HMGB1 promotes the proliferation and invasion of oral squamous cell carcinoma via activating epithelial-mesenchymal transformation

This study aimed to investigate the role of high mobility group box-1 (HMGB1) expression in oral squamouscell carcinoma; HMGB1 promoted the proliferation and invasion of oral squamous cell carcinoma via activatingepithelial-mesenchymal transformation (EMT). In this study, RNA transfection was used to silence the expression ofHMGB1 in oral squamous cell carcinoma cells. CCK-8, cell clone formation and trans-well assays were used to detectthe proliferation and invasion of cells before and after HMGB1 silencing. qRT-PCR and Western blot were used todetect changes in EMT marker protein expression before and after transfection. HMGB1 was significantly higher inOSCC tissues than in adjacent tissues, and of the cell lines examined, HMGB1 was highest in SCC-9 cells. Additionally,HMGB1 silencing decreased SCC-9 cell proliferation and viability. Down-regulation of HMBG1 expression inhibitednot only the proliferation but also the invasion of SCC-9 cells. The expression of N-cadherin, Snail, and Slug, but notE-cadherin, were promoted after silencing HMGB1. The expression of HMGB1 in OSCC tissue and cell lines washigher, and HMGB1 silencing decreased SCC-9 cell proliferation and invasion, suggesting that HMGB1 has positiveeffects on OSCC development. Down-regulation of HMBG1 expression regulates EMT markers, suggesting thatHMBG1 promotes OSCC cell proliferation and invasion is likely to be associated with EMT activation.     

UCK2 promotes the proliferation,migration, and invasion of trophoblast cells in preeclampsia by activating the STAT3 pathway

Background: Preeclampsia (PE), characterized by hypertension and proteinuria, leads to serious maternal andinfant complications. Uridine-cytidine kinase 2 (UCK2) belongs to the UCK family, a class of enzymes that catalyzes theconversion of uridine and cytidine to monophosphate form. However, the role of UCK2 in PE has not been reported.Methods: The expression of UCK2 was detected in the placenta of PE patients and N(ω)-nitro-L-arginine methyl esterinduced PE mouse model. Through forced up-regulation or down-regulation of UCK2 in vitro, we examined the effects ofUCK2 on the proliferation, apoptosis, migration, and invasion of trophoblast cells. Stattic, the inhibitor of STAT3pathway, was used to investigate whether the STAT3 pathway mediates the biological function of UCK2 introphoblast cells. Results: The present study found that UCK2 showed low expression in the placenta of PE patientsand PE mouse model. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and flow cytometryassays verified that up-regulation of UCK2 promoted the proliferation of trophoblast cells, while the silence of UCK2suppressed cell proliferation. Besides, flow cytometry and TdT-mediated dUTP Nick-End Labeling assaysdemonstrated that knockdown of UCK2 resulted in apoptosis of trophoblast cells. The wound healing and transwellassays showed that the migration and invasion activities of the trophoblast cells were facilitated by the overexpressionof UCK2 and were blocked by the silence of UCK2. Furthermore, the expression of phosphorylated STAT3 wasincreased with the upregulation of UCK2 and decreased with the inhibition of UCK2. When the STAT3 pathway wasblocked by its inhibitor stattic, the promotion effects of UCK2 on trophoblast cells were suppressed. Conclusion:UCK2 promotes the proliferation, migration, and invasion of trophoblast cells, and these effects may be partlymediated by the activation of the STAT3 pathway.     

AKT regulates IL-1β-induced proliferation and activation of hepatic stellate cells

Background: Activated hepatic stellate cells (HSCs) are closely involved in the initiation, perpetuation, andresolution of liver fibrosis. Pro-inflammatory cytokine levels are positively correlated with the transition from liverinjury to fibrogenesis and contribute to HSC pathophysiology in liver fibrosis. Methods: In this study, we investigatedthe effect of the pro-inflammatory cytokine interleukin (IL)-1β on the proliferation and signaling pathways involvedin fibrogenesis in LX-2 cells, an HSC cell line, using western blotting and cell proliferation assays. Results: IL-1βincreased the proliferation rate and α-smooth muscle actin (SMA) expression of LX-2 cells in a dose-dependentmanner. Within 1 h after IL-1β treatment, c-Jun N-terminal kinase (JNK), p38, and nuclear factor-κB (NF-κB)signaling was activated in LX-2 cells. Subsequently, protein kinase B (AKT) phosphorylation and an increase in α-SMA expression were observed in LX-2 cells. Each inhibitor of JNK, p38, or NF-κB decreased cell proliferation, AKTphosphorylation, and α-SMA expression in IL-1β-treated LX-2 cells. Conclusion: These results indicate that JNK,p38, and NF-κB signals converge at AKT phosphorylation, leading to LX-2 activation by IL-1β. Therefore, the AKTsignaling pathway can be used as a target for alleviating liver fibrosis by the inflammatory cytokine IL-1β.     

Effects of polydatin on the proliferation,migration, and invasion of ovarian cancer

To investigate the effects of polydatin on the proliferation, migration, and invasion of ovarian cancer, thechange of proliferative ability, migration ability, and invasive ability of human ovarian cancer cell OVCAR-3, A2780,and HO-8910 was detected by using polydatin and up-regulating PI3K. The anticancer activity and mechanism ofpolydatin in ovarian cancer were analyzed. Polydatin could effectively inhibit the proliferation, migration, and invasionof OVCAR-3, A2780, and HO-8910, and inhibit the expression of PI3K protein. After the expression level of PI3Kprotein was up-regulated, the inhibitory effect of polydatin on the proliferative ability, migration ability, and invasiveability of OVCAR-3, A2780, and HO-8910 significantly decreased, suggesting that PI3K was the target of polydatin.Therefore, we concluded that polydatin could inhibit the proliferation, migration, and invasion of ovarian cancer cellsby inhibiting the expression of PI3K protein, which provides an experimental basis for polydatin in the treatment ofovarian cancer.     

Forkhead box protein O1 (FoxO1) regulates lipids metabolism and cell proliferation mediated by insulin and PI3K-Akt-mTOR pathway in goose primary hepatocytes

In order to explore the role of forkhead box protein O1 (FoxO1) in the lipid metabolism and cell proliferation, goose primary hepatocytes were isolated and incubated with insulin or PI3K-Akt-mTOR pathway dual inhibitor NVP-BEZ235, and then transfected with FoxO1 interference plasmid. The related parameters of lipid metabolism and cell proliferation were measured. The results firstly showed that FoxO1 interference increased the intracellular TG and lipids concentration (P < 0.05); and increased the proliferative index (PI), cell DNA synthesis, protein expression of Cyclin D1 in goose primary hepatocytes (P < 0.05). Secondly, the co-treatment of insulin and FoxO1 interference increased the mRNA level and protein content of Cyclin D1 (P < 0.05); however, there was no significant difference between the insulin treatment and the co-treatment of insulin and miR-FoxO1 interference in the intracellular TG and lipids concentration and PI (P > 0.05). Lastly, the decrease of intracellular TG and lipids concentration and PI induced by NVP-BEZ235 was up-regulated by FoxO1 interference significantly (P < 0.05). In summary, FoxO1 could regulate the lipids metabolism and cell proliferation mediated by PI3K-Akt-mTOR signaling pathway in goose primary hepatocytes. Further investigations are required to highlight the potential role of FoxO1 in the lipid metabolism and cell proliferation mediated by insulin in goose primary hepatocyte.     

Suspension state promotes extravasation of breast tumor cells by increasing integrin β1 expression

Mechanical microenvironment can strongly affect the metastatic efficiency of circulating tumor cells. However, the effect of suspension state on their extravasation and the mechanisms involved are still unclear. To explore the influence of suspension state on extravasation (including adhesion, spreading and transendothelial migration) of breast tumor cells and its relevant molecular mechanism, MDA-MB-231 cells were cultured on poly (2-hydroxyethyl methacrylate) coated 6-well plates to minic the suspension state. Suspension state promoted adhesion, spreading and transendothelial migration of MDA-MB-231 cells to EAhy926 endothelial cells (ECs) monolayer under both the static condition and 0.5 dyne/cm² flow shear stress (FSS). The number of cells adhered to ECs monolayer reached 2.15 (static condition, 3 d) and 1.67 (FSS, 3 d) times, and the number of migration reached 10.60 times, respectively, as compared to that in adhesion state. Moreover, MDA-MB-231 cells knockdown of integrin β1 provoked poor adhesion and transendothelial migration, as compared with MDA-MB-231 cells. But it made no difference in cell spreading. Our results implied the increasing expression of integrin β1 induced by suspension culture promoted the adhesion and transendothelial migration of MDA-MB-231 cells, but had no significant influence on their spreading.     

Silencing of long non-coding RNA CCHE1 inhibits the ovarian cancer SKOV3 cell invasion and migration and inactivates the p38-MAPK signaling pathway

Ovarian cancer (OC) is a major cause of cancer-related deaths among gynaecological malignancies. Emerging studiessuggest that the long non-coding RNA (lncRNA) may be the potential biomarker for the diagnosis and prognosis of the cancer.The current study was carried out to investigate the role of lncRNA CCHE1 silencing in OC cell invasion and migration.Expression of lncRNA CCHE1 in normal ovarian cell Hose and OC cell lines HO 8910, A2780 and SKOV3 was detected.LncRNA were transfected with siRNA, and then the proliferation of cells was detected by using MTT assay. Cell invasionand migration was measured by using Transwell assay and scratch test, respectively. The protein levels of E-cadherin,N-cadherin, ERK, p38-MAPK and the phosphorylation of ERK and p38-MAPK in cells after siRNA transfection weredetected by using Western blot analysis. Consequently, lncRNA CCHE1 expression was highly expressed in OC cell lines,especially in SKOV3 cells. siRNA1, siRNA2 and siRNA3 all decreased. lncRNA CCHE1 expression in SKOV3 cells andsiRNA2 showed the best silencing efficacy. Silencing of lncRNA CCHE1 decreased proliferation, invasion and migration,and reduced the protein levels of N-cadherin, ERK, p38-MAPK and the phosphorylation of ERK and p38-MAPK, whilereducing the protein level of E-cadherin in SKOV3 cells. Collectively, our study proved that the silencing of lncRNACCHE1 could inhibit SKOV3 cell invasion and migration via inactivating the p38-MAPK signaling pathway.     

Cardioprotective effect of ivabradine via the AMPK/SIRT1/PGC-1α signaling pathway in myocardial ischemia/reperfusion injury induced in H9c2 cell

Post-resuscitation myocardial dysfunction (PRMD) is the most severe myocardial ischemia-reperfusion injury(MIRI) and is characterized by difficult treatment and poor prognosis. Research has shown the protective effects of therational use of ivabradine (IVA) against PRMD; however, the molecular mechanisms of IVA remain unknown. In thisstudy, an ischemia-reperfusion injury (IRI) model was established using hypoxic chambers. The results demonstratedthat pretreatment with IVA reduced IRI-induced cytotoxicity and apoptosis. IVA attenuated mitochondrial damage,eliminated excess reactive oxygen species (ROS), suppressed IRI-induced ATP and NAD⁺, and increased theAMP/ATP ratio. We further found that IVA increased the mRNA levels of sirtuin 1 (SIRT1) and peroxisomeproliferator-activated receptor-γ coactivator 1α (PGC-1α) and upregulated the expression levels of phosphorylatedAMP-activated protein kinase (p-AMPK)/AMPK, SIRT1, and PGC-1α proteins. Interestingly, no change in AMPKmRNA levels was observed. Cardiomyocyte energy metabolism significantly changed after IRI. The aim of this studywas to demonstrate the cardioprotective effect of Ivabradine via the AMPK/SIRT1/PGC-1α signaling pathway inmyocardial ischemia/reperfusion injury-induced in H9c2 cell.     

STMN1 promotes the proliferation and inhibits the apoptosis of acute myeloid leukemiacells by activating the PI3K/Akt pathway

Recent studies have shown that the microtubule disrupting protein Stathmin 1 (STMN1) is differentiallyexpressed in AML patients and healthy control. The aim of this study was to explore the effects and molecularmechanism of STMN1 in AML. Here, the expression of STMN1 in peripheral blood cells (PBMCs) and bone marrowof AML patients and healthy volunteers was detected by RT-PCR and Western blot. STMN1 expression was regulatedby transfected with STMN1 overexpressed plasmid or shRNA in two human leukemia cell lines K562 and HL60. Cellproliferation was examined by CCK8 and Edu staining. Annexin V and TUNEL assays were applied to test cellapoptosis. Flow cytometry was used to test the cell cycle distribution. The activation of the PI3K signaling pathwayand the expression levels of cell cycle and cell apoptosis-related protein were determined by Western blot. In thisstudy, we found that STMN1 was overexpressed in PBMCs and bone marrow of AML patients. STMN1 expressionwas closely related to FAB subtypes, risk stratification, disease-free survival, and overall survival of AML. Functionalassays showed that overexpression of STMN1 in HL60 and K562 cells enhanced cell proliferation, decreased cellapoptosis, and caused G₁ phase arrest. In contrast, suppression of STMN1reduced cell proliferation and enhanced cellapoptosis in both HL60 and K562 cells. Moreover, the PI3K/Akt pathway was activated by STMN1, while suppressionof STMN1 dysregulated the PI3K/Akt pathway and upregulating the levels of caspases3 and Bax expression. Inconclusion, STMN1 was confirmed to promote the proliferation and inhibit the apoptosis of HL60 and K562 cells bymodulating the PI3K/Akt pathway. STMN1 might be a novel molecular target for treating AML.     

Overexpression of inhibin α (1-32) fusion protein promotes apoptosis and cell cycle arrest in a cervical cancer cell model (Hela cells)

Inhibins play important roles in the reproductive system. To evaluate whether inhibin α (1-32) fusion protein plays a role in cervical cancer growth, the plasmid pVAX-inhα was constructed and its effect on proliferation and apoptosis of the human cervical cancer cell line (Hela) was checked by flow cytometry and real-time PCR. The expression and localization of inhibin α protein were detected by RT-PCR and confocal microscopy which showed that inhibin α protein was expressed and localized in the nucleus of Hela cells. Over expression of inhibin α gene significantly induced cell apoptosis and ceased S phase of cell cycle. Furthermore, cell proliferation was significantly suppressed 96 h post-transfection and mRNA level of anti-apoptosis genes (Bcl-2, NFκB) were decreased but pro-apoptosis genes (Bax, wild type p53) and inhibin co receptor (TGFβR3) were increased, indicating that inhibin, through its co-receptor, might activate apoptotic and cell growth cascades which regulate proliferation and apoptosis in Hela cells. These results suggest that inhibin α (1-32) fusion protein, located in the cell nucleus, can regulate Hela cells growth and apoptosis by induction of apoptotic pathways such as NFκB, Bcl-2 and p53 families. These findings may have a significant impact on future research regarding cervical cancer cell lines     

Measurement method for the objective and early detection of the osteosarcoma tumors

This paper deals with the characterization, by means of measurement techniques typically used for ceramics and polymeric materials, of human bone samples affected by two aggressive tumors: osteolitic osteosarcoma and sclerotic osteosarcoma. These two common forms of osteosarcoma often affects children and young teenagers. To distinguish between healthy and diseased bone tissue, the Hydroxyapatite/Collagen ratio and the Hydroxyapatite composition (Calcium/Phosphorus molar ratio) are evaluated. The results allow two considerations to be drawn on the analysis of human bone samples. The first consideration is that the bone affected by osteosarcoma has a greater amount of Collagen with respect to the healthy one. This can be used to evaluate the pathologic status of bone tissues. The second consideration is that the Calcium/Phosphorus molar ratio is, with respect to the one of healthy bone, higher in bone tissue affected by osteolitic osteosarcoma, while is lower in the one affected by sclerotic osteosarcoma. On the basis of these considerations, a promising measurement method is proposed to support the early and objective detection of the osteosarcoma tumor and to distinguish between osteolitic and sclerotic forms. The proposed measurement method can be executed in a few minutes and by using few milligrams of bone tissue that can be drawn with a needle under local anesthesia.     

CDK5 inhibition promotes osteoblastic differentiation of MSCs and blocks the migration of osteosarcoma MG-63 cells

CDK5 belongs to the cyclin-dependent kinase family. CDK5 is multifunctional and plays an important role in neural differentiation. However, the role of CDK5 in osteoblastic differentiation remains unclear. The present study investigated functions and molecular mechanism of CDK5 in osteoblastic differentiation. It was found that, CDK5 inhibition promoted the expression of Runx2, ALP, OCN and OPN of MSCs and the mineralization of MC-3T3E1 cells and MSCs. CDK5 inhibition enhanced the development of F-actin, nuclear localization of β-catenin and YAP, as well as the expression of RMRP RNA. When F-actin was suppressed by Blebbistatin, the nuclear localization of YAP and β-catenin, and expression of RMRP RNA as well as Runx2 and ALP were decreased. These indicate Seliciclib promotes osteoblastic differentiation mainly by F-actin. Moreover, Seliciclib also suppressed the migration of MG-63, suggesting a potential application for Seliciclib in bone defect repair and inhibition of the migration of osteosarcoma cells after osteosarcoma surgical resection.     

Effect of Peroxiredoxin 1 on the biological function of airway epithelial cells and epithelial-mesenchymal transition

Peroxiredoxin 1 (PRDX1) participates in tumor cell proliferation, apoptosis, migration, invasion, and the epithelial-to-mesenchymal transition (EMT). This study aimed to investigate the effect of PRDX1 on the EMT of airway epithelial cells stimulated with lipopolysaccharide (LPS) and transforming growth factor-beta 1 (TGF-β1). PRDX1 overexpression significantly increased the proliferation and migration of human bronchial epithelial (BEAS-2B) cells, reduced cell apoptosis (p < 0.01), and induced EMT and collagen deposition by upregulating the expression of the matrix metallopeptidase (MMP)2, MMP9, α-smooth muscle actin (α-SMA), N-cadherin, vimentin and twist proteins and inhibiting E-cadherin expression (p < 0.05). PRDX1 overexpression promoted TGF-β1-mediated inhibition of cell proliferation and migration and significantly enhanced the TGF-β1-induced EMT and collagen synthesis (p < 0.05). Knockdown of PRDX1 inhibited cell proliferation, migration, EMT, and collagen synthesis (p < 0.01), reversed LPS-mediated inhibition of cell proliferation and migration, and significantly suppressed LPS-induced EMT and collagen synthesis (p < 0.01). The result indicating that PRDX1 may be involved in LPS/TGF-1-induced EMT and collagen synthesis in human bronchial epithelial cells.     

Temperature-dependent imaging of living cells by AFM

Characterization of lateral organization of plasma membranes is a prerequisite to the understanding of membrane structure-function relationships in living cells. Lipid-lipid and lipid-protein interactions are responsible for the existence of various membrane microdomains involved in cell signalization and in numerous pathologies. Developing approaches for characterizing microdomains associate identification tools like recognition imaging with high-resolution topographical imaging. Membrane properties are markedly dependent on temperature. However, mesoscopic scale topographical information of cell surface in a temperature range covering most of cell biology experimentation is still lacking. In this work we have examined the possibility of imaging the temperature-dependent behavior of eukaryotic cells by atomic force microscopy (AFM). Our results establish that the surface of living CV1 kidney cells can be imaged by AFM, between 5 and 37 degrees C, both in contact and tapping modes. These first temperature-dependent data show that large cell structures appeared essentially stable at a microscopic scale. On the other hand, as shown by contact mode AFM, the surface was highly dynamic at a mesoscopic scale, with marked changes in apparent topography, friction, and deflection signals. When keeping the scanning conditions constant, a progressive loss in the image contrast was however observed, using tapping mode, on decreasing the temperature.     

Single-cell sequencing analysis reveals the molecular mechanism of promotion of SCAP proliferation upon AZD2858 treatment

The Wnt/β-catenin signaling pathway is the main target of tooth regeneration regulation. Treatment of cells with AZD2858 stimulates the Wnt/β-catenin signaling pathway, yet the function of this pathway in tooth regeneration remains unclear. Here, we found that AZD2858 promotes the accumulation of β-catenin in the nuclei of stem cells from the apical papilla (SCAPs) and enhances cell proliferation. Single-cell sequencing was performed on SCAPs treated with AZD2858. Eight clusters were identified, namely SCAPs-CNTNAP2, SCAPs-DTL, SCAPs-MYH11, SCAPs-MKI67, SCAPs-CXCL8, SCAPs-TPM2, SCAPs-IFIT2 and SCAPs-NEK10. The pseudo-time trajectory analysis showed that AZD2858 enhanced the evolution of SCAPs from SCAPs-TMP2 clusters to SCAPs-MYH11, SCAPs-CNTNAPs and SCAPs-NEK10 clusters via up-regulation of PRKCA, SMURF2, MAGI2, RBMS3, EXT1, CAMK2D, PLCB4, and PLCB1. These results demonstrate that AZD2858 enhances the proliferation of SCAPs-TPM2 cluster by activating the non-canonical Wnt/β-catenin signaling pathway.     

Roles of cell adhesion molecules nectin and nectin-like molecule-5 in the regulation of cell movement and proliferation

In response to chemoattractants, migrating cells form protrusions, such as lamellipodia and filopodia, and structures, such as ruffles over lamellipodia, focal complexes and focal adhesions at leading edges. The formation of these leading edge structures is essential for directional cell movement. Nectin-like molecule-5 (Necl-5) interacts in cis with PDGF receptor and integrin alpha(v)beta(3), and enhances the activation of signalling molecules associated with these transmembrane proteins, which results in the formation of leading edge structures and enhancement of directional cell movement. When migrating cells come into contact with each other, cell-cell adhesion is initiated, resulting in reduced cell velocity. Necl-5 first interacts in trans with nectin-3. This interaction is transient and induces down-regulation of Necl-5 expression at the cell surface, resulting in reduced cell movement. Cell proliferation is also suppressed by the down-regulation of Necl-5, because the inhibitory effect of Necl-5 on Sprouty2, a negative regulator of the Ras signalling, is diminished. PDGF receptor and integrin alpha(v)beta(3), which have interacted with Necl-5, then form a complex with nectin, which initiates cell-cell adhesion and recruits cadherin to the nectin-based cell-cell adhesion sites to form stable adherens junctions. The formation of adherens junctions stops cell movement, in part through inactivation of integrin alpha(v)beta(3) caused by the trans-interaction of nectin. Thus, nectin and Necl-5 play key roles in the regulation of cell movement and proliferation.     

KIFC1 overexpression promotes prostate cancer cell survival and proliferation <i>in vitro</i> by clustering of amplified centrosomes via interaction with Centrin 2

Mitotic kinesin KIFC1 plays critical roles in mitosis by regulating the spindle length, pole formation, and known for clustering extra centrosomes in cancer cells. Centrosome clustering is associated with the survival of cancer cells, but this phenomenon remains obscure in prostate cancer (PCa). The present study demonstrated that PCa cells showed centrosome amplification and clustering during interphase and mitosis, respectively. KIFC1 is highly expressed in PCa cells and tumor tissues of prostatic adenocarcinoma (PAC) patients. Up-regulation of KIFC1 facilitated the PCa cell survival in vitro by ensuring bipolar mitosis through clustering the multiple centrosomes, suggesting centrosome clustering could be a leading cause of prostate carcinogenesis. Conversely, the silencing of KIFC1 resulted in normal centrosome number or multipolar mitosis by inhibiting the clustering of amplified centrosomes in PCa cells. Besides, knockdown of KIFC1 by RNAi in PCa cells reduced cancer cell survival, and proliferation. KIFC1 interacted with centrosome structural protein Centrin 2 in clustering of amplified centrosomes in PCa cells to ensure the bipolar mitotic spindle formation. Knockdown of Centrin 2 in PCa cells inhibited the centrosome amplification and clustering. Moreover, up-regulated KIFC1 promotes PCa cell proliferation via progression of cell cycle possibly through aberrant activation of cyclin dependent kinase 1(Cdk1). Therefore, KIFC1 can be a prognostic marker and therapeutic target of PCa for inhibiting the cancer cell proliferation.     

LncRNA LINC01772 promotes metastasis and EMT process in cervical cancer by sponging miR-3611 to relieve ZEB1

Cervical cancer (CC), has been identified as one of the most frequent malignant tumors all over the world,with high mortality in females. A growing number of investigations have confirmed that long noncoding RNAs(lncRNAs) play a crucial role in the progression of multiple cancers. Nonetheless, the biological function and regulatorymechanism of LINC01772 in CC haven’t been explored so far. In this study, LINC01772 expression was found to beupregulated in tissues and cells of CC. Knocking down LINC01772 suppressed CC cell proliferation, migration andepithelial-mesenchymal transition (EMT) process. Through molecular mechanism assays, LINC01772 was verifiedto be bound with miR-3611 and LINC01772 acted as a sponge for miR-3611. Zinc finger E-box binding homeobox 1(ZEB1) was a downstream target gene of miR-3611. ZEB1 was negatively regulated by miR-3611 but positively regulatedby LINC01772. Rescue assays confirmed that miR-3611 inhibitor or ZEB1 overexpression offset the inhibitive effectof LINC01772 depletion on cell proliferation, migration and EMT process in CC. In a word, our study validated thatLINC01772 promoted cell metastasis and EMT process in CC by sponging miR-3611 to upregulate ZEB1 expression,indicating that LINC01772 could serve as a new therapeutic target for patients with CC.