Cell Transwell Invasion Assays Research Articles

Retracted] Dual inhibition of COX‑2/5‑LOX blocks colon cancer proliferation, migration and invasion in vitro.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that there appeared to be a number of anomalies in the presentation of data, including both tabulated data and data in figures: First, a discrepancy was noted between the numbers of males and females reported in the Materials and methods section on p. 1681 (47 females and 47 males) and yet, in Table I, showing clinicopathological characteristics of the patients, different numbers of male and female patients were reported. Secondly, data in Fig. 1 on p. 1683 had been misassembled: Experiments with COX‑2 and 5‑LOX are shown, but the panels for the x40 and x100 magnified images are presented the wrong way around. Thirdly, regarding the western blotting data, there were a couple of instances where it appeared that different exposures of gels had been undertaken in an attempt to show the same data for different experimental conditions. Fourthly, western blotting data featured internally in Fig. 4C on p. 1686 appeared to be strikingly similar, such that the same data may have been used to show the results for differently performed experiments. Fifthly, the data shown in the left‑hand columns for the scratch‑wound assay experiments in Figs. 2A and 5A were the same, even though different experiments were intended to have been portrayed in these figures. Finally, after having conducted an independent investigation of this paper in the Editorial Office, the presence of overlapping sections was also noted comparing the Transwell cell invasion assay data in Figs. 3 and 5. Given the identification of these various issues in the paper, the Editor of Oncology Reports has decided that this article should be retracted from the Journal on account of the uncertainties, and an overall lack of confidence, in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 35: 1680‑1688, 2016; DOI: 10.3892/or.2015.4506].

Retracted] LncRNA TTN‑AS1 promotes endometrial cancer by sponging miR‑376a‑3p.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell migration and invasion assay data in Fig. 2E and F and 4E and F, tumor images in Fig. 7B and western blotting data shown in Fig. 4D had already appeared in previously published articles written by different authors at different research institutes (a few of which have been retracted). Owing to the fact that the contentious data in the above article had already been published prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 44: 1343‑1354, 2020; DOI: 10.3892/or.2020.7691].

Retracted] MEG3/miR‑21 axis affects cell mobility by suppressing epithelial‑mesenchymal transition in gastric cancer.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell invasion assay data shown in Fig. 2B on p. 42 and the immunofluorescence data shown in Fig. 4D on p. 44 were strikingly similar to data appearing in other articles written by different authors at different research institutes that were submitted to different journals at around the same time. Moreover, a further investigation of this paper undertaken by the Editorial Office identified a large number of overlapping data panels comparing the Transwell cell migration and invasion assay data and the scratch‑wound assay data both within and between Figs. 2 and 3, where data which were intended to have shown the results from differently performed experiments had apparently been derived from the same original source, including an overlapping section of data within the 'MEG3+mimic' panel in Fig. 3G that would be difficult to attribute to pure chance. Owing to the fact that the contentious data in the above article had already been submitted for publication at around the same time as its submission to Oncology Reports, and given an overall lack of confidence in the presented data, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 40: 39‑48, 2018; DOI: 10.3892/or.2018.6424].

Lecithin-cholesterol acyltransferase is a potential tumor suppressor and predictive marker for hepatocellular carcinoma metastasis

BACKGROUND Hepatocellular carcinoma (HCC) is a major cause of cancer mortality worldwide, and metastasis is the main cause of early recurrence and poor prognosis. However, the mechanism of metastasis remains poorly understood. AIM To determine the possible mechanism affecting HCC metastasis and provide a possible theoretical basis for HCC treatment. METHODS The candidate molecule lecithin-cholesterol acyltransferase (LCAT) was screened by gene microarray and bioinformatics analysis. The expression levels of LCAT in clinical cohort samples was detected by quantitative real-time polymerase chain reaction and western blotting. The proliferation, migration, invasion and tumor-forming ability were measured by Cell Counting Kit-8, Transwell cell migration, invasion, and clonal formation assays, respectively. Tumor formation was detected in nude mice after LCAT gene knockdown or overexpression. The immunohistochemistry for Ki67, E-cadherin, N-cadherin, matrix metalloproteinase 9 and vascular endothelial growth factor were performed in liver tissues to assess the effect of LCAT on HCC. Gene set enrichment analysis (GSEA) on various gene signatures were analyzed with GSEA version 3.0. Three machine-learning algorithms (random forest, support vector machine, and logistic regression) were applied to predict HCC metastasis in The Cancer Genome Atlas and GEO databases. RESULTS LCAT was identified as a novel gene relating to HCC metastasis by using gene microarray in HCC tissues. LCAT was significantly downregulated in HCC tissues, which is correlated with recurrence, metastasis and poor outcome of HCC patients. Functional analysis indicated that LCAT inhibited HCC cell proliferation, migration and invasion both in vitro and in vivo . Clinicopathological data showed that LCAT was negatively associated with HCC size and metastasis (HCC size ≤ 3 cm vs 3-9 cm, P < 0.001; 3-9 cm vs > 9 cm, P < 0.01; metastatic-free HCC vs extrahepatic metastatic HCC, P < 0.05). LCAT suppressed the growth, migration and invasion of HCC cell lines via PI3K/AKT/mTOR signaling. Our results indicated that the logistic regression model based on LCAT, TNM stage and the serum level of α-fetoprotein in HCC patients could effectively predict high metastatic risk HCC patients. CONCLUSION LCAT is downregulated at translational and protein levels in HCC and might inhibit tumor metastasis via attenuating PI3K/AKT/mTOR signaling. LCAT is a prognostic marker and potential therapeutic target for HCC.

Retracted] Schisandrin B inhibits epithelial‑mesenchymal transition and stemness of large‑cell lung cancer cells and tumorigenesis in xenografts via inhibiting the NF‑κB and p38 MAPK signaling pathways.

Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the Transwell cell invasion and migration assay data featured in Figs. 2D and 5E and the wound‑healing assay data in Fig. 2A were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published elsewhere prior to the submission of this paper to Oncology Reports, or which under consideration for publication at around the same time. In view of the fact that certain of these data had already apparently been published prior to the submission of this article for publication, the Editor of Oncology Reports has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 45: 115, 2021; DOI: 10.3892/or.2021.8066].

Retracted] MicroRNA‑336 directly targets Sox‑2 in osteosarcoma to inhibit tumorigenesis.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell migration and invasion assay data in Fig. 3C and D, and the tumour images shown in Fig. 4A were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes, which had already been published. In addition, certain of the data panels shown in Fig. 3C were overlapping, such that the data from the same original source had been selected to represent the results from allegedly differently performed experiments. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 15: 4217‑4224, 2017; DOI: 10.3892/mmr.2017.6493].

Retracted] Matrine inhibits ovarian cancer cell viability and promotes apoptosis by regulating the ERK/JNK signaling pathway via p38MAPK.

Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the Transwell cell invasion assay data featured in Fig. 1B and C, the immunofluorescence assay data in Fig. 2E and F, the TUNEL assay data in Fig. 4C and the immunohistochemical data in Fig. 4B and E were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published elsewhere prior to the submission of this paper to Oncology Reports, or which under consideration for publication at around the same time. In view of the fact that certain of these data had already apparently been published prior to the submission of this article for publication, the Editor of Oncology Reports has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 45: 82, 2021; DOI: 10.3892/or.2021.8033].

Role of the transient receptor potential melastatin 4 in inhibition effect of arsenic trioxide on the tumor biological features of colorectal cancer cell

Background To investigate the effects of arsenic trioxide (ATO) on human colorectal cancer cells (HCT116) growth and the role of transient receptor potential melastatin 4 (TRPM4) channel in this process. Methods The viability of HCT116 cells was assessed using the CCK-8 assay. Western blot analysis was employed to examine the protein expression of TRPM4. The apoptosis of HCT116 cells was determined using TUNEL and Flow cytometry. Cell migration was assessed through the cell scratch recovery assay and Transwell cell migration assay. Additionally, Transwell cell invasion assay was performed to determine the invasion ability of HCT116 cells. Results ATO suppressed the viability of HCT116 cells in a dose-dependent manner, accompanied by a decline in cell migration and invasion, and an increase in apoptosis. 9-phenanthroline (9-Ph), a specific inhibitor of TRPM4, abrogated the ATO-induced upregulation of TRPM4 expression. Additionally, blocking TRPM4 reversed the effects of ATO on HCT116 cells proliferation, including restoration of cell viability, migration and invasion, as well as the inhibition of apoptosis. Conclusion ATO inhibits CRC cell growth by inducing TRPM4 expression, our findings indicate that ATO is a promising therapeutic strategy and TRPM4 may be a novel target for the treatment of CRC.

CADM2 participates in endometriosis development by influencing the epithelial-mesenchymal transition.

Endometriosis (EM) is a common gynecologic condition that often leads to infertility in women of reproductive age. Cell adhesion molecule 2 (CADM2) is involved in maintaining cell adhesion and polarity, as well as suppressing tumors. However, the role and mechanism of CADM2 in endometriosis is unclear. Therefore, this study evaluated the expression levels of CADM2 and epithelial-mesenchymal transition (EMT)-related marker proteins (E-cadherin, α-SMA, and N-cadherin). Compared to normal endometrial tissue, CADM2 was expressed at low levels in ectopic endometrial tissue from patients with EM. We performed clone formation assays, wound healing assays, and Transwell cell invasion assays to investigate the effects of CADM2 on the biological behavior of endometriosis epithelial cells (11Z) and ectopic endometrial stromal cells (EESCs). The growth, migration, and invasion abilities of these cells were significantly inhibited by overexpression of CADM2. The results were reversed after the knockdown of CADM2. Finally, western blotting (WB) was utilized to detect the effect of CADM2 on EMT in endometriosis cells. CADM2 inhibited EMT in endometriosis cells. In conclusion, our study suggests that CADM2 is a negative regulator of endometriosis development and may inhibit endometriosis development by suppressing EMT.

Abstract PO3-24-07: The role of Hepatitis A Virus Cellular Receptor 1 (HAVCR1) in breast cancer and the impact on penetration of blood brain barrier

Abstract Background: Hepatitis A Virus Cellular Receptor 1 (HAVCR1) is associated with the biological behaviour of several cancers, and has been shown to regulate junctional complexes. However, its role in breast cancer remains unexplored. This study aimed to investigate the effects of HAVCR1 on human breast cancer. Methods: We explored the UALCAN web portal, which is linked to the TCGA database, to determine the expression of HAVCR1 in breast cancer and the Kaplan-Meier plotter to evaluate the correlation with the survival of the patients. HAVCR1 siRNA was used to knock down the HAVCR1 expression in MCF-7 and MDA-MB-231 cell lines. In vitro cell growth, wounding healing, and electric cell impedance sensing (ECIS for assessing cellular proliferation, migration and adhesion) assays were used. Transepithelial resistance (TEER) and paracellular permeability (PCP) were assessed to determine changes in the barrier function of human breast cancer cells. The expression of HAVCR1 and prospective interactive binding molecules of HAVCR1 protein was assessed using quantitative polymerase chain reaction (qPCR). Cellular response to docetaxel was evaluated and shown (IC50). The invasiveness of breast cancer cells through the human cerebral microvessel endothelial cells (hCMEC/D3) cell layers was measured using an in vitro transwell cell invasion assay. Results: HAVCR1 gene expression levels were significantly lower (P< 0.001) in breast cancer tissue compared with normal tissues. Patients with high expression of HAVCR1 had a significantly better relapse-free survival than low expression (P< 0.001). There was no significant difference in overall survival (OS) between the HAVCR1 high and the low expression groups (P=0.22). However, in subgroup analysis, high HAVCR1 expression was associated with better OS in luminal A (P=0.04). Knockdown (KD) HAVCR1 in breast cancer cells influence cell function by enhanced adhesion, proliferation, and migration compared to wild type (WT) cell lines. It was noted that loss of HAVCR1 rendered both MCF-7 and MDA-MB-231 cells resistant to docetaxel (IC50 for WT and HAVCR1 KD respectively being 0.86nM vs 1.75nM for MCF-7 and 1.35nM vs 15.48nM for MDA-MB-231). HAVCR1 KD increase adhesion to hCMEC/D3 cells (53.14±8.23 vs ±99.37±8.97 for MCF-7, P< 0.001; 109.5±97.56 vs 147.1±96.63 for MDA-MB-231, P=0.228, WT and HAVCR1 KD). In the cerebral endothelial cell invasion assay, we found that HAVCR1 KD resulted in a significantly increased invasion of the breast cancer cells through the endothelium (19.27±8.74 vs 33.58±16.81 for MDA-MB-231, P=0.0114, WT and HAVCR1 KD). For the barrier function, the knockdown led to a decrease in TEER and an increase in PCP when compared with WT cells in both cell lines. HAVCR1 KD cells showed decreased barrier function, together with reduced expression of Claudin-1/8/10, occludin, MarvelD3, Tricellulin and ZO1. Conclusions: HAVCR1 is a potential biomarker for breast cancer prognosis. HAVCR1 influences the integrity of barrier function by influence the gene expression of tight junction in breast cancer, and influence the penetration to blood brain barrier. Together, it suggests that HAVCR1 may be a potential therapeutic target in breast cancer. Citation Format: Xiaoshan Cao, Binbin Cong, Wen Jiang, Tracey Martin. The role of Hepatitis A Virus Cellular Receptor 1 (HAVCR1) in breast cancer and the impact on penetration of blood brain barrier [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO3-24-07.

Retracted] MicroRNA‑329‑3p targets MAPK1 to suppress cell proliferation, migration and invasion in cervical cancer.

Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the Transwell cell migration and invasion assay data featured in Figs. 5C and 6C were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had already been published elsewhere prior to the submission of this paper to Oncology Reports, or were submitted for consideration for publication at around the same time. In view of the fact that certain of these data had already apparently been published prior to the submission of this article for publication, the Editor of Oncology Reports has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 37: 2743‑2750, 2017; DOI: 10.3892/or.2017.5555].

Retracted] lncRNA ROR promotes the progression of renal cell carcinoma through the miR‑206/VEGF axis.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell invasion and migration assay data shown in Fig. 2D and F on p. 3786 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes, which had already been published. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 20: 3782‑3792, 2019; DOI: 10.3892/mmr.2019.10636].

Retracted] Tissue‑specific transplantation antigen P35B functions as an oncogene and is regulated by microRNA‑125a‑5p in lung cancer.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the immunohistochemical data shown in Fig. 1A on p. 5, colony formation data shown in Figs. 2C, H and M and 6D on p. 6 and p. 10 respectively, the western blots in Fig. 2B, Transwell cell migration and invasion assay data in Fig. 3B, D and F, and immunofluorescence data in Fig. 4C had already appeared in previously published articles written by different authors at different research institutes (some of which have subsequently been retracted). Owing to the fact that the contentious data in the above article had already been published prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 45: 72, 2021; DOI: 10.3892/or.2021.8023].

Abstract 3034: Krüppel-like factors in regulation of gastric cancer progression

Abstract Introduction: Gastric cancer (GC) is the third leading cause of cancer-associated mortality and the fifth most frequently diagnosed cancer worldwide. The development and progression of GC is a complicated multistage process subjected to dynamic changes in gene regulation. Investigating the effects of these changes is therefore critical for improving our knowledge about GC initiation and progression. Krüppel-like factors (KLFs) are evolutionarily conserved zinc finger-containing transcription factors with altered expressions and diverse regulatory functions in GC. We previously reported that there is loss of KLF4 in GC. Here we report that KLF4 is a crucial regulator of KLF5 expression and vice versa and together they regulate GC cell behavior. Methods: The Cancer Genome Atlas (TCGA) and pan cancer data of differential expressions of KLFs in GC was analyzed. TCGA RNAseq and clinical data for the differential expression status of KLF genes in normal and cancerous tissues and the clinicopathological association was accessed from the UALCAN web portal. The expressions of KLF4 and KLF5 in human normal stomach and GC and orthotopic xenografts were detected by immunohistochemistry (IHC). KLF4, KLF5 cross regulation was evaluated by gene manipulation of each gene individually and checking the expression of the other factor in GC cells. The effect of KLFs on GC cell proliferation, migration, and invasion was determined by Ki67 staining of tissues, PrestoBlue cell viability assay, scratch wound and transwell cell invasion assays. Results and Conclusion: Our results indicated that not only KLF4 and KLF5 have contrasting expressions and effects in GC but also these two factors cross regulate each other. While lower expressions of KLF4 was found in human GC and orthotopic xenografts, increased expression of KLF5 was found in both human GC tissue and orthotopic xenografts. KLF4 silencing and CRISPR/Cas9 knockdown in human GC cells resulted in increased expression of KLF5 which was associated with increased GC cell proliferation and invasiveness. Interestingly, KLF5 knockdown by CRISPR/Cas9 in human GC cells on the other hand resulted in increased expression of KLF4, which was associated with decreased GC cell growth. Our data therefore suggests that the differential expressions of KLF4 and KLF5 might serve as valuable prognostic markers in GC. Citation Format: Sooraj Kakkat, Prabhat Suman, Sandeep Goswami, Sujit Basu, Martin J. Heslin, Elba A. Turbat-Herrera, Veronica Ramirez Alcantara, Chandrani Sarkar, Debanjan Chakroborty. Krüppel-like factors in regulation of gastric cancer progression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 3034.

Retracted] Tanshinone IIA enhances the inhibitory effect of imatinib on proliferation and motility of acute leukemia cell line TIB‑152 invivo and invitro by inhibiting the PI3K/AKT/mTOR signaling pathway.

Following the publication of the above article, a concerned reader drew to the Editor's attention that the Transwell cell invasion assay data featured in Figs.2D and 4E, certain of the tumor images in Fig.5A and the TUNEL assay data in Fig.5C were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published elsewhere prior to the submission of this paper to OncologyReports, or which under consideration for publication at around the same time (some papers of which have been retracted). In view of the fact that certain of these data had already apparently been published prior to the submission of this article for publication, the Editor of OncologyReports has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 43: 503‑515, 2020; DOI: 10.3892/or.2019.7453].

Retracted] miR‑34a is downregulated in human osteosarcoma stem‑like cells and promotes invasion, tumorigenic ability and self‑renewal capacity.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell invasion assay data shown in Fig.4B on p.1635 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes, which had either already been published or were submitted at around the same time. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 15: 1631‑1637, 2017; DOI: 10.3892/mmr.2017.6187].

Retracted] MicroRNA‑140 represses glioma growth and metastasis by directly targeting ADAM9.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell invasion and migration assay data shown in Figs.2C and 5D were strikingly similar to data in different form in other articles written by different authors at different research institutes, which had either already been published or had been submitted for publication at around the same time (some of which have now been retracted). Owing to the fact that certain of the data in the above article had already been published prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 36: 2329‑2338, 2016; DOI: 10.3892/or.2016.5007].

Characterization of m6A RNA methylation mediated immune heterogeneity and functional validation in hepatocellular carcinoma.

N6 -methyladenosine (m6 A) mediates RNA modification in various biological processes. It plays a key role in hepatocellular carcinoma (HCC) through regulating methyltransferase. The present study aims to analyze the correlation between the m6 A and the immune status of HCC, and to construct an m6 A-related prognostic signature for HCC. HCC subtypes with different m6 A modification activities were identified based on the m6 A-related genes. Lasso Cox regression was applied to construct an m6 A-related prognostic model for HCC. Then, the prognostic potential of the constructed signature was evaluated and validated in the external validation dataset. Small interfering RNAs were designed to knockdown FBXO5. CCK-8 assay, Edu staining, wound healing assay, and Transwell cell invasion assay were used to detect cell proliferation, migration, and invasion ability. Two m6 A-related HCC subtypes were identified. The m6 A modification active group showed an immune suppressive microenvironment compared to the m6 A modification inactive group. The differentially expressed genes (DEGs) between the HCC subtypes were screened. Enrichment analysis was performed using the DEGs. Subsequently, an m6 A-related prognostic model was established. The prognostic model performed well in both training and validation datasets. Moreover, knockdown of FBXO5, one of the genes in the prognostic model, inhibited the proliferation, migration, and invasion of HepG2 cells. The heterogeneity of m6 A RNA methylation is associated with immune status in HCC. The constructed m6 A-related gene-based signature can predict the prognosis of HCC patients. The genes in the prognostic model also have therapeutic potential for HCC.

Retracted] Effect of RhoC on the epithelial‑mesenchymal transition process induced by TGF‑β1 in lung adenocarcinoma cells.

Following the publication of the above article, a concerned reader drew to the Editor's attention that the Transwell cell invasion assay data featured in Figs.3 and 5, and the cell microscopic/morphological images shown in Fig.4A and C, were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published elsewhere prior to the submission of this paper to OncologyReports, or which under consideration for publication at around the same time (several of which have now been retracted). In addition, overlapping sections of data were noted within Figs.3 and 5, such that data which were intended to represent the results from differently performed experiments had apparently been derived from the same original source(s). In view of the fact that certain of these data had already apparently been published prior to the submission of this article for publication, the Editor of OncologyReports has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 36: 3105‑3112, 2016; DOI: 10.3892/or.2016.5146].

Network Pharmacology Analysis and In Vitro Validation of the Active Ingredients and Potential Mechanisms of Gynostemma Pentaphyllum Against Esophageal Cancer.

Esophageal cancer (EC) is one of the deadliest malignancies worldwide. Gynostemma pentaphyllum Thunb. Makino (GpM) has been used in traditional Chinese medicine as a treatment for tumors and hyperlipidemia. Nevertheless, the active components and underlying mechanisms of anti-EC effects of GpM remain elusive. This study aims to determine the major active ingredients of GpM in the treatment of EC and to explore their molecular mechanisms by using network pharmacology, molecular docking, and in vitro experiments. Firstly, active ingredients and potential targets of GpM, as well as targets of EC, were screened in relevant databases to construct a compound-target network and a protein-protein interaction (PPI) network that narrowed down the pool of ingredients and targets. This was followed by gene ontology (GO) functional and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Next, molecular docking, ADME and toxicity risk prediction, cell viability assays, in vitro scratch assays, Transwell cell invasion assays, and Western blotting analysis were subsequently applied to validate the results of the network analysis. The screening produced a total of 21 active ingredients and 167 ingredient-related targets for GpM, along with 2653 targets for EC. The PPI network analysis highlighted three targets of interest, namely AKT1, TP53, and VEGFA, and the compound-target network identified three possible active ingredients: quercetin, rhamnazin, and isofucosterol. GO and EKGG indicated that the mechanism of action might be related to the PI3K/AKT signaling pathway as well as the regulation of cell motility and cell migration. Molecular docking and pharmacokinetic analyses suggest that quercetin and isoprostanoid sterols may have therapeutic value and safety for EC. The in vitro experiments confirmed that GpM can inhibit EC cell proliferation, migration, and invasion and suppress PI3K and AKT phosphorylation. Our findings indicate that GpM exerts its anti-tumor effect on EC by inhibiting EC cell migration and invasion via downregulation of the PI3K/AKT signaling pathway. Hence, we have reason to believe that GpM could be a promising candidate for the treatment of EC.