scholarly journals SOX2 Knockdown with Sirna Reverses Cisplatin Resistance in NSCLC by Regulating APE1 Signaling

2021 ◽  
Author(s):  
Taiyu Chen ◽  
Ji Zhou ◽  
Peng-cheng Li ◽  
Chun-han Tang ◽  
Fang Yang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Binding Sites ◽  
Colony Formation ◽  
Cisplatin Resistance ◽  
A549 Cells ◽  
Underlying Mechanism ◽  
Luciferase Reporter ◽  
Sox2 Expression ◽  
Reporter Assays ◽  
Nsclc Patients

Abstract Objective: SOX2 is related to drug resistance in many types of cancer, including lung cancer, but the underlying mechanism is still not fully understood. Herein, we investigated the role of SOX2 and its regulatory signaling in cisplatin-treated non-small-cell lung cancer (NSCLC).Methods: Cisplatin-resistant NSCLC A549/CDDP cells, parental A549 cells and NCI-H460 cells were selected for experiments. The effects of SOX2 on cell viability, proliferation, and apoptosis were evaluated in vitro. Western blotting, real-time quantitative PCR (qPCR), immunohistochemistry (IHC), and luciferase reporter assays were used to investigate the underlying mechanism of SOX2. Kaplan-Meier survival analysis and the log-rank test were used to assess the relationship between SOX2 expression levels and patient survival.Results: A549/CDDP cells had marked resistance to cisplatin and stronger colony formation ability than A549 cells. The expression of SOX2 protein or mRNA in A549/CDDP cells was higher than that in A549 cells. Knockdown of SOX2 in A549/CDDP cells induced apoptosis by inhibiting colony formation and decreasing viability, but overexpression of SOX2 reversed these effects. Interestingly, Genomatix software predicted that the APE1 promoter has some SOX2 binding sites, while the SOX2 promoter has no APE1 binding sites. Furthermore, luciferase reporter assays proved that SOX2 could bind the promoter of APE1 in 293T cells. We further verified that SOX2 expression was not affected by small hairpin RNA against APE1 (shAPE1) in A549/CDDP cells. As expected, colony formation was obviously inhibited and apoptosis was strongly enhanced in A549/CDDP cells treated with SOX2 small-interfering RNA (siSOX2) alone or combined with CDDP compared with control cells. Meaningfully, SOX2 expression was variable in 45 advanced NSCLC patients, and patients with high expression of SOX2 survived longer than those with low expression of SOX2.Conclusion: siSOX2 overcomes cisplatin resistance in NSCLC by regulating APE1 signaling, providing a new therapeutic target for overcoming cisplatin resistance in NSCLC patients.

scholarly journals SOX2 knockdown with siRNA reverses cisplatin resistance in NSCLC by regulating APE1 signaling

2021 ◽  
Author(s):  
Taiyu Chen ◽  
Ji Zhou ◽  
Peng-cheng Li ◽  
Chun-han Tang ◽  
Fang Yang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Binding Sites ◽  
Colony Formation ◽  
Cisplatin Resistance ◽  
A549 Cells ◽  
Luciferase Reporter ◽  
Rank Test ◽  
Sox2 Expression ◽  
Reporter Assays

Abstract Objective SOX2 is related to drug resistance in many types of cancer, including lung cancer. Herein, we investigated the role of SOX2 and its regulatory signaling in cisplatin-treated non-small-cell lung cancer (NSCLC). Methods The effects of SOX2 on cell viability, proliferation, and apoptosis were evaluated in vitro. Western blotting, real-time quantitative PCR (qPCR), immunohistochemistry (IHC), and luciferase reporter assays were used to investigate the underlying mechanism. Kaplan-Meier survival analysis and the log-rank test were used to assess the relationship between SOX2 expression and patient survival. Results A549/CDDP cells had marked resistance to cisplatin and stronger colony formation ability than A549 cells. The expression of SOX2 protein or mRNA in A549/CDDP was higher than that in A549. Knockdown of SOX2 in A549/CDDP induced apoptosis by inhibiting colony formation and decreasing viability, but overexpression of SOX2 reversed these effects. Interestingly, Genomatix software predicted that the APE1 promoter has some SOX2 binding sites, while the SOX2 promoter has no APE1 binding sites. Furthermore, luciferase reporter assays proved that SOX2 could bind the promoter of APE1 in 293T cells. We further verified that SOX2 expression was not affected by shAPE1 in A549/CDDP. As expected, colony formation was obviously inhibited and apoptosis was strongly enhanced in A549/CDDP treated with SOX2 siSOX2 alone or combined with CDDP compared with control cells. Meaningfully, patients with high expression of SOX2 survived longer than those with low expression of SOX2. Conclusion siSOX2 overcomes cisplatin resistance by regulating APE1 signaling, providing a new target for overcoming cisplatin resistance in NSCLC.

scholarly journals Knockdown of Lncrna PVT1 Enhances Radiosensitivity in Non-Small Cell Lung Cancer by Sponging Mir-195

2017 ◽  
Vol 42 (6) ◽  
pp. 2453-2466 ◽  
Author(s):  
Dapeng Wu ◽  
Yong Li ◽  
Huixiang Zhang ◽  
Xigang Hu
Keyword(s):  
Lung Cancer ◽  
Colony Formation ◽  
Underlying Mechanism ◽  
Tumor Xenograft ◽  
Luciferase Reporter ◽  
Nsclc Patients ◽  
The Relationship ◽  
Variant Translocation

Background/Aims: Plasmacytoma variant translocation 1 (PVT1) exerts an oncogenic role in many tumors, including lung cancer. However, the roles of PVT1 in regulating radiosensitivity of NSCLC and its underlying mechanism are still unclear. Methods: Expression levels of PVT1 and miR-195 in NSCLC tissues and cells were examined by qRT-PCR. Effects of PVT1 and miR-195 on cell proliferation, apoptosis and colony formation abilities were assessed by MTT assay, flow cytometry and colony formation assay. Luciferase reporter assay was performed to confirm the relationship between PVT1 and miR-195. Tumor xenograft experiments were conducted to observe the effect of PVT1 on radiosensitivity of NSCLC in vivo. Results: PVT1 was negatively correlated with miR-195 expression in NSCLC tissues and associated with poor prognosis of NSCLC patients. Expression of PVT1 and miR-195 varied inversely after irradiation in NSCLC cells. PVT1 knockdown or miR-195 overexpression enhanced radiosensitivity of NSCLC in vitro by inhibiting proliferation and inducing apoptosis. PVT1 directly interacted with miR-195 and regulated its expression. Moreover, PVT1 knockdown improved radiosensitivity of NSCLC cells in vitro and in vivo by sponging miR-195. Conclusion: Knockdown of PVT1 enhances radiosensitivity of NSCLC by sponging miR-195, providing a novel therapeutic target to improve radiotherapy efficiency in NSCLC.

scholarly journals microRNA-1236-3p regulates DDP resistance in lung cancer cells

Open Medicine ◽  
2019 ◽  
Vol 14 (1) ◽  
pp. 41-51 ◽  
Author(s):  
Zhigang Wang ◽  
Limei Liu ◽  
Xiaofeng Guo ◽  
Chunmei Guo ◽  
Wenxia Wang
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Chemotherapy Resistance ◽  
A549 Cells ◽  
B Cell Lymphoma ◽  
Underlying Mechanism ◽  
Expression Level ◽  
Lung Cancer Cells ◽  
Luciferase Reporter ◽  
Direct Target Gene

AbstractLung cancer is a malignant tumor leading to the most cancer-related deaths worldwide. The treatment efficiency of lung cancer remains poor mainly due to chemotherapy drug resistance, including cisplatin. MicroRNAs (miRNAs) are closely related to chemotherapy resistance of tumor cells. Here, we illustrated the underlying mechanism of miR-1236-3p on the DDP resistance in lung cancer cells. In this study, we found that the expression level of miR-1236-3p was significantly decreased in lung cancer tissues and A549 cell line. In addition, the half maximal inhibitory concentration (IC50) of DDP in A549 cells was significantly lower than that in A549/DDP cells, while the expression level of miR-1236-3p was prominently down-regulated in A549/DDP cells. Combining the online tool TargetScan and a dual-luciferase reporter assay, tumor protein, translationally-controlled 1 (TPT1) was proved to be the direct target gene of miR-1236-3p. The MTT and flow cytometry assays demonstrated that up-regulation of miR-1236-3p could markedly inhibit A549/DDP cell proliferation but promote apoptosis, which could be significantly reversed by pcDNA3.1-TPT1 plasmids. Finally, we further demonstrated that miR-1235-3p could restrain the expression levels of TPT1, Pim-3, phosphate-Bcl-2-associated death promoter (p-BAD) and B-cell lymphoma-extra large (Bcl-XL) in A549/DDP cells, while the inhibition could be reversed by pcDNA3.1-TPT1 as well. In a word, our study demonstrated that miR-1236-3p could reverse DDP resistance by modulation of TPT1 gene and inhibition of Pim-3 signaling pathway in lung cancer cells.

scholarly journals NBM-T-BMX-OS01, an Osthole Derivative, Sensitizes Human Lung Cancer A549 Cells to Cisplatin through AMPK-Dependent Inhibition of ERK and Akt Pathway

2015 ◽  
Vol 36 (3) ◽  
pp. 893-906 ◽  
Author(s):  
Tian-Jun Chen ◽  
Yue-Fei Zhou ◽  
Jie-Juan Ning ◽  
Tian Yang ◽  
Hui Ren ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Colony Formation ◽  
Human Lung ◽  
Cisplatin Resistance ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Ros Generation ◽  
Fluorescence Staining ◽  
Inhibition Of Proliferation

Background: Drug combination therapies using cisplatin and natural products are common practice in the treatment of human lung cancer. Osthole is a natural compound extracted from a number of medicinal plants and has been shown to exert strong anticancer activities with low toxicity. Methods: In the present study, NBM-T-BMX-OS01 (BMX), derived from the semi-synthesis of osthole, was evaluated in cisplatin treated A549 cells to investigate its effect on cisplatin resistance in human lung cancer. The anticancer effect of BMX were measured by cell viablity‚ colony formation‚ TUNEL staining‚ flow cytometry and cell cycle assay. The fluorescence staining was performed to detect intracellular and mitochondrial reactive oxygen species (ROS) generation. Western blot analysis, antagonists pretreatment and small interfering RNA (siRNA) transfection were used to determine the potential mechanism. Results: It was found that, in comparison with single cisplatin treatment, the combination of BMX and cisplatin resulted in greater efficacy in inhibition of proliferation and colony formation, apoptosis induction and cell cycle arrest. The results of fluorescence staining showed that the combination effect of BMX and cisplatin was due to oxidative stress induced by mitochondrial ROS generation. In addition, BMX significantly attenuated the phosphorylation of ERK and Akt, two important pro-survival kinases. In contrast, BMX inhibited the activation of AMPK, and knockdown of AMPK using specific siRNA partially reversed BMX-induced inhibition of ERK and Akt, as well as its synthetic effects on cisplatin induced anticancer activity in A549 cells. Conclusion: Taken together, this study provides that BMX might modulate cisplatin resistance through AMPK-ERK and AMPK-Akt pathways. These results also support the role of BMX as a potential drug candidate for use in combination with cisplatin in the treatment of human lung cancer.

scholarly journals Pseudogene KRT17P3 Drives Cisplatin Resistance of Human NSCLC Cells by Modulating miR-497-5p/mTOR

2020 ◽  
Author(s):  
Zhibo Hou ◽  
Qianwen Zhou ◽  
Ning Xia ◽  
Tang-feng Lv ◽  
Xiaoqin Yuan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Cisplatin Resistance ◽  
Annexin V ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Functional Interaction ◽  
Nsclc Patients

Abstract Background: Chemoresistance is a major obstacle in non-small-cell lung cancer (NSCLC) treatment. The pseudogene KRT17P3 has been shown to be up-regulated in lung cancer tissues from patients with cisplatin resistance. However, its molecular mechanism in promoting chemoresistance has not been elucidated.Methods: Real-time PCR was performed to evaluate KRT17P3 levels in plasma samples collected from 30 cisplatin-resistance patients and 32 cisplatin-sensitive patients. KRT17P3 was overexpressed or knocked down in A549 and SK-MES-1 NSCLC cells to evaluate the effects of KRT17P3 on the in vitro and in vivo resistance of NSCLC to cisplatin. Cell Counting Kit 8, Annexin V/propidium iodide staining, and PARP-1 cleavage assays were performed to evaluate cell viability and apoptosis. Dual luciferase reporter, RNA immunoprecipitation, Western blot assays, and rescue experiments were used to evaluate the functional interaction of KRT17P3, miR-497-5p and mTOR.Results: Our results demonstrate that KRT17P3 overexpression in cultured NSCLC cells increases cell viability and decreases apoptosis upon cisplatin treatment, while KRT17P3 knockdown has the opposite effect. KRT17P3 overexpression promotes NSCLC tumor growth upon in cisplatin-treated xenografted mice. Mechanistically, KRT17P3 acts as a molecular sponge for miR-497-5p and relieves the binding of miR-497-5p to its target gene mTOR. Rescue experiments validated the functional interaction among KRT17P3, miR497-5p, and mTOR. Moreover, the plasma level of KRT17P3 is up-regulated in cisplatin-resistance patients.Conclusions: Our findings indicate that KRT17P3/miR497-5p/mTOR regulates the chemosensitivity of NSCLC, suggesting a potential therapeutic target for cisplatin-resistant NSCLC patients. KRT17P3 may be a potential peripheral blood marker of NSCLC patients resistant to cisplatin.

scholarly journals Midazolam increases cisplatin-sensitivity in non-small cell lung cancer (NSCLC) via the miR-194-5p/HOOK3 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Tingting Sun ◽  
Jing Chen ◽  
Xuechao Sun ◽  
Guonian Wang
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Cisplatin Resistance ◽  
Small Cell ◽  
Luciferase Reporter ◽  
Small Cell Lung ◽  
Cisplatin Sensitivity

Abstract Backgrounds As previously reported, midazolam anesthesia exerts tumor-suppressing effects in non-small cell lung cancer (NSCLC), but the regulating effects of this drug on cisplatin-resistance in NSCLC have not been studied. Thus, we designed this study to investigate this issue and preliminarily delineate the potential molecular mechanisms. Methods We performed MTT assay and trypan blue staining assay to measure cell proliferation and viability. Cell apoptosis was examined by FCM. qRT-PCR and immunoblotting were performed to determine the expression levels of genes. The targeting sites between genes were predicted by bioinformatics analysis and were validated by dual-luciferase reporter gene system assay. Mice tumor-bearing models were established and the tumorigenesis was evaluated by measuring tumor weight and volume. Immunohistochemistry (IHC) was used to examine the pro-proliferative Ki67 protein expressions in mice tumor tissues. Results The cisplatin-resistant NSCLC (CR-NSCLC) cells were treated with high-dose cisplatin (50 μg/ml) and low-dose midazolam (10 μg/ml), and the results showed that midazolam suppressed cell proliferation and viability, and promoted cell apoptosis in cisplatin-treated CR-NSCLC cells. In addition, midazolam enhanced cisplatin-sensitivity in CR-NSCLC cell via modulating the miR-194-5p/hook microtubule-tethering protein 3 (HOOK3) axis. Specifically, midazolam upregulated miR-194-5p, but downregulated HOOK3 in the CR-NSCLC cells, and further results validated that miR-194-5p bound to the 3’ untranslated region (3’UTR) of HOOK3 mRNA for its inhibition. Also, midazolam downregulated HOOK3 in CR-NSCLC cells by upregulating miR-194-5p. Functional experiments validated that both miR-194-5p downregulation and HOOK3 upregulation abrogated the promoting effects of midazolam on cisplatin-sensitivity in CR-NSCLC cells. Conclusions Taken together, this study found that midazolam anesthesia reduced cisplatin-resistance in CR-NSCLC cells by regulating the miR-194-5p/HOOK3 axis, implying that midazolam could be used as adjuvant drug for NSCLC treatment in clinical practices.

scholarly journals Ovalitenone Inhibits the Migration of Lung Cancer Cells via the Suppression of AKT/mTOR and Epithelial-to-Mesenchymal Transition

Molecules ◽  
2021 ◽  
Vol 26 (3) ◽  
pp. 638
Author(s):  
Kittipong Sanookpan ◽  
Nongyao Nonpanya ◽  
Boonchoo Sritularak ◽  
Pithi Chanvorachote
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Colony Formation ◽  
Cancer Metastasis ◽  
Epithelial To Mesenchymal Transition ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Mesenchymal Transition

Cancer metastasis is the major cause of about 90% of cancer deaths. As epithelial-to-mesenchymal transition (EMT) is known for potentiating metastasis, this study aimed to elucidate the effect of ovalitenone on the suppression of EMT and metastasis-related behaviors, including cell movement and growth under detached conditions, and cancer stem cells (CSCs), of lung cancer cells. Methods: Cell viability and cell proliferation were determined by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazo-liumbromide (MTT) and colony formation assays. Cell migration and invasion were analyzed using a wound-healing assay and Boyden chamber assay, respectively. Anchorage-independent cell growth was determined. Cell protrusions (filopodia) were detected by phalloidin-rhodamine staining. Cancer stem cell phenotypes were assessed by spheroid formation. The proteins involved in cell migration and EMT were evaluated by Western blot analysis and immunofluorescence staining. Results: Ovalitenone was used at concentrations of 0–200 μM. While it caused no cytotoxic effects on lung cancer H460 and A549 cells, ovalitenone significantly suppressed anchorage-independent growth, CSC-like phenotypes, colony formation, and the ability of the cancer to migrate and invade cells. The anti-migration activity was confirmed by the reduction of filopodia in the cells treated with ovalitenone. Interestingly, we found that ovalitenone could significantly decrease the levels of N-cadherin, snail, and slug, while it increased E-cadherin, indicating EMT suppression. Additionally, the regulatory signaling of focal adhesion kinase (FAK), ATP-dependent tyrosine kinase (AKT), the mammalian target of rapamycin (mTOR), and cell division cycle 42 (Cdc42) was suppressed by ovalitenone. Conclusions: The results suggest that ovalitenone suppresses EMT via suppression of the AKT/mTOR signaling pathway. In addition, ovalitenone exhibited potential for the suppression of CSC phenotypes. These data reveal the anti-metastasis potential of the compound and support the development of ovalitenone treatment for lung cancer therapy.

BAI1 acts as a tumor suppressor in lung cancer A549 cells by inducing metabolic reprogramming via the SCD1/HMGCR module

2020 ◽  
Author(s):  
Lei Liu ◽  
Li Chai ◽  
Jingjing Ran ◽  
Ying Yang ◽  
Li Zhang
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Colony Formation ◽  
Warburg Effect ◽  
Poor Prognosis ◽  
A549 Cells ◽  
Angiogenesis Inhibitor ◽  
Metabolic Reprogramming ◽  
The Warburg Effect

Abstract Brain-specific angiogenesis inhibitor 1 (BAI1) is an important tumor suppressor in multiple cancers. However, the mechanisms behind its anti-tumor activity, particularly the relationship between BAI1 and metabolic aberrant of a tumor, remained unveiled. This study aimed to investigate whether BAI1 could inhibit biological functions in lung cancer A549 cells and the critical regulating molecules that induce metabolic reprogramming. Immunohistochemistry staining was performed to analyze whether variations in the expression of BAI1 in tumor tissues contributes to poor prognosis of lung cancer. Overexpressed BAI1 (BAI1-OE-A549) and control (Vector-NC-A549) were generated by lentiviral transfection. Biological function assays (proliferation, apoptosis, colony formation, invasion and in vivo metastasis), as well as metabolic reprogramming (by the Warburg effect and the glycolytic rate), were performed in both groups. Our results indicated that lower levels of BAI1 contributed to poor prognosis of lung cancer patients. Furthermore, overexpressed of BAI1 dramatically inhibited proliferation, migration, invasion, colony formation and in vivo metastasis of A549 cells. The Warburg effect and the Seahorse assay revealed that BAI1-OE induced metabolism reprogramming by inhibiting the Warburg effect and glycolysis. Further exploration indicated that BAI1 induced metabolic reprogramming by upregulating stearoyl-CoA desaturase 1 (SCD1) and inhibited 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR). Our study revealed a novel mechanism through which BAI1 acted as tumor suppressor by inducing metabolic reprogramming via the SCD1 and HMGCR module.

scholarly journals Emetine Synergizes with Cisplatin to Enhance Anti-Cancer Efficacy against Lung Cancer Cells

2019 ◽  
Vol 20 (23) ◽  
pp. 5914 ◽  
Author(s):  
Ti-Hui Wu ◽  
Shan-Yueh Chang ◽  
Yu-Lueng Shih ◽  
Tsai-Wang Huang ◽  
Hung Chang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Clinical Problem ◽  
Driver Mutations ◽  
Anticancer Efficacy ◽  
Lung Cancers ◽  
Anticancer Effects ◽  
Therapeutic Choice ◽  
Reporter Assays

Cisplatin is still the primary therapeutic choice for advanced lung cancers without driver mutations. The occurrence of cisplatin resistance is a major clinical problem in lung cancer treatment. The natural extracted agent emetine reportedly has anticancer effects. This study aimed to explore the possible role of emetine in cisplatin resistance. We used cell viability, Western blot, and Wnt reporter assays to show that emetine suppresses proliferation, β-catenin expression, and Wnt/β-catenin signaling in non-small cell lung cancer (NSCLC). The synergism of emetine and cisplatin was assessed by constructing isobolograms and calculating combination index (CI) values using the Chou-Talalay method. Emetine effectively synergized with cisplatin to suppress the proliferation of cancer cells. Furthermore, nuclear β-catenin and cancer stem cell-related markers were upregulated in the cisplatin-resistant subpopulation of CL1-0 cells. Emetine enhanced the anticancer efficacy of cisplatin and synergized with cisplatin in the cisplatin-resistant subpopulation of CL1-0 cells. Taken together, these data suggest that emetine could suppress the growth of NSCLC cells through the Wnt/β-catenin pathway and contribute to a synergistic effect in combination with cisplatin.

scholarly journals MiR-7-5p suppresses tumor metastasis of non-small cell lung cancer by targeting NOVA2

2019 ◽  
Vol 24 (1) ◽  
Author(s):  
Haiping Xiao
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Tumor Metastasis ◽  
Underlying Mechanism ◽  
Small Cell ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Small Cell Lung

Abstract Background Non-small cell lung cancer (NSCLC) is the leading cause of cancer mortality worldwide. Distant metastasis is thought to be one of the most important factors responsible for the failure of NSCLC therapy. MicroRNA-7-5p (miR-7-5p) has been demonstrated to be a tumor suppressor in breast cancer, hepatocarcinoma, prostate cancer and glioblastoma multiforme (GBM). However, its role in NSCLC is still not fully understood. This study evaluated the role of miR-7-5p in the progression of NSCLC and explored the underlying mechanism. Materials & methods The quantitative real-time PCR (qPCR), MTT, migration and invasion assays were used to evaluate the effects of miR-7-5p on the proliferation, migration and invasion of A549 and SPCA-1 cells. A tumor xenograft model was created to determine the effects of miR-7-5p on metastasis in vivo. The dual-luciferase reporter gene, neuro-oncological ventral antigen 2 (NOVA2) overexpression and western blotting assays were performed to explore the underlying mechanism. Results MiR-7-5p is downregulated in NSCLC tissues and lung cancer cell lines. It suppresses proliferation, migration, invasion and EMT marker expression in vitro and in vivo. Further study showed that miR-7-5p suppresses tumor metastasis of NSCLC by targeting NOVA2. Overexpression of NOVA2 attenuates the miR-7-5p-mediated inhibitory effect on lung cancer cells. Conclusion MiR-7-5p suppresses NSCLC metastasis. Targeting miR-7-5p may contribute to the success of NSCLC therapy.

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