The aim of this study was to examine the effects of the crude extract of Acanthus ebracteatus Vahl (AE) on tumor growth and angiogenesis by utilizing a tumor model in which nude mice were implanted with cervical cancer cells containing human papillomavirus 16 DNA (HPV-16 DNA).

Angiopoietin-2 (Ang-2) has been proven to be a potential agent for malignant cancer treatment. The aim of the current study was to investigate the inhibitory effects of chitosan magnetic nanoparticles (CMNPs) loaded with Ang-2 small interfering RNA (Ang2-siRNA) plasmids (Ang2-CMNPs) on malignant melanoma.

Gallbladder cancer (GBC) is a common malignancy of the biliary tract and is characterized by rapid progression and early metastasis. Elucidating the molecular mechanisms of GBC could help to develop better treatment strategies.

Large-scale studies have revealed that appropriate antiangiogenic treatment enables the recovery of the normal structure and function of solid tumor vessels. Epigallocatechin-3-gallate (EGCG), a natural extract of green tea, has multiple effects on angiogenesis. However, normalization of blood vessels due to natural ingredients has not yet been reported. Therefore, we examined the microvasculature, microenvironment, and efficacy of EGCG combined with chemotherapy in a xenograft model.

Patient-derived tumor xenografts (PDX) are considered as a more reliable experiment model for screening chemotherapeutic drugs. However, the tumorigenic rate differs depending on mouse strains, which generates the experimental variability.

Monitoring the fate of implanted cells over time in an experimental animal may provide a new way to track the metastatic process. Lymph node metastase is of extremely importance for the prognostic prediction of gastric carcinoma. The aim of this study was to assess the feasibility of magnetic resonance imaging (MRI), using micron-sized superparamagnetic iron oxide particles (MPIO), for monitoring of the fate of gastric cancer cells and detecting the migration of gastric cancer cells through the lymphatic system in a mouse model.

Purpose: In this study, we used a nude mouse model of human laryngeal squamous cell carcinoma (LSCC) to investigate inhibition of tumor growth by microRNA-145 (miR-145) and the mechanisms underlying this inhibition. Methods: Tumors were established in nude mice by transplantation of the LSCC AMC-HN-8 cell line. Forty-eight nude mice were randomly divided into groups of eight mice each and treated with high (1.0 optical density [OD]) or low (0.5 OD) doses of miR-145, or relevant control treatments. Tumor growth was observed in each group and used to calculate the inhibition rate. Routine pathological and electron microscopic examinations were used to determine tumor apoptosis and proliferation. Changes in levels of miR-145 and PI3K and Akt protein levels were also analyzed. Results: MiR-145 inhibited LSCC growth in a dose-dependent manner, as tumor growth was significantly inhibited in mice injected intratumorally with high-dose miR-145 compared with both the untreated and low-dose miR-145 groups (p<0.05). Pathological examination showed increased tumor necrotic and apoptotic changes in treated mice, which was confirmed by electron microscopy. PI3K and Akt protein expression were significantly lower in tumors treated with high-dose miR-145 group compared with those in the untreated and low-dose miR-145 groups (p<0.05). Conclusions: MiR-145 was associated with inhibited tumor growth in a nude mouse model of LSCC. The underlying mechanism may be inhibition of the PI3K/Akt signaling pathway, which regulates tumor growth, invasion, and metastasis and also plays an important role in tumor angiogenesis and proliferation of tumor stem cells. MiR-145 may act as a tumor suppressor gene and is a promising candidate for cancer treatment.

To assess the expression levels of COTL1 in human GBM tissues and evaluate the potential involvement of COTL1 in cancer progression.

Obesity is defined as a chronic, low-grade inflammatory disease that can cause obesity-associated disorders, such as cancer. Obesity has traditionally been thought to be a risk factor for ovarian cancer. Few reports have focused on the specific pathogenesis of obesity-related ovarian cancer. When considering the correlation between obesity and the relative risk of death from ovarian cancer, we investigated whether obesity promotes tumor immune escape in ovarian cancer.

Long noncoding RNA has been involved in tumorigenesis of colorectal cancer (CRC). This study aimed to illustrate the functions and mechanisms of LINC00173 in CRC progression.

SET has been proven to be an oncogene, which promotes the initiation and progression in several kinds of malignant carcinomas. However, the expression and its functional roles in colorectal carcinoma (CRC) remained unknown.

Glioma is one the most common and aggressive primary tumors of adult central nervous system worldwide, which tends to develop dysplasia and metastasis. Recently, toosendanin (TSN) has shown pharmacological effects in several cancers. However, little is known about the underlying mechanism of the effect of TSN on glioma and its relationship between miRNA in glioma.

Non-small-cell lung cancer (NSCLC) comprises approximately 80% of all lung malignancies. The 5-year survival rate of patients with advanced lung cancer who lost their chances of surgery is approximately 15%. Suitable animal models are important in screening individualized treatment plans for patients with lung cancer, evaluating the pre-clinical efficacy of new drugs, and conducting basic research.

Objective: This study aimed to investigate the role of fibroblast growth factor-5 (FGF5) in osteosarcoma (OS) and explore the potential mechanisms. Methods: OS gene expression data was downloaded from the Gene Expression Omnibus (GEO; GSE12865) and analyzed by R software. OS tissues and cell lines were collected. The expression level of FGF5 in tumor tissues and cell lines was detected using qRT-PCR. Knockout of FGF5 was performed using CRISPR/Cas9 system. The effects of FGF5 knockout on OS cell proliferation and tumor growth were determined through cell counting kit-8 assay and xenograft nude mice, respectively. Additionally, recombinant FGF5 (rFGF5) was added into OS cell and the effects of rFGF5 on the proliferation and apoptosis of OS cell lines were assayed. Furthermore, the protein expression levels of mitogen-activated protein kinase (MAPK) signaling pathway were detected through Western blot. Results: FGF5 was significantly upregulated in OS tissues and cells, and closely associated with poor differentiation, larger tumor size, lymph node metastasis, and advanced TNM stage. FGF5 knockout could inhibit proliferation of OS cells and tumor growth in nude mouse model. Addition of exogenous rFGF5 promoted OS cell proliferation while inhibited OS cell apoptosis. The expression levels of MAPK signaling pathway proteins in FGF5 knockout group were significantly lower than that in control when there was no rFGF5. Additionally, their expression level in rFGF5 addition group was higher than that in without rFGF5 group. Conclusion: We demonstrated for the first time that FGF5 was overexpressed in OS cell lines and clinical tissue samples and promotes OS cell proliferation by activating MAPK signaling pathway, which indicated that FGF5 was a potential therapeutic target for OS.

The dysregulated circular RNAs (circRNAs) are relevant to lung adenocarcinoma development. Nevertheless, the function and mechanism of hsa_circ_0020850 (circ_0020850) in lung adenocarcinoma development are uncertain.

Objective: CD166 is known as a tumor stem cell specific marker, associating with tumor metastasis. The purpose of this study was to further discuss CD166 gene on cell proliferation, invasion, metastasis, and the epithelial-mesenchymal transition (EMT) in CNE-2R cell line of nasopharyngeal carcinoma (NPC). Materials and methods: CNE-2R cells were transfected with lentivirus CD166-shRNA, and quantitative reverse transcription polymerase chain reaction (RT-qPCR), and Western blotting were used to confirm the silencing effects. The wound healing test and transwell test were carried out to assess cell invasive and migratory abilities in vitro. With the establishment of xenograft nude mouse model, Western blotting and immunohistochemistry were undertaken to detect the expression level of E-cadherin, N-cadherin, and vimentin. In vivo metastasis detection was carried out by injecting tumor cells into nude mice via the tail vein. Results: The invasive and migratory abilities of CNE-2R cells were significantly reduced after CD166 was downregulated. In addition, silencing of CD166 of CNE-2R cells increased the expression of E-cadherin, while down-regulated the expression of N-cadherin and vimentin. Immunohistochemistry of tumors showed consistent results with in-situ tumor formation experiment. Additionally, the growth of transplanted tumor was inhibited. In addition, in vivo metastasis test proved that knockdown of CD166 suppressed pulmonary metastasis and liver metastasis according to hematoxylin and eosin (H&E) staining. Expression of E-cadherin increased, while expression of N-cadherin and vimentin decreased, as revealed by Western blotting of metastatic lung tumors. Conclusion: Silencing of CD166 in CNE-2R cells evidently inhibited proliferation, invasion, metastasis, and EMT process in vivo and in vitro.

Glucose-6-phosphate isomerase (GPI) is a glycolytic-related enzyme that inter-converts glucose-6-phosphate and fructose-6-phosphate in the cytoplasm. This protein is also secreted into the extracellular matrix by cancer cells and is, therefore, also called autocrine motility factor (AMF).

The dysregulation of microRNA (miRNAs) is broadly participated in cancer progression, resulting in sustained cell proliferation by directly targeting various targets. This study investigated the expression of miR-582 in GC and its association with liver metastasis.

Bladder Carcinoma (BC) is a malignant carcinoma with a high incidence in masculinity. We preliminarily researched the efficacy and mechanism of matrine (MAT) in T24 and 5637 cells.

Objective: To understand the role of WFDC2 in metastasis of ovarian cancer. Methods: By knockdown or overexpression of WFDC2, we demonstrated the role of WFDC2 in epithelial-mesenchymal transition (EMT). Results: We demonstrated that stable knockdown of WFDC2 suppressed EMT along with the upregulation of E-cadherin and the downregulation of Vimentin. In addition, WFDC2 knockdown decreases matrix metalloproteinase-2 (MMP-2) expression in in vitro cell model and in in vivo nude mice xenografts. The correlation of WFDC2 and MMP-2 expression in the clinical sample confirmed that WFDC2 was tightly correlated with the development of tumor. More importantly, the EMT phenotype and cell invasion induced by WFDC2 overexpressing can be reversed by the siMMP-2 and P13K/AKT signaling inhibitor. Conclusion: WFDC2 contributed to ovarian cancer metastasis and EMT as a positive regulator by activating AKT signaling pathway and inducing MMP-2 expression.