tomography, X-Ray Computed , Xenograft Model Antitumor Assays/instrumentationABSTRACT
In this paper, we summarize the major problems existing in establishing gastric cancer patient-derived xenograft ( PDX) models and its solutions, and introduce its advantages on screening targeted drugs. As many previous re?search emphasized on individual characteristics too much, we argue that we should pay more attention to the generality of what we are studying in order to analyze the genotype of PDX models before taking a targeted therapy.
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Objective To investigate the effects of nuclear factor-kappaB(NF-κB)/p65 signaling transduction on the apoptosis and expressions of apoptosis-related genes Bax in nude mouse lung tumour cell xenografts. Methods The nude mice Lewis lung carcinoma cell xenograft model was established,and then the mice were intraperitoneally injected with NF-κB/p65 small interfering RNA(siRNA). The apoptosis of xenografted tumor cells in nude mice was detected by TUNEL assay. Expressions of Bax mRNA and protein were detected by RT-PCR and Western blotting. Results The result of TUNEL assay demonstrated that p65 siRNA evidently evoked cell apoptosis. Compared to the PBS treatment group or the normal control mice,both mRNA and protein expression levels of Bax in tumor xenografts were significantly up-regulated. There were significant differences among three groups(P<0.05). Conclusion NF-κB/p65 subunit may play an essential role in cell apoptosis of Lewis lung tumor.
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Background and purpose: Current colorectal cancer patient-derived xenografts (PDXs) models were established by samples taken during surgery. However, metastatic colorectal cancer (mCRC) patients have less surgical opportunities, and it was difcult to obtain enough tumor fragment. The aim of the present study was to es-tablish mCRC PDXs by image-guided biopsy. Methods: A total of 12 patients with colorectal cancer who underwent surgery were included. All patients had recurrent lesions or metastatic lesions needed to be histologically confirmed, and none of them had contraindication to biopsy. Tumor tissues not required for clinical diagnosis were used to establish mCRC PDXs. Results: Seven PDXs grew sufficiently for transfer into mice. The success rate was 77.8%. Conclusion:The PDXs established by image-guided biopsy had the advantage of convenient operation, good reproducibility, high achievement ratio, short experimental periodicity and reliably retain specific genetic and morphological features of the primary patient tumors.
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Objective To explore the effects and mechanisms of ursolic acid on drug-resistant SKOV3/DDP ovarian carcinoma xenografts in nude mice. Methods The models of drug-resistant SKOV3/DDP ovarian carcinoma on athymic mouse were established and randomly divided into four groups with intraperitoneal injection of different drugs: blank control (0. 9%sodium chloride solution ) , cisplatin ( 4 mg·kg-1 ·d-1 ) , ursolic acid low dose ( 30 mg·kg-1 ·d-1 ) , and high dose (60 mg·kg-1·d-1). All drugs were injected at volumes of 10 mL·kg-1 perday for 15 days. The tumor volumes were measured during the process of drug treatment every three days. After 14 days, The tumorigenic rate and tumor inhibition rate were calculated. RT-PCR and Western blotting were performed to detect the expression of Bcl-2 and Bax. Results Anti-tumor rates of cisplatin group , low dose ursolic acid group, and high dose ursolic acid group was 33. 3%, 43. 3%, and 71. 0%, respectively. Bcl-2 expressions were down-regulated, while Bax expressions were up-regulated in all three groups. Conclusion Ursolic acid has some anti-tumor activity on cisplatin-resistant human ovarian cancer SKOV3 /DDP cell in nude mice. It can inhibit tumor growth with dose-effect relationship. The mechanism may be to suppress the expression of anti-apoptotic factor Bcl-2 and to increase the expression of apoptosis-promoting factors Bax.
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Cancer is a group of heterogeneous disease caused by diverse genomic alterations in oncogenes and tumor suppressor genes .Despite recent advances in high-throughput sequencing technologies and development of targeted therapies, novel cancer drug development is limited due to the high attrition rate from clinical studies .Patient-derived xenografts ( PDX) models are generated by implanting sectioned patient tumor fragments into immunodeficient mice .PDX models retain many of the key characteristics of patients ' tumors including histology , genomic signature , cellular heterogeneity , and drug responsiveness .These models cannot only serve as a platform for co-clinical trials by enabling the integration of clinical data , genomic profiles , and drug responsiveness data to determine precisely targeted therapies , but also be applied to the development of biomarkers for drug responsiveness and personalized drug selection .This review summarizes our current knowledge of this field , including methodologic aspects , applications in drug development , challenges and limitations , and utilization for precision cancer medicine .
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Objective: To study the effect of lentivirus-mediated integrin αVβ3-shRNA on tumor growth of mice with lung cancer xenograft. Methods: Lung cancer tissue, paracancer tissue and normal tissue were collected and integrin αVβ3 expression was detected; BALB/c nude mice were selected, divided into integrin αVβ3 knockdown group (KD group) and negative control group (NC group), and inoculated with cells stably infected by integrin αVβ3-shRNA lentivirus and cells stably infected by negative control-shRNA lentivirus, respectively, the growth of tumor tissue was continuously observed, and the number of apoptosis cells as well as the expression of angiogenesis, apoptosis and invasion genes in tumor tissue were detected. Results: mRNA content and protein content of integrin αVβ3 in lung cancer tissue were significantly higher than those in paracancer tissue and normal tissue; increasing trend of tumor tissue volume of KD group was weaker than that of NC group, and tumor volume at various points in time of KD group was lower than that of NC group; mRNA contents and protein contents of VEGF, FGF, EGF, Bcl-2, MMP-9, MMP-12 and MMP-13 in tumor tissue of KD group were lower than those of NC group, and apoptosis index as well as mRNA content and protein content of Bax were higher than those of NC group. Conclusions: The expression of integrin αVβ3 increases in lung cancer tissue, and lentivirus-mediated integrin αVβ3-shRNA can inhibit tumor growth of mice with lung cancer xenografts.