Objective: To investigate the clinicopathological features and differential diagnoses of paratesticular liposarcoma. Methods: The cases were collected from 2012-2020, from the archives of the Department of Pathology, Peking University Third Hospital, with diagnosis confirmed by histology, immunostaining and FISH tests. Results: Totally 19 patients were enrolled (including 11 in-hospital patients and 8 consultant cases). The patients aged 37-84 years (mean 57 years). The preoperative clinical diagnoses were spermatic cord/inguinal masses (nine patients), scrotal masses (seven patients), and inguinal hernia (three patients). Six lesions recurred after local resection, including one case extending from pelvic liposarcoma. Histologically, there were 10 cases of well-differentiated liposarcoma (WDLPS) and nine cases of dedifferentiated liposarcoma (DDLPS). WDLPSs mostly showed the combined features of lipoma-like, inflammatory and sclerosing subtypes (six patients); the other four WDLPSs had pure lipoma-like subtype features. DDLPSs were low-grade (three patients) or high-grade (six patients), with the morphology resembling myxofibrosarcoma, inflammatory myofibroblastoma, spindle cell sarcoma, pleomorphic undifferentiated sarcoma and pleomorphic liposarcoma. Intense inflammatory cells infiltration was commonly observed in five WDLPSs and two DDLPSs. Ossification was observed in three tumors. Immunohistochemically, the tumors were positive for MDM2 (8/10) and CDK4 (10/10), which were expressed in lipo-differentiating cells, spindle cells in WDLPS, and in dediffferentiated components. S-100 was only expressed by lipocytes (10/10). CD34 expression was positive and diffuse in the stromal cells of WDLPSs and focal or diffuse in dedifferentiated areas (10/10). FISH tests with an MDM2 gene probe were positive (12/12). Conclusions: Paratesticular liposarcoma may be overlooked by both clinicians and pathologists. WDLPS and DDLPS predominate, showing various histologic divergences. The presence of amplification of the 12q14-q15 region (containing the MDM2 and CDK4 genes) is helpful for making the correct diagnosis.

Objective: To investigate the clinicopathological features, immunophenotype, ultrastructure, genetic alterations and prognosis of succinate dehydrogenase-deficient renal cell carcinoma (SDH RCC). Methods: A total of 11 SDH RCCs, diagnosed from 2010 to 2019, were selected from the Department of Pathology of Nanjing Jingling Hospital, Nanjing University School of Medicine for clinicopathologic, immunohistochemical (IHC), ultrastructural investigation and follow-up. The molecular features of seven cases were analyzed by the panel-targeted DNA next generation sequencing (NGS). Results: There were seven males and four females, with ages ranging from 24 to 62 years (mean 41.4 years, median 41 years). Microscopically, SDH RCC was mainly composed of solid and tubular structures with local cystic change. Four cases showed nested or trabecular structure distributed in a loose hypocellular connective tissue or around scar, similar to oncocytoma. The neoplastic cells demonstrated flocculent eosinophilic cytoplasm with typical intracytoplasmic vacuoles. Immunohistochemically, eight cases were negative for SDHB; three cases showed focal and weak expression, whereas normal renal tubular and vascular endothelial cells demonstrated strong cytoplasmic staining. NGS of DNA targeted-panel detected pathogenic mutations of SDHB gene in seven cases (including three cases with equivocal IHC expression of SDHB), without any mutations in other SDH related genes. There were four cases of SDHB missense mutation, one case of frameshift mutation, one case of splicing mutation, and one case of acquired stop codon mutation. Conclusions: SDH RCC is a distinct variant of RCCs with genetic tendency or with hereditary cancer syndrome. NGS is recommended to detect the related gene mutations for a definitive diagnosis. The patients should be closely followed up.

Oncogene StarD4 had the function of promoting proliferation and metastasis of triple-negative breast cancer (TNBC), but its clinical value and molecular mechanism are unknown. This paper found that StarD4 was highly expressed in cancer tissues of TNBC patients, and higher expression level of StarD4 in TNBC patient resulted in poorer prognosis. Based on transcriptomics of MDA-MB-231 cell model, the results of bioinformatics analysis showed that down-regulated expression level of StarD4 led to overall downregulation of cholesterol-relative genes and significant enrichment of cancer mechanism and pathway. Further analysis and investigation verified that StarD4 might cross-promote the protein stability of receptor ITGA5 through the cholesterol pathway to enhance TNBC progression, which provides guidance for clinical application of TNBC diagnosis and treatment.

Using modular identification methods in gene-drug multiplex networks to infer new gene-drug associations can identify new therapeutic target genes for known drugs. In this paper, based on the gene expression data and drug response data of lung cancer in the genomics of drug sensitivity in cancer (GDSC) database, a multiple network algorithm is proposed. First, a heterogeneous network of genes of lung cancer and drugs in different cell lines is constructed, and then a network module identification method based on graph entropy is used. In this heterogeneous network, network modules are identified, and five lung cancer gene-drug association modules are identified through iterative convergence. Compared with other methods, the algorithm has better results in terms of running time, accuracy and robustness, and the identified modules have obvious biological significance. The research results in this article have guiding significance for the medication and treatment of lung cancer, and can provide references for the treatment of other diseases with the same targeted genes.

To observe the effect of electroacupuncture (EA) on tumor number, body conditions, inflammatory factors and expression levels of silent information regulator 1 (sirtuin 1, SIRT1) and autophagy-related proteins Beclin-1, P62, and LC3 in colorectal tissues in inflammatory-transformed colorectal cancer mice, so as to explore its underlying mechanisms in resisting tumor growth.

To analyze variants of TSC1 and TSC2 genes in a Chinese patient with tuberous sclerosis complex (TSC).

The purpose of the present study was to investigate the effect and potential mechanism of knockdown of sphingosine kinase-1 (SPHK1) on the proliferation, cell cycle and apoptosis of non-small cell lung cancer (NSCLC) cells. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect SPHK1 mRNA expression in human healthy lung fibroblasts (MRC-5 cells) and four NSCLC cell lines. Then, A549 and H1299 cells were transfected with SPHK1-shRNA and corresponding negative control. CCK-8, Annexin V-FITC/PI dual staining and cell cycle assay were performed to evaluate cell proliferation, apoptosis and cell cycle distribution, respectively. JC-1 mitochondrial membrane potential measurement kit was adopted to measure mitochondrial membrane potential. Western blot was used to detect the protein expression levels of cell cycle and mitochondrial apoptotic pathway-related proteins, as well as MEK/ERK signaling pathway. The results showed that the mRNA expression of SPHK1 in NSCLC cells was higher than that in MRC-5 cells. SPHK1-shRNA significantly inhibited the proliferation of A549 and H1299 cells, blocked the cell cycle in G0/G1 phase, and promoted cell apoptosis through the mitochondrial pathway. Compared with the control group, the expression of p-MEK and p-ERK proteins in the SPHK1-shRNA group was significantly down-regulated. Moreover, MEK/ERK inhibitor could dramatically suppress cell proliferation and promote cell apoptosis. These results suggest that SPHK1 knockdown can inhibit the proliferation of NSCLC cells and might promote mitochondrial apoptotic pathway by inhibiting MEK/ERK signaling pathway.

Objective: To investigate the role of ubiquitin-specific peptidase 22 (USP22) in colorectal cancer multidrug resistance and its correlation with multidrug resistance genes P-gp and MRP1, and to preliminarily explore the mechanism of USP22 affecting colorectal cancer resistance. Methods: USP22 over-expression plasmid was transfected into colorectal cancer cells (RKO, SW480)with low expression of USP22. Cell counting kit (CCK-8) assay was used to detect the effect of USP22 on oxaliplatin resistance in colorectal cancer cells. The cells were treated with oxaliplatin of the same concentration. Western blot method was used to detect the expression of apoptosis-related proteins cleaved-caspase3, Bcl-2, and drug resistance proteins MRP1, P-gp in the cells. The cell efflux test was used to detect the effect of up-regulated USP22 on Calcein-AM and rhodamine123. Immunohistochemical methods were used to detect the expressions of USP22 and P-gp in the oxaliplatin chemotherapy-sensitive group and the drug-resistant group and to analyze the correlation between USP22 and MRP1, P-gp. Results: CCK-8 assay showed that the IC50 values of SW480-USP22 (SW480 cells overexpressing USP22) treated with oxaliplatin for 24 h and 48 h was (4.62±0.05)μmol/L and (2.32±0.04)μmol/L respectively; which was 2.7 times and 3.0 times higher than that in control cells, respectively. After treating with 1.25 μmol/L oxaliplatin for 48 h, USP22 overexpression can inhibit SW480 cells apoptosis. The fluorescence intensity of calcein-AM and rhodamine123 in the SW480-USP22 group were significantly increased when compared with that in the control cells (both P<0.01). The protein expression levels of MRP1 and P-gp in SW480-USP22 cells were significantly increased when compared with that in the control cells(both P<0.01). Immunohistochemistry showed that the positive expression rates of USP22, MRP1, and P-gp in the oxaliplatin chemotherapy-sensitive group were significantly lower than those in the chemotherapy-resistant group, the difference was statistically significant (all P<0.05), and USP22 was positively correlated with the expressions of MRP1 and P-gp in colorectal cancer tissues (r1=0.377, r2=0.423, both P<0.05). Conclusions: The up-regulation of USP22 is related to the acquired resistance of colorectal cancer cells to oxaliplatin. USP22 may be involved in the process of platinum-based chemotherapy resistance of colorectal cancer by regulating the expressions of P-gp and MRP1.

To explore the mechanism of Hedyotis Diffusae Herba-Smilacis Glabrae Rhizoma(HDH-SGR) in treating lung adenocarcinoma based on big data bioinformatics combined with network pharmacology analysis and molecular docking technology. The chemical components and potential therapeutic targets of HDH-SGR were obtained from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP). Lung adenocarcinoma-related genes were obtained from The Cancer Genome Atlas(TCGA), Therapeutic Target Database(TTD), Pharmacogenetics and Pharmacogenomics Knowledge Base(PharmGKB), Online Mendelian Inheritance in Man(OMIM), DrugBank, and GeneCards. &quot;Drug component-target&quot; network was constructed using Cytoscape to screen out key compounds. STRING was used to build protein-protein interaction(PPI) network and core targets were screened out by Cytoscape-CytoNCA topology analysis. Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) analyses of target genes were performed by R-clusterProfiler. Finally, key compounds were docked to core target genes using AutoDock. The results showed that 22 active compounds and 499 potential therapeutic targets were obtained from HDH-SGR. A total of 14 332 lung adenocarcinoma-related targets were screened out through six data platforms, including 182 common targets. Fifteen core targets were screened out from the PPI network. GO and KEGG analyses revealed significant enrichment of relevant target genes in various biological processes, cellular functions(e.g., response to lipopolysaccharide, nuclear receptor activity, and ligand-activated transcription factor activity) and close relationship between target genes and non-small cell lung cancer signaling pathways. Based on the results of molecular docking validation, diosgenin, quercetin, naringenin, taxifolin, 2-methoxy-3-methyl-9,10-anthraquinone, stigmasterol, and β-sitosterol were able to bind tightly to the core targets. HDH-SGR can intervene in lung adenocarcinoma through multiple targets and signaling pathways, such as non-small cell lung cancer signaling pathways. The binding of active components in Chinese medicine to key targets is presumedly one of the mechanisms that produce therapeutic effects.

Colorectal cancer is a malignancy with high mortality. Huangqin Tea(HQT) can exert potential preventive and therapeutic effects on colorectal cancer. Flavonoids are the main compounds in HQT, but the pharmacodynamic material basis and mechanism are unclear. Network pharmacology and molecular docking were used to predict and analyze the targets and signaling pathways of HQT in the prevention and treatment of colorectal cancer. The active components of flavonoids in HQT were searched and screened out by literature review and FAFDrugs4. The related targets of active components were predicted by SwissTargetPrediction, STITCH, and TCMSP. Colorectal cancer-related genes were collected from OMIM, TTD, and GeneCards. The common targets were obtained as the potential targets of HQT in the prevention and treatment of colorectal cancer. Metascape was used for GO function enrichment and KEGG pathway enrichment analyses. Cytoscape was used to construct the protein-protein interaction(PPI) network and &quot;component-target-disease-pathway&quot; network to obtained and analyze core targets and key components. AutoDock Vina was used for molecular docking verification of key components and core targets. The results showed that apigenin, luteolin, wogonin, and baicalein were presumedly the key active components in the prevention and treatment of colorectal cancer, and core targets included TP53, AKT1, VEGFA, PIK3 CA, and SRC. The key KEGG signaling pathways mainly involved PI3 K-AKT, AGE-RAGE, p53, NF-κB, Wnt, Hippo, and calcium signaling pathways. Further molecular docking results showed that four key components showed strong hydrogen bonding ability with the five core targets. This study preliminarily reveals the pharmacodynamic material basis and potential mechanism of HQT in the prevention and treatment of colorectal cancer and provides a theoretical and scientific basis for the application of HQT.

To investigate the effect of trending up-regulation LncRNA CASC11 which is differentially expressed during the malignant transformation of human bronchial epithelial cells(16 HBE) induced by glycidyl methacrylate(GMA).

The concept of spread through air spaces (STAS) was first proposed in the World Health Organization (WHO) Classification of Tumors of the Lung, Pleura, Thymus and Heart (version 2015). STAS is defined as the micropapillary clusters, solid nests or single cells of tumor that exist in the air spaces of the surrounding lung parenchyma beyond the edge of the main tumor. Meanwhile, apart from the traditional invasion modes of lung adenocarcinoma (interstitial, visceral pleura and lym-phovascular invasion), STAS has been identified as the fourth invasion mode of lung adenocarcinoma. In recent years, the research on STAS has been a hot spot in the field of lung adenocarcinoma. The existence of STAS is related to lung cancer histopathology, gene mutation and other factors, and many studies have also confirmed that it can be used as an independent factor for tumor recurrence and prognosis. However, according to some studies, human factors can cause morphological artifacts of STAS, which still needs to be distinguished in clinical work. This paper reviews the research progress of STAS classification, related pathological features, genetic status changes, and human factors that may cause STAS artifacts.
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To identify the key hub genes in prostate cancer metastasis based on weighted gene co-expression network analysis (WGCNA) and verify the identified genes.

Objective: To investigate the effect of apoptosis-associated protein kinase-like 1 (DAPL1) hypomethylation on prognosis of lung cancer patients with epidermal growth factor receptor gene exon 19 deletion (EGFR Del19) mutation. Methods: The clinicopathological data of lung cancer patients in databases of genomic data sharing (GDC) TCGA lung adenocarcinoma, TCGA lung adenocarcinoma, and TCGA lung cancer were collected to analyze the effect of DAPL1 methylation level on the prognosis of patients with EGFR Del19 mutation. Linear regression model was used for correlation analysis, Kaplan-Meier method was used to draw the survival curve, and the difference of survival curve between the two groups was tested by Log rank. Results: In GDC TCGA lung adenocarcinoma, TCGA lung adenocarcinoma and TCGA lung cancer databases, the 5-year survival rates of lung cancer patients with high DAPL1 expression (31.9%, 27.5% and 33.0%, respectively) were higher than those with low DAPL1 expression (11.0%, 11.6% and 13.8%, respectively). The differences were statistically significant (P=0.006, 0.028 and 0.025, respectively). The median expression levels of DAPL1 in patients with EGFR Del19 mutation (12.8, 2.75 and 2.9, respectively) were higher than those in patients with other EGFR mutations (11.6, 1.75 and 1.8, respectively, P<0.05). In TCGA lung adenocarcinoma and TCGA lung cancer database, the 5-year survival rate of lung cancer patients with lower DAPL1 methylation levels (22.4% and 16.4%, respectively) were higher than those of lung cancer patients with higher DAPL1 methylation levels (15.1% and 14.2%, respectively), with statistical significance (P<0.05). The expression level of DAPL1 was positively correlated with the EGFR mutant subtype (r=0.909, P<0.05), and negatively correlated with DNA methylation (r=-0.891, P<0.05). The expression of DAPL1 in lung cancer patients was regulated by DNA methylation, which affected the prognosis of lung cancer patients. Conclusion: High DAPL1 expression, or hypomethylation, is associated with lung cancer EGFR Del19 mutation subtype, and DAPL1 hypomethylated lung cancer patients have longer overall survival.

Objective: To explore the relationship between expression levels of CLOCK mRNA and protein and the clinical characteristics of patients with nasopharyngeal carcinoma. Methods: The frozen tissue specimens from 33 patients with nasopharyngeal carcinoma in the Affiliated Tumor Hospital of Guizhou Medical University from 2018 to 2019 were collected. Seventeen cases of tissue specimens from patients with nasopharyngeal chronic inflammation in the Affiliated Hospital of Guizhou Medical University in 2019 were collected. From 2008 to 2014, 68 cases of formalin-fixed paraffin-embedding (FFPE) nasopharyngeal carcinoma tissue and 37 cases of FFPE nasopharyngeal chronic inflammation tissue were collected from the Affiliated Tumor Hospital of Guizhou Medical University. Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot (WB) were used to detect the mRNA and protein expression levels of CLOCK. The nasopharyngeal carcinoma cells including CNE1, CNE2, 5-8F and the normal nasopharyngeal epithelial cell NP69 were cultured. qRT-PCR was used to detect the expression level of CLOCK mRNA in each cell line at the time points of ZT2, ZT6, ZT10, ZT14, ZT18 and ZT22. The cosine method was used to fit the rhythm of CLOCK gene in nasopharyngeal carcinoma. The protein expression of CLOCK protein was detected by using immunohistochemical method in 68 cases of nasopharyngeal carcinoma and 37 cases of nasopharyngeal chronic inflammation tissue. Survival was analyzed by Kaplan-Meier method and Log rank test, and the influencing factors was analyzed by Cox regression model. Results: The expression levels of CLOCK mRNA in CNE1, CNE2 and 5-8F cells (0.63±0.07, 0.91±0.02 and 0.33±0.04, respectively) were lower than that in NP69 cell (1.00±0.00, P<0.05). The expression levels of CLOCK protein in CNE1, CNE2 and 5-8F cells (0.79±0.06, 0.57±0.05 and 0.74±0.10, respectively) were lower than that of NP69 cells (1.00±0.00, P<0.05). The expressions of CLOCK mRNA in nasopharyngeal carcinoma cells including CEN1, CNE2, 5-8F and normal nasopharyngeal epithelial cell NP69 were different at different time points, with temporal fluctuations. The fluctuation periods of CLOCK mRNA in CNE1, CNE2, 5-8F, and NP69 cells were 16, 14, 22 and 24 hours, respectively. The peak and trough times were ZT10: 40 and ZT18: 40, ZT10 and ZT3, ZT14: 30 and ZT3: 30, ZT12: 39 and ZT0: 39, respectively. CLOCK mRNA and protein expression levels in nasopharyngeal carcinoma tissues (0.37±0.20 and 0.20±0.26, respectively) were lower than those in nasopharyngeal chronic inflammation tissues (1.00±0.00 and 0.51±0.41, respectively, P<0.05). The 1, 3, and 5-year survival rates of patients in the CLOCK protein high expression group (CLOCK protein expression level ≥ 0.178) were 96.2%, 92.1%, and 80.1%, respectively, which were higher than those in the low expression group (CLOCK protein expression level <0.178, 92.9% , 78.6% and 57.1%, respectively, P=0.009). The 1, 3, and 5-year progression-free survival (PFS) rates of patients in the CLOCK protein high expression group were 96.2%, 87.8%, and 87.7%, respectively, which were higher than those in the low expression group (92.7%, 82.2%, and 70.8%, respectively, P=0.105). Compared with the low-expression group (100.0%, 96.9%, and 90.0%, respectively), the 1, 3, and 5-year recurrence-free survival rates of patients in the CLOCK protein high expression group (100.0%, 95.7%, and 95.7%, respectively) were not statistically significant (P=0.514). Compared with the low-expression group (92.7%, 82.2%, and 79.3%), the 1, 3, and 5-year survival rates without metastasis in the CLOCK protein high expression group (96.2%, 92.0%, and 92.0%, respectively) were not statistically significant (P=0.136). CLOCK protein expression and T stage were independent prognostic factors of overall survival (P<0.05). Conclusions: The expression of CLCOK is downregulated in the nasopharyngeal carcinoma cell and nasopharyngeal carcinoma tissues. Clock gene CLOCK is rhythmically expressed in the nasopharyngeal carcinoma cells and normal nasopharyngeal epithelial cells. Compared with normal nasopharyngeal epithelial cells, the fluctuation period of CLOCK in nasopharyngeal carcinoma cells is shortened. The overall survival of patients in the CLOCK protein high expression group is better than that of low expression group. The expression of CLOCK protein is an independent influencing factor for overall survival. CLOCK gene may be a potential tumor suppressor gene in the nasopharyngeal carcinoma.

Objective: To investigate the effect of siRNA targeting inhibition of α-enolase (ENO1) combined with paclitaxel on the proliferation, invasion and apoptosis of hepatocellular carcinoma SK-HEP-1 cell and its mechanism. Methods: siRNA-ENO1 (siRNA-ENO1 group) and siRNA-negative control (siRNA-NC group) were transfected into SK-HEP-1 cells in vitro, the untransfected SK-HEP-1 cells were used as the control group, and the transfection effect was detected by real-time fluorescent quantitative polymerase chain reaction and western blotting. After SK-HEP-1 cells were treated with 0, 2.5, 5, 10, 20 and 40 μg/L paclitaxel for 48 hours, the cell survival rate was measured by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) method and the semi inhibitory concentration of paclitaxel was calculated. SK-HEP-1 cells transfected with siRNA-ENO1 or siRNA-NC were treated with 10 μg/L paclitaxel as paclitaxel+ siRNA-ENO1 group and paclitaxel+ siRNA-NC group. The proliferation, clonogenesis, invasion and apoptosis of siRNA-NC group, siRNA-ENO1 group, paclitaxel+ siRNA-ENO1 group and paclitaxel+ siRNA-NC group were detected by MTT, clonogenesis, Transwell chamber and flow cytometry respectively. The expression levels of the phosphorylation of phosphatidylinositol-3-kinase (p-PI3K), p-protein kinase B (Akt) and proliferating cell nuclear antigen (PCNA), matrix metalloproteinase 9 (MMP-9) and B lymphocytoma-2 gene (Bcl-2) were detected by western blotting. Results: Compared with the control group (1.00±0.00 and 0.69±0.04, respectively), the expression levels of ENO1 mRNA and protein (0.25±0.03 and 0.23±0.02, respectively) in siRNA-ENO1 group decreased significantly (P<0.05), but there were no significant differences in the expression levels of ENO1 mRNA and protein in siRNA-NC group (P>0.05). Compared without treatment group [(100.00±0.00)%, P<0.05], the survival rates of SK-HEP-1 cells treated with 2.5, 5, 10, 20 and 40 μg/L paclitaxel [(88.65±6.46)%, (72.36±6.08)%, (60.48±4.23)%, (38.52±3.56)% and (20.75±2.32)%, respectively] decreased significantly (P<0.05), and the semi inhibitory concentration of paclitaxel was 13.26 μg/L. The cell survival rate and clone formation rate of siRNA-ENO1 group [(68.86±5.12)% and (18.12±2.25)%, respectively] were lower than those of siRNA-NC group [(100.00±0.00)% and (29.65±3.06)%, respectively, P<0.05]. The cell survival rate and clone formation rate of the paclitaxel+ siRNA-ENO1 group [(43.28±2.64)% and (8.72±0.52)%, respectively] were significantly different from those of the paclitaxel+ siRNA-NC group [(61.75±5.06)% and (13.48±2.16)%, respectively, P<0.05] and siRNA-ENO1 groups [(68.86±5.12)% and (18.12±2.25)%, respectively, P<0.05]. Cell invasion number in paclitaxel+ siRNA-ENO1 group (23.64±2.12) was lower than that in siRNA-ENO1 group and paclitaxel+ siRNA-NC group (42.16±2.75 and 37.35±2.42, respectively, P<0.05). The apoptosis rates of paclitaxel+ siRNA-NC group and siRNA-ENO1 group [(17.49±1.35)% and (15.29±1.50)%, respectively] were higher than that of siRNA-NC group [(7.21±0.70)%, P<0.05]. The apoptosis rate in the paclitaxel+ siRNA-ENO1 group [(24.59±2.40)%] was higher than those in the paclitaxel+ siRNA-NC group and siRNA-ENO1 group [(17.49±1.35)% and (15.29±1.50)%, respectively, P<0.05]. The expression levels of ENO1, PI3K/Akt signaling pathway related proteins including p-PI3K and p-Akt and the expression levels of PCNA, MMP-9 and Bcl-2 in siRNA-ENO1 group and paclitaxel+ siRNA-NC group were lower than those in siRNA-NC group (P<0.05). The expression levels of ENO1, p-PI3K, p-Akt, PCNA, MMP-9 and Bcl-2 in paclitaxel+ siRNA-ENO1 group were lower than those in siRNA-ENO1 group or paclitaxel+ siRNA-NC group (P<0.05). Conclusion: siRNA targeting inhibition of ENO1 expression can enhance the inhibitory effect of paclitaxel on proliferation, invasion and apoptosis of SK-HEP-1 cells, and its mechanism may be related to the inhibition of PI3K/AKT signaling pathway.

To investigate the differentially expressed genes related to the survival of testicular seminoma patients and the pathogenesis of the malignancy.

To identify the key genes associated with the pathogenesis of PCa using the bioinformatics approach for a deeper insight into the molecular mechanisms underlying the development and progression of PCa.

To search for the potential genes associated with the recurrence of prostate cancer (PCa) after radical prostatectomy so as to improve the prognosis of the patient.

Prostate cancer (PCa) is a maligmancy with high morbidity and mortality. Bone metastasis is the main cause of short survival time and difficulties in the treatment and prevention of PCa. Previous findings of our team showed 155 bone-specific genes highly expressed in bone metastatic PC3 cells, which is considered to be the key to their adaptation to the bone micro-environment, proliferation and formation of metastatic tumor, and extensively exists in cancer metastasis in multiple systems. This review summarizes the published literature on the highly expressed bone-specific genes, focusing on the roles and values of these genes in the metastasis, progression, clinical diagnosis, treatment and prognosis of PCa, offering a prospect of the direction and targets in the studies of PCa bone metastasis so as to enrich the bone metastatic theories and clinical treatment principles of this disease in the future.