Experimental study on the inhibitory effects of recombinant bee venom peptide on the malignant biological behavior of cervical cancer

Trichosanthin inhibits the proliferation of cervical cancer cells and downregulates STAT-5/C-myc signaling pathway

The study aimed to investigate the mechanism by which the sonic Hedgehog (SHH) gene silencing acts upon epithelial-mesenchymal transition (EMT), proliferation, invasion, and migration of cervical cancer (CC) cells via the Hedgehog signaling pathway. RT-qPCR and Western blotting were all employed to detect the SHH mRNA and protein expressions. HeLa and CasKi cells were cultured and subsequently divided into the blank, negative control (NC), and SHH-RNAi groups. A cell counting kit-8 (CCK-8) assay was utilized for cell proliferation. Cell migration and invasion ability were evaluated through scratching test and Transwell assay. The mRNA and protein expressions of the Hedgehog signaling pathway-related factors were detected using RT-qPCR and Western blotting, respectively. After tumor xenograft in nude mice, tumor growth was subsequently observed. SHH mRNA and protein expressions were greater in the SHH-RNAi group than in the blank and NC groups. Compared with the blank group and NC groups, the SHH-RNAi group displayed inhibited levels of proliferation, migration, invasion abilities, as well as a decreased in the Hh signaling pathway-related factors, as well as a reduction in the mRNA and protein expressions of N-cadherin and Vimentin, however, on the contrary increased expressions of E-cadherin were observed. Following tumor xenograft in nude mice, tumor growth was exhibited vast levels of inhibition, particularly in the SHH-RNAi group in comparison to the blank and the NC groups. During the study it was well established that SHH gene silencing suppresses EMT, proliferation, invasion, and migration of CC cells through the repression of the Hedgehog signaling pathway.

In recent years the anti-diabetic drug metformin has been shown to inhibit tumor growth, but the underlying mechanism is unclear. Our previous results showed that metformin can destroy the sponge effect of long-chain non-coding RNA MALAT1/miR-142-3p and inhibit the proliferation of cervical cancer cells. Metformin can inhibit the PI3K/Akt signaling pathway and synergizes with Nelfinavir to inhibit the proliferation and invasion of cervical cancer cells. In this study, we used iTRAQ-based proteomics, mass spectrometry-based targeted proteomics, immunoblotting, and bioinformatics to analyze the molecular mechanism by which metformin inhibits the proliferation and invasion of cervical cancer cells. We found that 53 proteins were differentially expressed in cervical cancer cells after metformin treatment, of which 20 were up-regulated and 33 were down-regulated. Bioinformatics analysis showed that the 53 differentially expressed proteins are negative regulators of receptor signaling that inhibit cell growth and are mainly enriched in cell growth and apoptosis signaling pathways. We performed PRM verification on 11 of the differentially expressed proteins and found that they were all associated with apoptosis. We also found that metformin up-regulated the expression of the tumor suppressor IGFBP7 to inhibit the proliferation and invasion of cervical cancer cells. Our results indicate that metformin mainly regulates the insulin signaling pathway and interferes with cell proliferation and apoptosis to inhibit proliferation and invasion of cervical cancer cells. These differentially expressed proteins may become new targets for the treatment of cervical cancer.

Cervical cancer seriously threatens both the health and life of women. We aimed to investigate whether RNA interference of long non-coding RNA (lncRNA) DCST1-AS1 could promote miR-874-3p expression to affect the proliferation, migration and invasion of cervical cancer cells. DCST1-AS1 expression levels in cervical cancer cells and transfection effects were detected by quantitative reverse transcriptase-polymerase chain reaction analysis. Proliferation, invasion and migration of cells were separately shown by cell-counting kit-8, wound healing and transwell assays, and relative protein expression was determined by western blot analysis. Dual-luciferase reporter and RNA immunoprecipitation assays verified the interaction of DCST1-AS1 and miR-874-3p. DCST1-AS1 expression was increased in cervical cancer tissues and cells. The DCST1-AS1 expression in Hela and SiHa cells was the highest, and so the cells were selected for the next experiment. Inhibition of DCST1-AS1 suppressed the proliferation, invasion and migration of cervical cancer cells and decreased the expression of KI67, proliferating cell nuclear antigen, matrix metalloproteinase (MMP)-2 and MMP-9. miR-874-3p expression was increased when cells were transfected with miR-874-3p mimic or shRNA-DCST1-AS1-1, and DCST1-AS1 expression was down-regulated when cells were transfected with miR-874-3p mimic. DCST1-AS1 can directly target miR-874-3p. Furthermore, inhibition of miR-874-3p could effectively alleviate the effect of inhibition of DCST1-AS1 with respect to the proliferation, invasion and migration of cervical cancer cells. Inhibition of DCST1-AS1 suppressed the proliferation, migration and invasion of cervical cancer cells by increasing miR-874-3p expression, which could be alleviated by the inhibition of miR-874-3p.

The purpose of the present study is to figure out the role of miRNA-148a (miR-148a) in growth, apoptosis, invasion, and migration of cervical cancer cells by binding to regulator of ribosome synthesis 1 (RRS1). Cervical cancer and adjacent normal tissues, as well as cervical cancer cell line Caski, HeLa, C-33A, and normal cervical epithelial cell line H8 were obtained to detect the expression of miR-148a and RRS1. Relationship between miR-148a and RRS1 expression with clinicopathological characteristics was assessed. The selected Caski and HeLa cells were then transfected with miR-148a mimics, miR-148a inhibitors or RRS1 siRNA to investigate the role of miR-148a and RRS1 on proliferation, apoptosis, colony formation, invasion, and migration abilities of cervical cancer cells. Bioinformatics information and dual luciferase reporter gene assay was for used to detect the targetting relationship between miR-148a and RRS1. Down-regulated miR-148a and up-regulated RRS1 were found in cervical cancer tissues and cells. Down-regulated miR-148a and up-regulated RRS1 are closely related with prognostic factors of cervical cancer. RRS1 was determined as a target gene of miR-148a and miR-148a inhibited RRS1 expression in cervical cancer cells. Up-regulation of miR-148a inhibited cell proliferation, migration, and invasion while promoting apoptosis in Caski and HeLa cells. Our study suggests that miR-148a down-regulates RRS1 expression, thereby inhibiting the proliferation, migration, and invasion while promoting cell apoptosis of cervical cancer cells.

Objective: To elucidate the impact of over-expression of S100A7 on migration, invasion, proliferation, cell cycle, and epithelial-mesenchymal transition (EMT) in human cervical cancer HeLa and CaSki cells. Methods: (1) Immunohistochemistry of SP was used to examine the expression of S100A7 in 40 cases of squamous cervical cancer tissues and 20 cases of normal cervical tissues. (2) The vectors of pLVX-IRES-Neo-S100A7 and pLVX-IRES-Neo were used to transfect human cervical cancer HeLa and CaSki cells, and the positive clones were screened and identified. Next, transwell migration assay, cell counting kit-8 (CCK-8) assay and fluorescence activating cell sorter (FACS) were used to detect the effect of S100A7-overexpression on the migration, invasion, proliferation and cell cycle of cervical cancer cells. Furthermore, western blot was performed to observe the expression of epithelial marker (E-cadherin) and mesenchymal markers (N-cadherin, vimentin, and fibronectin) of EMT. Results: (1) S100A7 expression was significantly higher in cervical squamous cancer tissues (median 91.6) than that in normal cervical tissues (median 52.1; Z=-2.948, P=0.003) . (2) Stable S100A7-overexpressed cells were established using lentiviral-mediated gene delivery in HeLa and CaSki cells. S100A7 was detected by real-time quantitative reverse transcription PCR, S100A7 mRNA of S100A7-overexpressed cells were 119±3 and 177±16, increased significantly compared with control groups of median (P<0.01) . Compared with the control cells, the number of S100A7-overexpressed HeLa and CaSki cells that passed the transwell membrane assay were increased significanatly (572±51 vs 337±25, P<0.01; 100±8 vs 41±4, P<0.01) .Matrigel invasion assay showed that the number of S100A7-overexpressed HeLa and CaSki cells that passed the transwell membrane were respectively 441±15 and 110±14, elevated significantly compared with control cells (156±21 and 59±7; P<0.05) . However, S100A7 overexpression didn't influence the proliferation and cell cycle progression of HeLa and CaSki cells (P>0.05) . Expression of E-cadherin was dramatically decreased, while N-cadherin, vimentin, and fibronectin increased in S100A7-overexpressed cells. Conclusion: S100A7 enhances the migration, invasion and EMT of HeLa cells and CaSki cells, and may be plays an important role in the development of cervical cancer.

Cervical cancer is the second most common gynecological cancer worldwide and remains one of the leading causes of cancer-associated mortality among women. S100A6 has been reported to be associated with the development of many types of cancer. The aim of the present study was to investigate the effect of S100A6 on the proliferation, apoptosis and migration of cervical cancer cells and its underlying molecular mechanisms. Quantative polymerase chain reaction (qPCR) was used to detect the basic mRNA level of S100A6 in HeLa, SiHa and CaSki cells. Western blot analysis was used to detect the protein level of S100A6, epithelial cadherin, neuronal cadherin, phosphorylated protein kinase B (p-Akt), t-Akt, p-glycogen synthase kinase 3β (GSK3β), t-GSK3β and β-catenin. Semi-qPCR was used to detect the mRNA level of Snail, Twist and Vimentin. MTT and Hoechst staining assays were used to detect the proliferation and apoptosis of cells, and wound healing and Transwell assays were used to detect the migration of cells. The results of the present study demonstrate that the levels of S100A6 were decreased in HeLa cells compared with in SiHa and CaSki cells. Overexpression of S100A6 in HeLa and CaSki cells promoted the proliferative and migratory ability, and had no significant effect on cellular apoptosis. Whereas the knockdown of S100A6 in SiHa and CaSki cells inhibited the proliferative and migratory ability, it had no significant effect on apoptosis. The overexpression of S100A6 in HeLa cells increased the levels of neuronal (N)-cadherin, vimentin, Snail and Twist. Conversely, knockdown of S100A6 in SiHa cells decreased the levels of N-cadherin, vimentin, Snail and Twist and increased the levels of epithelial (E)-cadherin. Furthermore, overexpression of S100A6 in HeLa cells activated the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, and treatment with the PI3K inhibitor LY294002 partially repressed S100A6-enhanced proliferation and migration of cervical cancer cells. These results indicate that S100A6 facilitates the malignant potential of cervical cancer cells, particularly metastatic ability and epithelial-mesenchymal transition, which is mediated by activating the PI3K/Akt signaling pathway.

Objective: To investigate the expression of Bcl-2 associated athanogene 3 (BAG3) in cervical cancer tissues and cells and its role in epithelial mesenchymal transition (EMT) of cervical cancer. Methods: (1) Cervical cancer samples were collected from September 2015 to March 2017 in the Qilu Hospital of Shandong University and Shangdong Provincial Hospital. While, 50 normal tissues were collected from August 2015 to March 2017 in the Dezhou Municiple Hospital, which were obtained from patients with uterine myoma underwent hysterectomy and patients with cervical biopsy. Reverse transcription (RT)-PCR and western blot were used to detect the expression of BAG3 mRNA and protein, and their clinical significances were analyzed. (2) The expression of BAG3 mRNA and protein was detected using RT-PCR and western blot method in HeLa and SiHa cell lines and normal cervical epithelial cells. The experiment was divided into two groups, BAG3 small interfering RNA transfected group (si-BAG3) and the control group transfected with small interfering RNA (siRNA). Cell counting kit 8 (CCK-8) analysis was used to detect cell proliferation of two groups. Wound-healing and transwell assay were used to detect the migration and invasion ability of HeLa and SiHa cells. The xenograft model of cervical cancer in nude mice was used to observe the effect of BAG3 on tumor xenografts and the tumor-related biomarkers were tested by western blot. Results: (1) The expression levels of BAG3 mRNA and protein in cervical carcinoma tissues were 1.20±0.15 and 1.10±0.16, which were significantly higher than that in normal cervical tissue, 0.23±0.04 and 0.29±0.03 (both P<0.01). The results showed that the expression levels of BAG3 mRNA and protein were significantly correlated with cervical carcinoma staging and lymph node metastasis (P<0.05).However, its expression was not correlated with the patient's age, pathological grade, and diameter of tumor (all P>0.05). (2) Compared with normal cervical epithelial cells, the expression of BAG3 mRNA and protein levels in HeLa and SiHa cells were significantly increased (P<0.01), the expression levels of BAG3 mRNA and protein in HeLa and SiHa cells transfected with si-BAG3 were significantly lower than that in control group (all P<0.01). After post-transfected 72 hours, A value of HeLa and SiHa with transfection were significantly lower than those in control group [(0.88±0.08) vs (1.22±0.13), (0.92±0.09) vs (1.35±0.12); both P<0.01]. After post-transfected 24 hours, the migration level of HeLa and SiHa cells with transfection were significantly lower than those in the control group [(20.1±2.1)% vs (58.6±5.6)%, and (21.1±2.1)% vs (61.7±5.4)%; both P<0.01]. The transmembrane cell number in HeLa and SiHa cells with transfection were 76±11 and 71±8, which were significantly less than those in control group (131±12 and 129±14; both P<0.01). After the inoculation into nude mice, tumor formation time of HeLa and SiHa cells with transfection were (9.5±0.5) and (10.5±1.3) days, respectively, which were significantly longer than those in control group [(4.5±0.5) and (5.2±1.1) days; both P<0.05]. Compared with those in the control group, the expression level of Slug, N-cadherin and matrix metalloproteinase-2 (MMP-2) protein in HeLa and SiHa cells with transfected in tumor tissues were significantly decreased (all P<0.01), while the expression level of E-cadherin protein was significantly increased (P<0.01). Conclusion: BAG3 could be involved in the proliferation, migration and invasion of cervical cancer cells by affecting cervical cancer EMT, and BAG3 may be an effective target for the treatment of cervical cancer.

The long non-coding RNA (lncRNA) NF-κB interaction lncRNA (NKILA) has been found to exert tumor suppressive effects in numerous types of carcinoma; however, the relationship between NKILA and cervical cancer (CC) remains largely unclear. The present study aimed to investigate the effects of NKILA on the proliferation and metastasis of CC cell lines, in addition to the related molecular mechanisms. Reverse transcription-quantitative PCR was used to detect the expression levels of NKILA in cancer tissues and cell lines. The constructed overexpression vector, pcDNA3.1NKILA, and its corresponding negative control sequence were transfected into CaSki cells and short hairpin RNA targeting NKILA and the corresponding negative control sequence were transfected into C-33A cells. Subsequently, the proliferative, migratory and invasive ability, as well as the process of epithelial-mesenchymal transition (EMT) of C-33 A and CaSki cells were analyzed by performing Cell Counting Kit-8, wound healing, Matrigel invasion and western blot assays, respectively. The expression levels of proteins were detected using western blot analysis. The expression levels of NKILA were decreased in CC tissues and CC cell lines (SiHa, C-33A, CaSki and HeLa) and the downregulation of NKILA expression using shRNA was observed to significantly increase the proliferation of CC cells. Conversely, the upregulation of NKILA inhibited the proliferation of CC cells, in addition to significantly inhibiting the migration and invasion of CaSki cells, whereas the knockdown of NKILA promoted the invasion of C-33A cells. Thus, it was hypothesized that NKILA may inhibit the migration and invasion of CC cells via regulation of EMT processes, which was reflected by the expression of ZO-1, E-cadherin, N-cadherin and Vimentin. Furthermore, the overexpression of NKILA significantly inhibited the activation of NF-κB in CaSki cells, whereas the knockdown of NKILA expression promoted the degradation of inhibitory protein-κB and promoted the transfer of p65 into the nucleus in C-33A cells. In conclusion, the results from the present study suggested that NKILA may be involved in the inhibition of migration and invasion in CC cells through regulating EMT processes, which may be related to its inhibition of NF-κB activation.

The oncogenic miR-21 has been widely recognized to promote the development and progression of various types of malignant tumors, but not cervical cancers. The aim of this study was to examine the expression of miR-21 and PTEN in cervical cancer specimens using quantitative PCR. The miR-21 level was then manipulated in the cervical cancer lines and the regulation of miR-21 on the proliferation, migration and invasion of cervical cancer cells was determined. Additionally, we determined the role of PTEN in the miR-21-regulated proliferation, migration and invasion of cervical cancer cells. miR-21 was upregulated in the cervical cancer specimens, negatively correlating with the PTEN mRNA level. Transfection of the miR-21 mimics was markedly promoted, whereas the miR-21 inhibitor suppressed the proliferation, migration and invasion of cervical cancer cells, with a significant inhibition of PTEN expression. In addition, the overexpression of PTEN markedly inhibited the proliferation and migration of the cervical cancer cells. The present study showed the upregulation of miR-21 in invasive cervical cancers, and confirmed the promotion of miR-21 with regard to the proliferation, migration and invasion in cervical cancer cells via inhibiting the PTEN expression. To the best of our knowledge, this is the first study to confirm that the miR-21/PTEN pathway promotes cervical cancer.

Replication factor C subunit 2 (RFC2) is a component of the replication factor C (RFC) complex, which plays a critical role in DNA replication and repair. Recent studies have reported the involvement of RFC2 in several cancers. In this study, we investigated the functional role of RFC2 in cervical cancer progression. RFC2 expression in cervical cancer cells was analyzed using quantitative real-time PCR (qRT-PCR) and western blotting. HeLa, ME-180, and SiHa cells were transfected with siRNAs targeting RFC2. Cell viability and proliferation were assessed using the MTT and colony formation assays, and cell cycle distribution was analyzed by flow cytometry. Migration and invasion abilities were evaluated through Transwell assays with or without Matrigel. RFC2 knockdown significantly reduced cell proliferation in cervical cancer cells. Flow cytometry analysis revealed cell cycle arrest at the S phase. Additionally, RFC2 knockdown markedly inhibited the migration and invasion of cervical cancer cells. These results demonstrate the critical involvement of RFC2 in regulating proliferation and metastatic potential in cervical cancer cells. RFC2 plays a pivotal role in promoting cervical cancer progression by enhancing cell growth, regulating the cell cycle, and promoting metastatic behavior. Further studies on the molecular mechanisms of RFC2 in cancer-associated pathways may provide a novel therapeutic target for developing cervical cancer treatment strategies.

BackgroundThis study aimed to elucidate the roles of miR-1254 in cervical cancer progression and to explore the underlying mechanisms.MethodsThe expression levels of miR-1254 in normal-cancer cervical tissues and cells were measured using quantitive real-time polymerase chain reaction (qRT-PCR). The invasive and proliferative abilities of cervical cancer cell lines transfected with negative control (NC) mimic or miR-1254 mimic were measured using transwell, CCK-8, and colony formation assays. The binding sites between CD36 and miR-1254 were determined using luciferase reporter assays. The correlation of CD36 and miR-1254 with cervical cancer development was re-confirmed by co-transfection of miR-1254 mimic and CD36 overexpression using CCK-8, colony formation, transwell and western blot assays.ResultsMiR-1254 was expressed at significantly lower levels in the cervical cancer cell lines and tissues than in the controls. The functional assays revealed that upregulation of miR-1254 inhibited the invasion and proliferation of cervical cancer cells. The luciferase reporter assays demonstrated that CD36 messenger RNA and miR-1254 bound to one another. CD36 overexpression reversed the inhibitory effects of upregulated miR-1254 in the cervical cancer cells, suggesting that miR-1254 regulates cervical cancer progression by modulating CD36.ConclusionmiR-1254 attenuated the invasion and proliferation of cervical cancer cells by modulating the expression levels of CD36.

Objective: To investigate the role of DDX3 up-regulation in the proliferation of human cervical cancer cells and its correlation with clinical prognosis. Methods: Expression levels of DDX3 in the 59 specimens of cervical cancer and adjacent non-neoplastic tissue collected at Henan Provincial People's Hospital from April 2012 to March 2013 were detected using immunohistochemistry. A lentivirus-mediated DDX3-over-expression cell line was constructed based on HeLa cells of cervical cancer. CCK-8 assay was used to evaluate cell survival rate. Boyden chamber was used to measure the cell migration and invasion. Real-time fluorescence quantitative PCR was used to detect DDX3 expression level and Western blot was used to detect the expression of EMT and PI3K/Akt signal pathway-related proteins. Results: DDX3 overexpression was associated with FIGO stage, depth of cervical invasion and lymph node metastasis (P<0.05). Kaplan-Meier analysis revealed that cervical cancer patients with high expression of DDX3 had a poor overall survival (P<0.05). Compared with the cells transfected with pLVX-Con vector, the expression of DDX3 protein and mRNA was significantly increased in the cells transfected with pLVX-DDX3 (all P<0.01). Cell proliferation was significantly increased following transfection with pLVX-DDX3 for 72 h in HeLa cells compared with that transfected with pLVX-Con (P<0.05). Compared with the controls, DDX3 overexpression significantly promoted the migration and invasion of HeLa cells (P<0.05), and increased the expression of N-Cadherin, vimentin and Snail in HeLa cells (P<0.05). In pLVX-DDX3 group, the expression levels of β-catenin, phosphorylated Akt, and pAkt's downstream target p-GSK3β were significantly higher than those of pLVX-Con group (P<0.05). The expression levels of p-Akt, p-GSK3β and β-catenin were decreased when the PI3K/Akt pathway was blocked using the PI3K inhibitor LY294002 (P<0.05), and the expression levels of N-Cadherin, vimentin and Snail were also significantly decreased (P<0.05). Conclusions: DDX3 overexpression promotes proliferation, migration and invasion of cervical cancer cells, and induces epithelial-mesenchymal transition (EMT). Its mechanism may be related to activation of the PI3K/Akt signaling pathway.

Objective:This study aims to explore the modulatory effect of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) protein in the Notch1 signaling pathway in cervical cancer (CC) cells and assess how this modulation affects the proliferation and migration of CC cells. Moreover, this study offers fresh perspectives on the molecular mechanisms underlying CC by thoroughly analyzing the relationship between 15-PGDH and the Notch1 signaling pathway, and investigates the therapeutic potential of 15-PGDH.Material and Methods:Human normal cervical epithelial cells and CC cell lines (human CC cell line [HeLa], human cervical squamous carcinoma cell line [Caski], and human cervical epidermoid carcinoma cells [ME180]) were selected as experimental models. Western blotting (WB) and quantitative reverse transcription polymerase chain reaction were performed to evaluate the protein and messenger RNA levels of 15-PGDH and Notch receptor 1 (Notch1) signaling pathway-related proteins (Jagged canonical Notch ligand 1 [Jagged1] and Hes family bHLH transcription factor 1 [Hes1]). Results suggested that the HeLa and Caski cells exhibited significant expression of 15-PGDH and Notch1 signaling-related proteins. A series of experiments, including WB, cell counting kit-8 assay, Transwell migration assay, and 5-ethynyl-2'-deoxyuridine assay, was conducted in the HeLa and Caski cells to obtain an extensive understanding of how 15-PGDH influences Notch1 signaling regulation. This study also utilized the 15-PGDH inhibitor SW033291 and a Notch1 overexpression vector to evaluate the effect of 15-PGDH on CC cell growth, motility, and Notch1 signaling pathway modulation.Results:Results demonstrated that in the normal human cervical epithelial cells, 15-PGDH was highly expressed, while the Notch1 signaling pathway-related proteins exhibited low expression quantities. However, in HeLa and Caski CC cells, 15-PGDH expression was significantly downregulated (P < 0.001 or P < 0.01), whereas the Notch1 signaling pathway was activated. Further studies revealed that 15-PGDH or its inhibitor influenced the stimulation of the Notch1 signaling pathway in the HeLa and Caski cells. Specifically, the 15-PGDH inhibitor SW033291 reduced 15-PGDH expression (P < 0.001 or P < 0.01) and promoted Notch signaling activation. Meanwhile, 15-PGDH upregulation suppressed Notch signaling activation. Furthermore, 15-PGDH successfully prevented the proliferation and migration of CC cells induced by Notch1 overexpression and reduced the activation of the Notch signaling pathway, as shown by the downregulation of Notch1 and its downstream effectors, Jagged1 and Hes1.Conclusion:This study highlights the role of 15-PGDH in regulating the Notch1 signaling pathway in CC cells, focusing on its effect on cell proliferation and migration. The results demonstrate that 15-PGDH suppresses CC cell proliferation and migration by downregulating the Notch1 signaling pathway. These findings provide new insights into the molecular mechanisms underlying CC and suggest 15-PGDH as a promising therapeutic target.

Cervical cancer (CC) ranks as the fourth most prevalent malignancy among women worldwide, necessitating effective therapeutic interventions to mitigate its detrimental impact on both physical and mental health. Parthenolide (PTL), a natural product of the sesquiterpene lactone derived from Feverfew leaves, has exhibited promising anti-tumor properties in previous studies; however, its precise effects and underlying molecular mechanisms in CC remain elusive. In this work, we investigated the effect of PTL on the proliferation and migration of CC cells. Western blot analysis and Reverse transcription‑quantitative PCR were used for mechanistic elucidation. Our findings indicated that PTL substantially inhibited the proliferation of HeLa and SiHa CC cell lines in a dose- and time-dependent manner. Moreover, PTL significantly suppressed the migration of CC cells by down-regulating the expression of vascular endothelial growth factor (VEGF), metastasis-associated protein 1 (MTA1), and transforming growth factor-β1 (TGF-β1). Mechanistically, PTL blocked the phosphorylation of focal adhesion kinase (FAK) and glycogen synthase kinase-3β (GSK3β) induced by epidermal growth factor (EGF). Further investigations revealed that PTL suppressed the proliferation of CC cells by inhibiting the EGF-mediated phosphorylation of the FAK/GSK3β signaling pathway. Taken together, the present in vitro results suggest that PTL may inhibit the proliferation and migration of CC cells through down-regulating the FAK/GSK3β signaling pathway, providing new insights for the application of PTL in the treatment of CC.