scholarly journals Exosome Component 4 Promotes Epithelial Ovarian Cancer Cell Proliferation, Migration, and Invasion via the Wnt Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Chang Xiong ◽  
Zhongfeng Sun ◽  
Jinjin Yu ◽  
Yaying Lin
Keyword(s):  
Ovarian Cancer ◽  
Protein Expression ◽  
Epithelial Ovarian Cancer ◽  
Cyclin D1 ◽  
Cell Lines ◽  
Wnt Pathway ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Expression Levels ◽  
E Cadherin

BackgroundOf gynecologic malignancies, ovarian cancer is the leading cause of death, mainly due to the lack of sensitive tumor markers, which means it almost always presents at an advanced stage. Exosome Component 4 (EXOSC4) is involved in RNA degradation, but its role in epithelial ovarian cancer (EOC) is unclear.MethodsThe expression levels of EXOSC4 in EOC and normal ovarian tissue specimens were determined by immunohistochemical staining. The overall survival (OS) and progression-free survival (PFS) of patients with EOC were evaluated after patients were classified into high and low EXOSC4 expression groups, and the Cox regression model was established to identify independent predictors of patient prognosis. The effects of EXOSC4 on proliferation, colony formation, migration, and invasion were examined in the SKOV-3 and HO8910 cell lines by lentivirus-mediated shRNA knockdown. Flow cytometry was used to detect cell cycle changes. The mRNA levels of cyclin D1, CDK4, and c-myc were detected by RT-PCR. The protein expression levels of β-catenin, cyclin D1, CDK4, c-myc, vimentin, N-cadherin, and E-cadherin were assessed by western blot. Wnt/β-catenin activation was measured by TCF/LEF reporter assay.ResultsEXOSC4 was significantly elevated in EOC tissues and cell lines. High EXOSC4 expression was correlated with the International Federation of Gynecology and Obstetrics (FIGO) stage and pathological grade, and identified as an independent predictor of shorter OS and PFS. EXOSC4 knockdown suppressed proliferation, migration, and invasion in EOC cell lines. Cells were arrested at G0/G1 phase after EXOSC4 knockdown. The mRNA levels of cyclin D1, CDK4, and c-myc were decreased. β-catenin, cyclin D1, CDK4, c-myc, vimentin, and N-cadherin protein expression levels were reduced, while those of E-cadherin was increased. Wnt/β-catenin activity was suppressed after the EXOSC4 knockdown.ConclusionsEXOSC4 is involved in EOC. Knockdown of EXOSC4 can inhibit the proliferation, migration, and invasion ability of EOC by suppressing the Wnt pathway. EXOSC4 is expected to be a novel biomarker and molecular target in EOC.

scholarly journals NANOG regulates epithelial–mesenchymal transition and chemoresistance in ovarian cancer

2017 ◽  
Vol 37 (1) ◽  
Author(s):  
Shan Qin ◽  
Yanfang Li ◽  
Xuexia Cao ◽  
Jiexian Du ◽  
Xianghua Huang
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Cell Lines ◽  
Mesenchymal Cell ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Mesenchymal Transition ◽  
Cell Markers ◽  
Nanog Expression ◽  
E Cadherin

A key transcription factor associated with poor prognosis and resistance to chemotherapy in ovarian cancer is NANOG. However, the mechanism by which NANOG functions remains undefined. It has been suggested that epithelial-to-mesenchymal transition (EMT) also contributes to development of drug resistance in different cancers. We thus determined whether NANOG expression was associated with EMT and chemoresistance in epithelial ovarian cancer cells. NANOG expression was increased in epithelial ovarian cancer cell lines compared with its expression in normal epithelial ovarian cell lines. NANOG expression in SKOV-3 or OV2008 cells directly correlated with high expression of mesenchymal cell markers and inversely with low expression of epithelial cell marker. RNAi-mediated silencing of NANOG in SKOV-3 reversed the expression of mesenchymal cell markers and restored expression of E-cadherin. Reversibly, stable overexpression of NANOG in Moody cells increased expression of N-cadherin whereas down-regulating expression of E-cadherin, cumulatively indicating that NANOG plays an important role in maintaining the mesenchymal cell markers. Modulating NANOG expression did not have any effect on proliferation or colony formation. Susceptibility to cisplatin increased in SKOV-3 cells on down-regulating NANOG and reversible results were obtained in Moody cells post-overexpression of NANOG. NANOG silencing in SKOV-3 and OV2008 robustly attenuated in vitro migration and invasion. NANOG expression exhibited a biphasic pattern in patients with ovarian cancer and expression was directly correlated to chemoresistance retrospectively. Cumulatively, our data demonstrate that NANOG expression modulates chemosensitivity and EMT resistance in ovarian cancer.

Red Raspberry Extracts Inhibit A549 Lung Cancer Cell Migration, Invasion, and Epithelial-Mesenchymal Transition Through the Epidermal Growth Factor Receptor/Signal Transducer and Activator of Transcription-3 Signaling Pathway

2021 ◽  
Vol 11 (3) ◽  
pp. 439-444
Author(s):  
Jiayi Ren ◽  
Lifang Wang ◽  
Jia Fu ◽  
Chunyang Wang ◽  
Yan Gong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Cyclin D1 ◽  
Signaling Pathway ◽  
A549 Cells ◽  
Advanced Lung Cancer ◽  
Migration And Invasion ◽  
Red Raspberry ◽  
A549 Lung ◽  
E Cadherin

The incidence and mortality of lung cancer ranks first among all malignant tumors in the world. Because it is relatively asymptomatic at early stages, most patients do not become aware of the disease until it has progressed to an advanced stage. Advanced lung cancer metastasis results in systemic cachexia and effective treatment becomes challenging, leading to poor response and outcome. Therefore, the development of new drugs for the treatment of lung cancer is paramount. In this study, A549 cells were treated with different concentrations of red raspberry extract and the proliferation, migration, and invasion of cells were evaluated. The results indicated that red raspberry extract reduced the proliferation, migration, and invasion of A549 cells. Western blot analysis was used to detect the expression of the cyclin D1, N-cadherin, vimentin, E-cadherin, EGFR, and STAT3 proteins. Treatment with red raspberry extract reduced the expression of cyclin D1, N-cadherin, vimentin, EGFR, and STAT3, whereas the expression of E-cadherin increased. Following transfection of an EGFR overexpression vector into A549 cells, we observed a reduced inhibitory effect of the red raspberry extract on the proliferation, migration, and invasion of A549 cells. In addition, EGFR overexpression abrogated the increased expression of cyclin D1, N-cadherin, vimentin, EGFR, and STAT3 protein expression in A549 cells following extract treatment. In contrast, E-cadherin protein expression was decreased under these treatment conditions. Overall, this study suggests that red raspberry extract may reduce the proliferation, migration, invasion, and epithelialmesenchymal transition of A549 lung cancer cells by inhibiting the activation of the EGFR/STAT3 signaling pathway. These findings may lead to the development of new strategies to treat advanced lung cancer.

scholarly journals Upregulation of cyclase-associated actin cytoskeleton regulatory protein 2 in epithelial ovarian cancer correlates with aggressive histologic types and worse outcomes

2020 ◽  
Vol 50 (6) ◽  
pp. 643-652 ◽  
Author(s):  
Masataka Adachi ◽  
Yohei Masugi ◽  
Ken Yamazaki ◽  
Katsura Emoto ◽  
Yusuke Kobayashi ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Actin Cytoskeleton ◽  
Epithelial Ovarian Cancer ◽  
Cell Lines ◽  
Regulatory Protein ◽  
Control Cell ◽  
Type I ◽  
Type Ii ◽  
Expression Levels ◽  
Histologic Types

Abstract Objective Cyclase-associated actin cytoskeleton regulatory protein 2 (CAP2) regulates actin dynamics to control cell cycles and cell migration. CAP2 overexpression contributes to cancer progression in several tumor types; however, the role of CAP2 expression in ovarian cancer remains unclear. This study aimed to clarify the significance of CAP2 expression in epithelial ovarian tumor. Methods We evaluated CAP2 expression in ovarian cancer cell lines using quantitative real-time polymerase chain reaction, western blotting and immunocytochemistry and examined the effect of CAP2 silencing in migration and proliferation assays. CAP2 immunohistochemistry was conducted using tissue specimens from 432 ovarian carcinoma patients; a further 55 borderline and benign 65 lesions were analyzed. CAP2 expression levels were defined as low, intermediate or high, for correlation analysis with clinicopathological factors. Results CAP2 expression was significantly higher in cell lines from Type II ovarian cancer than in those in Type I, and knockdown of CAP2 showed decreased migration and proliferation. Higher levels of CAP2 expression in human tissues were associated with Type II histology, residual lesion, lymph node metastasis, ascites cytology and higher clinical stage. High CAP2 expression levels were observed in 26 (23.4%) of 111 Type II ovarian cancers and in 16 (5.0%) of 321 Type I cancers but not in any borderline or benign lesions. Multivariate analyses showed that CAP2 expression in ovarian cancer is an independent prognostic factor for recurrence-free survival (P = 0.019). Conclusion CAP2 expression is upregulated in aggressive histologic types of epithelial ovarian cancer and serves as a novel prognostic biomarker for patient survival.

scholarly journals Silencing of the TROP2 gene suppresses proliferation and invasion of hepatocellular carcinoma HepG2 cells

2019 ◽  
Vol 47 (3) ◽  
pp. 1319-1329 ◽  
Author(s):  
Jian Zhang ◽  
Hai Ma ◽  
Liu Yang ◽  
Hongchun Yang ◽  
Zhenxing He
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Cell Lines ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Human Trophoblast ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
Proliferation And Invasion

Objectives Overexpression of human trophoblast cell surface antigen 2 (Trop2) has been observed in many cancers; however, its roles in proliferation, apoptosis, migration, and invasion of hepatocellular carcinoma (HCC) remain unclear. Thus, this study aimed to characterize the function of Trop2 in HCC. Methods Trop2 protein expression was detected by immunohistochemistry in HCC tissues. Cell proliferation, apoptosis, and invasion were respectively measured by CCK-8, flow cytometry, Transwell, and wound healing assays. Expression levels of epithelial–mesenchymal transition-related proteins and Trop2 protein in HCC cell lines were detected by western blotting after silencing of the TROP2 gene. Results Trop2 protein was highly expressed in HCC tissues and HCC cell lines. Trop2 mRNA and protein expression levels decreased in HepG2 and HCCLM3 cells after transfection with Trop2 siRNA. Silencing of the TROP2 gene in HepG2 and HCCLM3 cells strongly inhibited cell proliferation and migration, while enhancing cell apoptosis. Investigation of the molecular mechanism revealed that silencing of the TROP2 gene suppressed epithelial–mesenchymal transition of HepG2 and HCCLM3 cells. Conclusions The results of the present study may improve understanding of the role of Trop2 in regulation of cell proliferation and invasion, and may aid in development of novel therapy for HCC.

scholarly journals Melatonin suppresses chronic restraint stress-mediated metastasis of epithelial ovarian cancer via NE/AKT/β-catenin/SLUG axis

2020 ◽  
Vol 11 (8) ◽  
Author(s):  
Shixia Bu ◽  
Qian Wang ◽  
Junyan Sun ◽  
Xiao Li ◽  
Tingting Gu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Cancer Cells ◽  
Restraint Stress ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Chronic Restraint Stress ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
Tumor Tissues

Abstract Chronic stress has been shown to facilitate progression of epithelial ovarian cancer (EOC), however, the neuro-endocranial mechanism participating in this process still remains unclear. Here, we reported that chronic restraint stress (CRS) promoted the abdominal implantation metastasis of EOC cells and the expression of epithelial–mesenchymal transition-related markers in tumor-bearing mouse model, including TWIST, SLUG, SNAIL, and β-catenin. We observed that β-catenin co-expressed with SLUG and norepinephrine (NE) in tumor tissues obtained from nude mice. Further ex vivo experiments revealed that NE promoted migration and invasion of ovarian cancer cells and SLUG expression through upregulating expression and improving transcriptional function of β-catenin in vitro. A human phosphor-kinase array suggested that NE activated various kinases in ovarian cancer cells, and we further confirmed that AKT inhibitor reduced NE-mediated pro-metastatic impacts and activation of the β-catenin/SLUG axis. Furthermore, the expression levels of NE and β-catenin were examined in ovarian tumor tissues by using tumor tissue arrays. Results showed that the expression levels of both NE and β-catenin were associated with poor clinical stage of serous EOC. Moreover, we found that melatonin (MLT) effectively reduced the abdominal tumor burden of ovarian cancer induced by CRS, which was partially related to the inhibition of the NE/AKT/β-catenin/SLUG axis. Collectively, these findings suggest a novel mechanism for CRS-mediated ovarian cancer metastasis and MLT has a potential therapeutic efficacy against ovarian cancer.

Protein Expression Patterns of Candidate Genes Involved in Apoptosis and Cell Cycle Control in Genetic Subgroups of Chronic Lymphocytic Leukemia.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2796-2796
Author(s):  
Christof Schneider ◽  
Dirk Winkler ◽  
Meike Loddenkemper ◽  
Alexander Krober ◽  
Peter Lichter ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Protein Expression ◽  
Cyclin D1 ◽  
Candidate Genes ◽  
Cell Lines ◽  
Normal Karyotype ◽  
Lymphocytic Leukemia ◽  
Expression Levels ◽  
Protein Levels ◽  
Atm Protein

Abstract Chronic lymphocytic leukemia (CLL) is a heterogeneous disease with a highly variable clinical course. Genomic aberrations (such as 13q−, 11q−, +12q, 17p−) can be found in about 80% of CLL cases and define pathogenic as well as clinical subgroups. Similarly, the mutational status of the variable region of the immunoglobulin heavy-chain gene (VH) identifies subgroups with different maturation stage and clinical outcome. In this study protein expression levels of candidate genes involved in cell cycle and apoptosis control (p53, ATM, Akt1, PI3-K, p21, p27, cdk4, Cyclin-D1, D2, D3, Bax, Bcl-2, Apaf-1, Smac, XIAP, cIAP2, survivin) were examined by Western Blotting. A total of 87 CLL cases derived from the subgroups with 11q- (n=22), 17p-/p53 mutation (n=18), +12q (n=24), 13q- (n=8) or a normal karyotype (n=15) were studied and compared to the cell lines EHEB and JVM-2. VH-mutation status was available for 65 cases (unmutated n=48, mutated n=17). Due to limitations in sample availability not all proteins could be examined in all cases. A highly homogenous expression pattern for all the proteins studied was observed in the CLL subgroup with a normal karyotype. This pattern was independent of the VH-status. CLL samples with normal karyotype, +12q and 13q deletion showed equal levels of ATM as compared to EHEB and JVM-2. As compared to cases with a normal karyotype the ATM level within the 11q- subgroup was reduced in 5 cases and absent in 1 case among 11 evaluable 11q- cases. The 17p- subgroup was comprised of 3 cases with concomitant 17p- and 11q- and 15 cases with 17p- but no 11q-. The latter group showed ATM protein levels comparable to the levels of the normal karyotype group. In the group with 17p- and 11q- there was an ATM expression level similar to the groups with 17p- and normal karyotype in two cases while one case had a reduced ATM protein level comparable to the 11q- subgroup. All cases with 17p- exhibited a stronger expression of p53 as compared to the cell lines and all other cases, except for one case with normal karyotype and one with an 11q-. No p53 mutations could be detected in exons 5–9 by sequencing in these two cases. High levels of survivin protein were found in all cases with 17p- and/or 11q-, 13q-, +12q while the subgroup with a normal karyotype showed lower levels. High levels of cdk4 protein were expressed in cases with 17p-, 11q- and 13q- while cdk4 protein levels were low in the subgroup with +12q and normal karyotype. Regarding p21, p27, Bcl2, Bax, Smac, Apaf-1, Cyclin D1–D3, cIAP2, XIAP, Akt1 and PI3K no variation in the expression levels were observed across the genetic CLL subgroups. Comparing the CLL cases to the cell lines the differences in expression levels were found for the cell cycle regulators Cyclin D1, D2, D3, p21 and p27. While the cell lines showed strong protein levels for Cyclin D1, D2, D3 and p21, they were nearly absent in the CLL cases. Expression of p27 was higher in all CLL cases as compared to JVM-2 and EHEB. In conclusion, the 17q- subgroup was the only group with a high level of p53 protein expression indicating that p53 is the affected gene in this subgroup. In contrast, the ATM protein levels are reduced only in a part of the 11q- cases indicating a possible role of additional candidate genes. Cases with +12q and normal karyotype showed weak expression of cdk4 pointing out a possible function in these subgroups.

scholarly journals miR-301-3p directly regulates Cx43 to mediate the development of gastric cancer

2021 ◽  
Vol 49 (9) ◽  
pp. 030006052110331
Author(s):  
Shasha Liu ◽  
Yang Zhao ◽  
Huan Liu ◽  
Xing Zhao ◽  
Xingbin Shen
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Clinical Prognosis ◽  
Expression Levels ◽  
Reporter Assays ◽  
Cx43 Mrna ◽  
Development Of Gastric Cancer

Objective Identifying novel biomarkers involved in the development of gastric cancer (GC) can provide potential therapeutic strategies and improve clinical prognosis. miR-301-3p and Cx43 are reportedly dysregulated in GC. miR-301-3p and Cx43 interaction, and their functions in GC progression, are still poorly understood. Methods The expression levels of miR-301-3p and Cx43 in GC tissues and cell lines with various differentiation degrees were evaluated by RT-qPCR. The interaction between miR-301-3p and Cx43 was assessed by dual-luciferase reporter assays. CCK8 and Transwell assays were employed to assess the effects of the miR-301-3p- Cx43 axis on GC cell proliferation, migration, and invasion. Results Cx43 was significantly downregulated in GC tissues and cell lines, while miR-301-3p expression was negatively correlated with Cx43 mRNA levels. The expression levels of Cx43 and miR-301-3p were closely associated with the differentiation, TNM stage, vascular invasion, and lymph node metastasis status of GC patients. Cx43 overexpression could suppress the proliferation, migration, and invasion of GC cells. Cx43 mRNA is a direct target of miR-301-3p, and transfection of an miR-301-3p mimic could reverse the inhibitory effects of Cx43. Conclusion The miR-301-3p- Cx43 axis is involved in the development and progression of GC by affecting the proliferation, migration, and invasion of GC cells.

scholarly journals LINC01094/miR-577 axis regulates the progression of ovarian cancer

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Jing Xu ◽  
Ping Zhang ◽  
Huajun Sun ◽  
Yang Liu
Keyword(s):  
Ovarian Cancer ◽  
Cyclin D1 ◽  
Cell Lines ◽  
Cancer Biology ◽  
Biological Effects ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Gene Assay

Abstract Background Long intergenic non-coding RNA 01094 (LINC01094) is probably a novel regulator in cancer biology. This study aimed to probe into the function and mechanism of LINC01094 in ovarian cancer (OC). Methods Quantitative real-time polymerase chain reaction (qRT-PCR) assay was utilized to measure LINC01094 and miR-577 expressions in OC tissues and cell lines. Western blot was used to examine the expressions of epithelial-mesenchymal transition (EMT)-related proteins, β-catenin, c-Myc and cyclin D1. Cell counting kit-8 (CCK-8) and Transwell assays were used to detect the proliferation, migration and invasion of SKOV3 and 3AO cells, respectively. Eventually, dual-luciferase reporter gene assay was employed to detect the regulatory relationship between miR-577 and LINC01094. Results LINC01094 expression was elevated in OC tissues and cell lines. High LINC01094 expression was associated with higher FIGO stage, lymph node metastasis and the shorter overall survival rate in patients with OC. Meanwhile, LINC01094 knockdown inhibited OC cell proliferation, migration, invasion and EMT. In addition, miR-577 was demonstrated to be a direct downstream target of LINC01094 in OC and inhibition of miR-577 reversed the biological effects of LINC01094 knockdown on OC cells. Additionally, LINC01094 / miR-577 axis regulated the expressions of β-catenin, c-Myc and cyclin D1 in OC cells. Conclusion LINC01094 promotes the proliferation, migration, invasion and EMT of OC cells by adsorbing miR-577.

Radix Tetrastigma Hemsleyani Flavone Inhibits the Occurrence and Development of Ovarian Cancer Cells by Regulating miRNA-4458 Expression

2021 ◽  
Vol 11 (3) ◽  
pp. 478-484
Author(s):  
Ping Liu ◽  
Yanjuan Guo ◽  
Yanfang He ◽  
Yajuan Tang
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Cyclin D1 ◽  
Cancer Cells ◽  
Diagnostic Methods ◽  
Migration And Invasion ◽  
Skov3 Cell ◽  
Advanced Stage ◽  
P21 Protein

Ovarian cancer (OC) has been identified to have the highest mortality rate among gynecological tumors. Most patients are diagnosed at an advanced stage because of its asymptomatic nature and a lack of effective early diagnostic methods. Advanced-stage cancer cells are prone to metastasis which reduces the efficacy of standard therapies. Thus, we evaluated the effect of different concentrations of radix tetrastigma hemsleyani flavone (RTHF) on SKOV3 OC cells. Our findings indicated a significant inhibition in cell proliferation, migration, and invasion. RTHF treatment resulted in a significant increase in p21 protein expression, whereas the expression of cyclin D1, MMP-2, and MMP-9 has reportedly decreased. In addition, the expression of miRNA-4458 expression increased significantly in a dose-dependent manner. Co-transfection of miRNA-4458 mimics into SKOV3 cells revealed that overexpressed miRNA-4458 can increase SKOV3 cell proliferation and p21 protein expression. Reduced cell migration and invasion were also observed along with decreased expression of cyclin D1, MMP-2, and MMP-9. Furthermore, inhibition of miRNA-4458 expression reversed the RTHF effect on SKOV3 cell proliferation, migration, invasion, and cyclin D1, MMP-2, and MMP-9 expression. These results indicate that RTHF reduces the proliferation, migration, and invasion of OC cells, and the underlying mechanism is associated with the upregulation of miRNA-4458 expression. These findings provide a new treatment strategy for advanced OC.

Carbonyl Reductase 3-Antisense RNA 1 Negatively Regulates microRNA-337-3p Expression: Effects on Proliferation, Migration, and Invasion of Lung Cancer Cells

2021 ◽  
Vol 11 (3) ◽  
pp. 433-438
Author(s):  
Shining Lin ◽  
Xiufeng Zhang ◽  
Huifang Shi ◽  
Fahui Wang ◽  
Shan Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Protein Expression ◽  
A549 Cells ◽  
Migration And Invasion ◽  
High Morbidity ◽  
Cancer Cell Proliferation ◽  
Expression Levels ◽  
Cancer Tissues ◽  
E Cadherin

Lung cancer, a malignant tumor, is associated with high morbidity and mortality worldwide. We studied the influence and mechanism of CBR3-AS1 on lung cancer cell proliferation, migration, and infiltration. The expression of CBR3-AS1 and miRNA-337-3p were higher and lower (P < 0.05), respectively, in lung cancer tissues than in paracancerous tissues. After inhibiting the expression of CBR3-AS1, the OD value of A549 cells, cloning formation numbers, migrating and invasive numbers, N-cadherin protein expression levels were lower. The G0-G1 cell cycle periods was longer. The S cell cycle periods was shorter. The E-cadherin protein expression levels higher (P < 0.05 in all cases). CBR3-AS1 negatively regulated miRNA-337-3p expression in A549 cells (P < 0.05). After inhibiting the expression of CBR3-AS1 and miRNA-337-3p, the OD value of A549 cells was lower, cloning formation numbers, migrating and invasive numbers, N-cadherin protein expression levels were lower. The G0-G1 cell cycle periods was longer. The S cell cycle periods was shorter. The E-cadherin protein expression levels was higher (P < 0.05 in all cases). CBR3-AS1 expression was increased in lung cancer tissues, and interference with CBR3-AS1 expression could inhibit the proliferation, migration, and infiltration of lung cancer A549 cells by negatively regulating miRNA-337-3p.

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