Effect of HMGB1 expression knockdown on invasion ability of breast cancer cells induced by TNF-α

AIM:To investigate the effect of high-mobility group box-1 (HMGB1) expression knockdown on the invasion ability of breast cancer cells induced by tumor necrosis factor-α (TNF-α). METHODS:HMGB1 siRNA was used to transfect into the breast cancer MDA-MB-231 cells. The expression of HMGB1 at mRNA and protein levels was determined by RT-qPCR and Western blot. After the MDA-MB-231 cells with HMGB1 expression knockdown were treated with TNF-α, the apoptosis rate was analyzed by flow cytometry, the cell invasion ability was measured by Transwell assay, and the cell migration ability was detected by cell scratch test. The protein expression of E-cadherin, MMP-2, N-cadherin, MMP-9 and Bax was determined by Western blot. RESULTS:The expression of HMGB1 at mRNA and protein levels in the MDA-MB-231 cells transfected with HMGB1 siRNA was significantly lower than that in the non-transfected cells (P<0.05). The apoptosis rate in the cells was increased after TNF-α treatment, and the cell invasion and migration abilities were also increased. The protein level of E-cadherin in the cells was decreased, the protein level of N-cadherin was increased, and the protein levels of MMP-2, MMP-9 and Bax were also increased (P<0.05). After the MDA-MB-231 cells with HMGB1 expression knockdown were induced by TNF-α, the apoptotic rate was increased, the invasion and migration abilities were decreased, the protein levels of E-cadherin and Bax were increased, and the protein levels of N-cadherin, MMP-2 and MMP-9 were decreased, as compared with the cells only induced by TNF-α without knockdown of HMGB1 expression (P<0.05). CONCLUSION:Knockdown of HMGB1 expression enhances the apoptosis of breast cancer cells induced by TNF-α, and inhibited the cell invasion, migration and epithelial-mesenchymal transition induced by TNF-α. The mechanism may be related with the changes of protein expression of MMP-2, MMP-9 and Bax.     

Effect of hirsutine on hypoxia-induced migration and invasion abilities in human breast cancer MCF-7 cells

AIM: To investigate the effect of hirsutine on hypoxia-induced migration and invasion abilities of human breast cancer MCF-7 cells and its possible mechanism. METHODS: CCK-8 assay was employed to detect the cytotoxic effect of hirsutine on the MCF-7 cells. Cell migration was observed by wound healing assay, and cell invasion ability was measured by Transwell invasion assay. Western blot was used to analyze the protein levels of hypoxia-inducible factor-1α (HIF-1α), Snail, E-cadherin and matrix metalloproteinase-9 (MMP-9). The mRNA levels of HIF-1α was detected by RT-PCR. RESULTS: Hirsutine remarkably reduced the cell viability from 32 μmol/L (P<0.05), and the IC₅₀ value was 62.82 μmol/L. In hypoxia state, MCF-7 cells showed more powerful capabilities of migration and invasion (P<0.05), higher protein levels of HIF-1α, Snail and MMP-9 (P<0.05), lower protein level of E-cadherin (P<0.05), and higher mRNA level of HIF-1α (P<0.05). These hypoxia-induced effects were all inhibited by hirsutine at 16 μmol/L (P<0.05), apart from the mRNA level of HIF-1α. CONCLUSION: Hirsutine inhibits hypoxia-induced migration and invasion in human breast cancer MCF-7 cells most likely via down-regulation of the protein levels of HIF-1α, Snail and MMP-9, and up-regulation of the protein level of E-cadherin.     

The suppressive effects of IFN-α on human gastric carcinoma cell line BGC-823

AIM:To observe the inhibitory effect of interferon-α (IFN-α) on the growth invasiveness and metastasis of human gastric carcinoma cell line BGC-823,and mechanism of its action.METHODS:We detected the influence of IFN-α on the proliferative ability of BGC-823 in cell culture system,the cell vitality with the MTT colorimetric assay,and the cell cycle with flow cytometer (FCM).The regulatory functions of IFN-α to the expression of E-cadherin and matrix metalloproteinase-2 (MMP-2) in tumor cells were estimated by immunohistochemical analysis (S-P).The ultrastructural changes of the junction among the tumor cells were observed under electron microscope.RESULTS:IFN-α can significantly inhibit the growth of human gastric carcinoma cell line BGC-823 in a dose-dependent manner.When the concentration of IFN-α was ≥106 U/L,the cell proliferation can be effectively suppressed，the suppression rate was ≥12.2%,and the blockage appeared at the phase of G1-S of the cell cycle.Under the induction of IFN-α,the expression level of the cell E-cadherin increased while the MMP-2 decreased.The changes on ultrastructure of the cells showed the increased adhesive junctions and the relative compact structure.CONCLUSION:IFN-α can suppress the growth of human gastric carcinoma cell line BGC-823 through its influence on cell cycle.IFN-α can regulate the expression of E-cadherin and MMP-2,make the cell junction closely,so that it has the potential on restricting the invasion and metastasis of gastric carcinoma cells.     

Effect of isoflavone genistein on activation and proliferation of mouse T cells in vitro

AIM: To study the effect of genistein on activation and proliferation of T cells, and explore the molecular mechanism of genistein. METHODS: Fluorescence conjugated monoclonal antibodies and flow cytometry were used to detect the express of CD69 and CD25 by activated T cells in vitro in response to Concanavalin (ConA )and Phorbol 12, 13-dibutyrate(PDB) or T cell proliferation stained by CFSE in response to PDB / Ionomycin or ConA. RESULTS: Genistein inhibited the expression of CD69 and CD25 in activated T cells in response to Con A in a concentration-dependent manner and in response to PDB in a high concentration. Genistein inhibited proliferation of T cells in both groups in a concentration-dependent manner. CONCLUSION: Genistein inhibited activation and proliferation of T cells in vitro in response to polyclonal stimulus, and it may hold potential as a new immunosuppressant.     

Effects of tangeretin on growth and invasion of human non-small-cell lung cancer cells

AIM: To study the influences of tangeretin (TGN) on the growth and invasion of non-small-cell lung cancer (NSCLC) cells, and to explore the molecular mechanisms. METHODS: The A549 cells were treated with different concentrations of TGN in vitro. The relative cell activity was determined by MTT assay. The apoptotic rate was analyzed by flow cytometry with Annexin V-FITC/PI staining. The number of the invasive cells was measured by Transwell assay. The mRNA expression of MMP-2 and MMP-9 was detected by RT-PCR, and the protein levels of Ki67, Cyt C, caspase-3, cleaved caspase-3, MMP-2, MMP-9, Akt, p-Akt and p-PI3K were determined by Western blotting analysis. RESULTS: TGN inhibited the proliferation of A549 cells in a dose-dependent manner (P<0.05) along with the low expression level of proliferation biomarker Ki67. TGN up-regulated the protein levels of Cyt C, caspase-3 and cleaved caspase-3 (P<0.01) and promoted the apoptosis of A549 cells in a dose-dependent manner. Moreover, TGN down-regulated the invasion-related molecules MMP-2 and MMP-9 at the mRNA and protein levels, and the number of invasive cells reduced with the increase in the concentration of TGN. The protein levels of p-Akt and p-PI3K in the A549 cells was reduced (P<0.05), and no difference of the cell viability in the cells treated with different concentrations of TGN was observed after blocking PI3K/Akt signaling pathway using LY294002. CONCLUSION: TGN inhibits the growth and invasion of A549 cells and promotes the cell apoptosis by potentially inhibiting PI3K/Akt signaling pathway activation. Therefore, this study will provide a new target for the prevention and control of NSCLC.     

The anticancer activity of genistein on implanted tumor of human primary gastric carcinoma cells in nude mice

AIM: To investigate the apoptosis of implanted tumor of primary human gastric cancer cells in nude mice induced by genistein and the relation between this apoptosis and expression of bcl-2 and bax.METHODS: Establishing a transplanted tumor model by injecting human primary gastric cancer cells into subcutaneous tissue of nude mice.The different doses of genistein (0.5mg/kg,1mg/kg and 1.5 mg/kg ) were directly injected beside tumor body respectively,for six times at an interval of two days.Then changes of tumor volume were measured continuously and tumor inhibition rate of each group was calculated.We observed the morphologic alteration by electron microscope,measured the apoptotic rate by TUNEL staining method,detected the expression of apoptosis-regulated gene bcl-2 and bax by immunohistochemical staining and RT-PCR.RESULTS: Genistein could significantly inhibit carcinoma growth when it was injected near the carcinoma.Genistein induced implanted tumors cells to undergo apoptosis with apoptotic characteristics by transmission electron microscope.The apoptosis index of above three groups was increased progressively.Positive rate of Bcl-2 protein of above three groups was decreased progressively and positive rate of Bax protein of above three groups was increased progressively by immunohistochemical staining.The density of bcl-2 mRNA decreased progressively and the density of bax mRNA increased progressively with elongation of time by RT-PCR.CONCLUSION: Genistein is able to induce the apoptosis of transplanted tumor cells.This apoptosis may be mediated by down-regulating bcl-2 and up-regulating bax mRNA and its protein.     

High mobility group box 1 protein promotes proliferation,migration and invasion of colon cancer cells

AIM: To investigate the expression of high mobility group box 1 protein (HMGB1) in colon can-cer cells, and to determine its regulatory roles in colon cancer cell proliferation, migration and invasion. METHODS: qPCR and Western blot were used to quantify the mRNA and protein expression levels of HMGB1 in human colon cancer SW620 cells and normal colonic epithelial FHC cells. HMGB1 shRNA was transfected into the SW620 cells to establish the stable HMGB1-downregulating colon cancer cells (shHMGB1 group), and negative control (shNC) group and blank control (blank) group were also set up. The proliferation, migration and invasion of the cells were determined by CCK-8 assay, colony formation experiment and Transwell chamber assays. Western blot was used to determine the protein levels of p-ERK, ERK, c-Myc, matrix metalloproteinase (MMP)-2/9, E-cadherin, N-cadherin, Bcl-2 and Bax. RESULTS: Both of the mRNA and protein levels of HMGB1 in colon cancer cells were higher than those in the normal colonic epithelial cells (P<0.05). HMGB1 gene was successfully knocked down in SW620 cells. Compared with blank group and shNC group, the proliferation, migration and invasion abilities of the cells in shHMGB1 group were significantly inhibited (P<0.05). The protein levels of MMP-2, MMP-9, N-cadherin, c-Myc, Bcl-2 and p-ERK were reduced notably, while the expression of Bax protein was increased (P<0.05) in shHMGB1 group compared with shNC group and blank group.CONCLUSION: HMGB1 effectively promotes the proliferation, migration and invasion of colon cancer cells through ERK/c-Myc signaling pathway.     

Effect of hypoxia on invasion and migration of lung carcinoma cells and its molecular basis

AIM: To investigate the effect of hypoxia on the invasion and migration of lung carcinoma cells. METHODS: Lung carcinoma cell H128 was exposed to normoxia (air, 5% CO₂), hypoxia (5% O₂,5% CO₂,90% N₂) or anoxia (95% N₂,5% CO₂) conditions for 48 hours. The migration ability of the cells was assayed by wound healing methods. The invasiveness ability was determined with HABM-HEM model. The cells exposed to hypoxia were inoculated under skin in nude mice, and then the growth of the tumor and the rate of metastasis to lymph node or lung were observed. The expression of E-cadherin and β1-integrin on the cells were also assayed by flow cytometry. RESULTS: Compared with normoxic group, the invasiveness and migration in hypoxic group were increased. The rates of tumorgenesis and metastasis to lung in anoxic group were evidently decreased. The expression of E-cadherin was decreased, and the expression of β1-integrin was increased in hypoxic group. In anoxia group, the invasiveness, migration, the expression of E-cadherin and β1-integrin were all decreased. CONCLUSIONS: Moderate hypoxia down-regulated the expression of E-cadherin, up-regulated the expression of β1-integrin, and increased the invasiveness and metastasis of carcinoma cells. Serious hypoxia decreased the expression of adhesive molecules, and the proliferation, invasiveness and migration were also decreased.     

Effect of formononetin on viability,migration and invasion of ovarian cancer cells in vitro

AIM To observe the effect of formononetin on the viability, migration and invasion of ovarian cancer cells, and to explore its mechanism. METHODS Human ovarian serous cystadenocarcinoma SKOV-3 cells were cultured in vitro. The cells were treated with formononetin at 0, 25, 50 and 100 μmol/L for 48 h. The cell viability was measured by MTS assay. The migration and invasion abilities of the SKOV-3 cells were detected by scratch wound assay and Transwell assay. RT-qPCR and Western blot were used to detect the mRNA and protein levels of E-cadherin and matrix metalloproteinase-9 (MMP-9). RESULTS The viability of SKOV-3 cells was decreased with the increase in the formononetin concentration compared with control group (P<0.01). The wound migration distance of the cells in 50 μmol/L formononetin group was less than that in control group (P<0.01). The number of invasive SKOV-3 cells across the Transwell sub-compartment was significantly decreased in 50 μmol/L formononetin group compared with control group (P<0.01). The mRNA and protein levels of E-cadherin in 50 μmol/L formononetin group were significantly higher than those in control group (P<0.01), while the mRNA and protein levels of MMP-9 in 50 μmol/L formononetin group were significantly lower than those in control group (P<0.01). CONCLUSION Formononetin inhibits the migration and invasion abilities of ovarian cancer SKOV-3 cells by increasing expression of E-cadherin and decreasing expression of MMP-9.     

Genistein inhibits proliferation of human oral cancer TCA8113 cells through suppression of VEGF expression

AIM: To investigate the effect of genistein on the proliferation of human oral cancer TCA8113 cells and to explore the underlying mechanisms.METHODS: The cell proliferation was examined by MTT assay, cell counting and colony formation assay. Western blotting was employed to examine the protein levels of vascular endothelial growth factor(VEGF), extracellular signal-regulated kinase(ERK) and p-ERK. RESULTS: Genistein significantly inhibited the proliferation of TCA8113 cells in a concentration-dependent fashion. Moreover, genistein dose-dependently decreased the protein levels of VEGF, ERK and p-ERK. The expression of VEGF was also blunted by U0126, a specific inhibitor of ERK. U0126 and axitinib, a VEGF receptor antagonist, both significantly inhibited the proliferation of TCA8113 cells. CONCLUSION: Genistein inhibits the proliferation of TCA8113 cells, which may be related to its inhibitory effect on ERK expression and activation, thus subsequently decreasing the expression of VEGF.     

Chronic hypoxia enhances aggressiveness of MCF-7 breast cancer cells through EMT

AIM: To investigate the effects of chronic hypoxia on the aggressiveness of MCF-7, a human breast cancer cell line, and the underlying mechanisms.METHODS: MCF-7 cells were cultured under hypoxia (1% O₂, 5% CO₂ and 94% N₂) or control (95% O₂ and 5% CO₂) condition. The viability, proliferation, and invasion and migration abilities of the MCF-7 cells were determined by MTT assay, CCK-8 assay, cell counting, and cell invasion and migration assays. Anchorage-independent growth and the alteration of cellular polarization of the MCF-7 cells were tested by soft agar colony formation assay and Matrigel-3D culture assay, respectively. The effects of chronic hypoxia on the growth and metastasis of MCF-7 cells in vivo were investigated by xenograft in nude mice. The morphological changes of the MCF-7 cells were observed under an inverted microscope. Hypoxia-induced alterations in the levels of hypoxia inducible factor-1 (HIF-1) and phosphorylated glycogen synthase kinase-3β (p-GSK-3β) as well as epithelial-mesenchymal transition (EMT) molecules, such as E-cadherin, N-cadherin, vimentin, matrix metalloproteinase (MMP)-3 and MMP-9, were determined by Western blot.RESULTS: Chronic hypoxia significantly increased the viability, proliferation, and invasion and migration abilities of MCF-7 cells in vitro, enhanced the anchorage-independent growth, facilitated cellular polarization alteration in Matrigel-3D culture, and promoted cancer metastasis in vivo. Hypoxia up-regulated HIF-1, activated GSK-3β, down-regulated E-cadherin and increased the protein levels of N-cadherin, vimentin, MMP-3 and MMP-9. CONCLUSION: Chronic hypoxia enhances the aggressiveness of breast cancer cells probably through EMT.     

Effect of PTEN gene overexpression on cell cycle and tumor invasion in a human ovarian carcinoma SKOV3 cell line

AIM:To investigate the role of phosphatase and tensin homology deleted on chromosome(PTEN) gene in the cell cycle and invasion ability of human ovarian carcinoma SKOV3 cell line in vitro. METHODS:Human ovarian carcinoma SKOV3 cells were transfected with a eukaryotic expression plasmid vector containing PTEN gene in vitro,and then the positive cell clones were selected and amplified. MTT method was used to observe the inhibitory rate,flow cytometry was used to detect the cycle of transfected PTEN cells and apoptosis level. Western blotting analysis was used to determine PTEN gene expression. The invasiveness of transfected cells were measured quantitatively by Matrigel invasion assays (Transwell chamber). RESULTS:The expression of PTEN mRNA in SKOV3 cells increased after transfection with PTEN gene. Flow cytometry showed that the percentage of cells in S phase increased,but that in G₂/M phase decreased. Invasiveness of SKOV3 was significantly decreased. CONCLUSION:The transfection of PTEN gene into SKOV3 cells can inhibit human ovarian carcinoma SKOV3 cell proliferation,invasion and induce SKOV3 cell apoptosis.     

Inhibitory effect of geinistein on apoptosis in hUVECs induced by MCP-1

AIM: To study the inhibitory effect of genistein on apoptosis in human umbilical vein endothelial cells (hUVECs) induced by monocyte chemotactic protein-1 (MCP-1). METHODS: The hUVECs were cultured in vitro and identified. Growth-arrested hUVECs were stimulated with genistein at different concentrations (0.1 μmol, 1.0 μmol, 10 μmol, 100 μmol) and co-treated with MCP-1 (10 μg/L). The survival rates of hUVECs were detected by MTT assay. The cell cycle and DNA content were detected by flow cytometry. To explore the possible mechanism of the genistein interventions, the expressions of Bcl-2, Fas and Bax proteins were detected by flow cytometry and Western blotting.RESULTS: Genistein increased the survival rate and the level of Bcl-2, inhibited Fas and Bax, decreased the ratios of apoptosis compared with MCP-1-induced hUVECs apoptotic group in a dose-dependent-manner. CONCLUSION: Genistein inhibits the apoptosis induced by MCP-1 and the inhibitory effect was relative to the dose of genistein. Its mechanism might be involved in the down-regulation of Fas and Bax expressions and the up-regulation of Bcl-2.     

Effects of lentivirus-mediated siRNA targeting IGF-1R on migration and invasion abilities of endometrial carcinoma cells

AIM:To investigate the down-regulation of insulin-like growth factor tgpe 1 receptor(IGF-1R) on the migration and invasion abilities of human endometrial cancer cell HEC-1B. METHODS:The siRNAs targeting IGF-1R gene were synthesized, cloned into a lentivirus expression vector and transfected into endometrial cancer HEC-1B cells(HEC-1B-KD group). The control cells(without virus transfection, HEC-1B-CON group) and negative virus transfection control cells(HEC-1B-NC group) were also set up. The gene silencing effect of siRNA targeting IGF-1R was determined by real-time PCR and Western blotting at mRNA and protein levels,respectively. The proliferation rate was detected by colony formation assay. The cell migration and invasion abilities were determined by Transwell experiment. The mRNA levels of matrix metalloproteinase(MMP)-2 and MMP-9 were measured by real-time PCR. RESULTS:The mRNA and protein levels of IGF-1R in HEC-1B-KD cells were significantly reduced by 81% and 91.5%, respectively(P<0.05). In anchorage-dependent growth by colony formation assay, HEC-1B-KD cells showed much less colonies than HEC-1B-CON cells and HEC-1B-NC cells. Compared with the control cells, knockdown of IGF-1R in HEC-1B cells resulted in significant reduction of cell motility. Down-regulation of IGF-1R in HEC-1B cells also significantly reduced the invasion potential(P<0.05). Down-regulation of IGF-1R substantially reduced the expression of MMP-2 and MMP-9 compared with the control cells. CONCLUSION:Knockdown of IGF-1R reduces the migration and invasion abilities of human endometrial cancer cells in vitro accompanied with a decrease in MMP-2 and MMP-9 expression.     

Linarin inhibits migration and invasion abilities of human breast cancer MDA-MB-231 cells through IKK/NF-κB signaling pathway

AIM: To investigate the effect of linarin (LIN) on the migration and invasion abilities of human breast cancer MDA-MB-231 cells and its underlying mechanism. METHODS: MCF-7, MDA-MB-231 and MCF-10A cells were cultured in vitro and treated with LIN at 5, 10, 20, 40, 80 and 160 μmol/L for 24 h, and the cell proliferation was measured by CCK-8 assay and colony formation assay. The protein levels of Snail, E-cadherin, matrix metalloproteinase-9 (MMP-9), IκBα, p-IKKα/β and p-p65 were determined by Western blot. RESULTS: LIN remarkably reduced the viability of MDA-MB-231 cells in a dose-dependent manner (P<0.05), and the IC₅₀ was 55.89 μmol/L for 24 h. LIN decreased the colony formation rate of MDA-MB-231 cells at the concentration of 20 μmol/L (P<0.05). After exposed to LIN at 5 μmol/L and 10 μmol/L for 24 h, the migration and invasion abilities of the MDA-MB-231 cells were significantly reduced (P<0.05), the protein expression levels of E-cadherin and IκBα were up-regulated (P<0.05), the protein expression levels of Snail and MMP-9 were down-regulated (P<0.05), and the phosphorylation levels of IKKα/β and p65 were decreased (P<0.05) in comparison with the control group. Meanwhile, IKK-16 (IKKα/β inhibitor) and PDTC (NF-κB inhibitor) also down-regulated the protein expression levels of Snail and MMP-9 (P<0.05), and up-regulated the protein expression level of E-cadherin (P<0.05). CONCLUSION: LIN down-regulates the protein expression levels of Snail and MMP-9, and up-regulates the protein expression level of E-cadherin most likely through inhibiting IKK/NF-κB signaling pathway, and ultimately lead to decreases in the migration and invasion abilities of MDA-MB-231 cells.     

Sinomenine inhibits viability,migration and invasion of human ovarian cancer SKOV3 cells

AIM:To investigate the effect of sinomenine on the viability, migration and invasion of human ovarian cancer SKOV3 cells and its possible mechanism. METHODS:The SKOV3 cells were treated with sinomenine at different concentrations for 12 h, 24 h and 48 h. CCK-8 assay was employed to detect the effects of sinomenine on the viability of the SKOV3 cells. Flow cytometry was used to analyze the cell cycle distribution. The cell migration and invasion abilities were measured by Transwell assay. Western blot was used to determine the protein levels of cyclin A, cyclin D1, E-cadherin and matrix metalloproteinase-9 (MMP-9). RESULTS:Sinomenine remarkably inhibited the viability of SKOV3 cells and IOSE80 cells in a time-dependent and dose-dependent manner (P<0.05), and the IC₅₀ values of 48 h were 2.12 mmol/L and 17.35 mmol/L, respectively. In a dose-dependent manner, sinomenine induced G₀/G₁ and S phase arrest in SKOV3 cells (P<0.05), suppressed the migration and invasion abilities of SKOV3 cells (P<0.05), down-regulated the protein levels of cyclin A, cyclin D1 and MMP-9 (P<0.05), and up-regulated the protein level of E-cadherin (P<0.05). CONCLUSION:Sinomenine inhibits the viability, migration and invasion of human ovarian cancer SKOV3 cells most likely via down-regulation of the protein levels of cyclin A, cyclin D1 and MMP-9, and up-regulation of the protein level of E-cadherin.     

Mechanism of microRNA-138-5p inhibiting proliferation,migration and invasion of lung cancer cells

AIM: To investigate the mechanism of microRNA-138-5p (miR-138-5p) inhibiting the proliferation, migration and invasion abilities of lung cancer cells.METHODS: The lung cancer A549 and H460 cells were transfected with miR-NC (control group) or miR-138-5p (experimental group). The bioinformatic analysis was performed to predict the target genes of miR-138-5p.The expression levels of miR-138-5p, forkhead box protein C1 (FOXC1) mRNA and vimentin mRNA were detected by RT-qPCR. The protein expression of FOXC1, vimentin, E-cadherin, N-cadherin and β-catenin was determined by Western blot. MTS method and colony formation assay were used to detect cell viability and proliferation ability. Wound healing assay and Transwell assay were used to detect cell migration and invasion ability.RESULTS: Over-expression of miR-138-5p significantly reduced the expression of FOXC1 and vimentin at mRNA and protein levels (P<0.05). The expression of E-cadherin and β-catenin were up-regulated and the expression of N-cadherin was down-regulated. The proliferation, migration and invasion abilities of the lung cancer cells were inhibited by the over-expression of miR-138-5p.CONCLUSION: miR-138-5p inhibits the proliferation, migration and invasion abilities of lung cancer cells by targeting FOXC1 and vimentin. It may be a potential target for lung cancer gene therapy.