The efficacy and safety of hydrotherapy in patients with knee osteoarthritis: a meta-analysis of randomized controlled trials.

BACKGROUND: Currently, there is poor evidence of the effect of hydrotherapy on patients with knee osteoarthritis (OA). The authors performed a meta-analysis from randomized controlled trials to determine the efficacy and safety of a hydrotherapy program on measures of pain and knee function in individuals living with knee OA. METHODS: A literature review included PubMed, EMBASE, Cochrane Library, Science Citation Index, ScienceDirect, and Ovid. Studies evaluating the efficacy of hydrotherapy for knee OA up to August 2023 were included. The research was reported based on the preferred reporting items for systematic reviews and meta-analysis guidelines to ensure the reliability and verity of results. Statistical analysis was performed using Stata/SE version 15.0. RESULTS: A total of six randomized controlled trials were included for data extraction and meta-analysis. The present study revealed that there were significant differences between the two groups regarding the pain intensity at 1 week (WMD=-0.429; 95% CI: -0.679 to -0.179; P =0.001), 4 week (WMD=-0.308; 95% CI: -0.587 to -0.030; P =0.030) and 8 week (WMD=-0.724; 95% CI: -1.099 to -0.348, P <0.001). Furthermore, hydrotherapy was associated with improved outcome of the Western Ontario and McMaster Universities Arthritis index at 1 week (WMD=-3.314; 95% CI: -6.484 to -0.145, P =0.040), 4 week (WMD= -3.630; 95% CI: -6.893 to -0.366, P =0.029) and 8 week (WMD=-3.775; 95% CI: -7.315 to -0.235; P =0.037). No serious adverse events were observed in all patients who received hydrotherapy. CONCLUSION: Hydrotherapy is efficacious and safe for reducing pain and improving functional status in individuals with knee OA, without increasing the risk of adverse effects.

Jiangqi Pingxiao formula regulates dendritic cell apoptosis in an autophagy-dependent manner through the AMPK/mTOR pathway in a murine model of OVA-induced asthma.

ETHNOPHARMACOLOGICAL RELEVANCE: Allergic asthma is a recurring respiratory condition that typically manifests during childhood or adolescence. It is characterized by a dominant type II immune response triggered by the identification and capturing of inhaled allergens by dendritic cells (DCs). Jiangqi Pingxiao Formula (JQPXF), a prescription medicine used for the treatment of pediatric asthma, has been clinically proven to be both safe and effective. However, its mechanism of action in the treatment of asthma has not been fully been fully elucidated. Recent research suggests that several natural compounds have the potential to target dendritic cells (DCs) and alleviate ovalbumin (OVA)-induced asthma, which may also be found within JQPXF. AIM OF THE STUDY: This study aimed to elucidate the effect of JQPXF on OVA-induced asthma model and its molecular mechanism targeting DCs. MATERIALS AND METHODS: The main constituents of JQPXF were analyzed by ultra performance liquid chromatography (UPLC). An asthma model was established by OVA. Hematoxylin-eosin staining and measurement of respiratory function was used to evaluate the treatment effect of JQPXF on asthmatic mice. Cytokine (IL-5, IL-13 and IgE) concentrations were determined by enzyme-linked immunosorbent assay (ELISA). Flow cytometry was employed to evaluate inflammatory cell infiltration (T helper 2 cells and DCs) in vivo and DC survival in vivo and vitro. Western blot and immunofluorescence were used to verify the molecular mechanisms. RESULTS: The results suggest that JQPXF can ameliorate pathological conditions and improve lung function in asthmatic mice, as well as the Th2 cells. Treatment with JQPXF significantly reduced the number of DCs and increased the number of Propidium iodide+ (PI) DCs. Furthermore, JQPXF upregulated protein levels of the pro-apoptotic factors Cleaved-caspase-3 and Bax, while downregulating the anti-apoptotic factor Bcl-2. Simultaneously, JQPXF increased autophagy levels by facilitating p62 degradation and promoting translation from LC3B I to LC3B II of DCs in vitro, as well as reducing the integrated optical density (IOD) of p62 within the CD11c-positive area in the lung. 3-Methyladenine (3-MA) was used to block autophagic flux and the apoptotic effect of JQPXF on DCs was abolished in vitro, with the number of DCs decreased by JQPXF being reversed in vivo. We further investigated the upstream key regulator of autophagy, the AMPK/mTOR pathway, and found that JQPXF increased AMPK phosphorylation while decreasing mTOR phosphorylation levels. Additionally, we employed Compound C (CC) as an AMPK inhibitor to inhibit this signaling pathway, and our findings revealed that both autophagic flux and apoptotic levels in DCs were abolished in vitro. CONCLUSIONS: In summary, we have demonstrated that JQPXF could alleviate type II inflammation in an asthmatic model by promoting the apoptosis of DCs through an autophagy-dependent mechanism, achieved by regulating the AMPK/mTOR signaling pathway.

Novel PPFIA1-ALK, ALK-C2orf91(intergenic) double-fusion responded well to alectinib in an advanced lung adenocarcinoma patient: a case report.

Non-small cell lung cancers (NSCLCs) with anaplastic lymphoma kinase (ALK)-rearrangement have favorable responses to ALK inhibitors. However, ALK fusion mutations harbored approximately 90 distinct fusion partners. Patients with different ALK fusions might respond distinctly to different-generation ALK inhibitors. In this case report, we identified a novel non-reciprocal ALK fusion, ALK-C2orf91(intergenic) (A19: intergenic) and PPFIA1-ALK (P2:A20), by next-generation DNA sequencing in an advanced lung adenocarcinoma patient. After 2 months of alectinib, the targeted lung lesion regressed significantly, and evaluation of therapeutic efficiency indicated partial response. To date, the patient had achieved 12 months of progression-free survival from alectinib treatment. Our study extended the spectrum of ALK fusion partners in ALK-positive NSCLC, and we reported a new ALK fusion, PPFIA1-ALK and ALK-C2orf91(intergenic), and its sensitivity to alectinib firstly in lung cancer. We believe that this case report has an important clinical reference.

Young LINE-1 transposon 5' UTRs marked by elongation factor ELL3 function as enhancers to regulate naïve pluripotency in embryonic stem cells.

LINE-1s are the major clade of retrotransposons with autonomous retrotransposition activity. Despite the potential genotoxicity, LINE-1s are highly activated in early embryos. Here we show that a subset of young LINE-1s, L1Md_Ts, are marked by the RNA polymerase II elongation factor ELL3, and function as enhancers in mouse embryonic stem cells. ELL3 depletion dislodges the DNA hydroxymethylase TET1 and the co-repressor SIN3A from L1Md_Ts, but increases the enrichment of the Bromodomain protein BRD4, leading to loss of 5hmC, gain of H3K27ac, and upregulation of the L1Md_T nearby genes. Specifically, ELL3 occupies and represses the L1Md_T-based enhancer located within Akt3, which encodes a key regulator of AKT pathway. ELL3 is required for proper ERK activation and efficient shutdown of naïve pluripotency through inhibiting Akt3 during naïve-primed transition. Our study reveals that the enhancer function of a subset of young LINE-1s controlled by ELL3 in transcription regulation and mouse early embryo development.

LncRNA DUXAP8 induces breast cancer radioresistance by modulating the PI3K/AKT/mTOR pathway and the EZH2-E-cadherin/RHOB pathway.

Radiation resistance poses a major clinical challenge in breast cancer (BC) treatment, but little is known about how long noncoding RNA (lncRNA) may regulate this phenomenon. Here, we reported that DUXAP8 was highly expressed in radioresistant BC tissues, and high expression of DUXAP8 was associated with poor prognosis. We found that the overexpression of DUXAP8 promoted radioresistance, while the knockdown of DUXAP8 expression increased radiosensitivity. Further studies revealed that DUXAP8 enhanced the radioresistance of BC cells by activating the PI3K/AKT/mTOR pathway and by repressing the expression of E-cadherin and RHOB through interaction with EZH2. Together, our work demonstrates that the overexpression of DUXAP8 promotes the resistance of BC cells toward radiation through modulating PI3K/AKT/mTOR pathway and EZH2-E-cadherin/RHOB axis. Targeting DUXAP8 may serve as a potential strategy to overcome radioresistance in BC treatment.

Comparison of Efficacy and Safety between Thrombolysis Plus Anticoagulation vs. Anticoagulation Alone for the Treatment of Acute Submassive Pulmonary Embolism: A Systematic Review and Meta-analysis.

OBJECTIVE: The objective of this study is to compare the efficacy and safety of thrombolysis plus anticoagulant therapy vs. anticoagulant therapy alone in acute submassive pulmonary embolism (PE). MATERIALS AND METHODS: The PubMed, Embase, and Cochrane Library databases were searched for randomized clinical trials comparing thrombolytic therapy and anticoagulation vs. anticoagulation alone in acute submassive PE patients from 1 Jan 1980 to 20 Jan 2021, with no drug or dose restrictions. Data on upgraded treatment of clinical deterioration, all-cause mortality, PE recurrence and bleeding events were extracted and analyzed using Revman 5.3 software. RESULTS: A total of 10 randomized controlled trials involving 1871 patients were included in the study after screening. In terms of efficacy, thrombolysis combined with anticoagulant therapy reduced the need for upgrading treatment (3.6 vs. 10.9%, risk ratio (RR) 0.36, 95% confidence interval (CI) 0.24- 0.54, p<0.00001) and PE recurrence (0.8 vs. 2.9%, RR 0.33, 95% CI 0.16-0.69, p=0.003) in patients with acute submassive PE. Compared with anticoagulant therapy alone, the concomitant use of thrombolysis was associated with lower all-cause mortality (1.3 vs. 3.0%, RR 0.47, 95% CI 0.26-0.87, p=0.02), but it increased minor bleeding rate (31.4 vs. 8.4%, RR 3.71, 95% CI 2.82-4.88, p<0.0001) and major bleeding rate (8.8 vs. 2.6%, RR 3.35, 95%CI 2.03-5.54, p<0.0001). CONCLUSION: The use of thrombolysis plus anticoagulant therapy in acute submassive PE was negatively associated with patients requiring escalation of treatment, PE recurrence, and all-cause mortality, but it was positively associated with bleeding.

Does bariatric surgery really benefit patients before total knee arthroplasty? A systematic review and meta-analysis.

PURPOSE: At present, whether bariatric surgery before total knee arthroplasty (TKA) affects the prognosis of subsequent TKA has been a topic of debate in the academic community. The primary purpose of this systematic review and meta-analysis was to investigate the effect of previous bariatric surgery on prosthetic revisions and postoperative complications after TKA. METHODS: We included prospective and observational studies published in English involving patients who had undergone bariatric surgery prior to TKA and compared them with morbidly obese patients with no history of bariatric surgery. The Newcastle-Ottawa Scale was used to assess the methodological quality of non-randomized case-control studies. The outcomes included revisions, infections, venous thromboembolism (VTE), blood transfusion, mortality, stiffness or manipulation under anesthesia (MUA), and medical complications. RESULTS: Of the 9 included studies with 166047 patients, 4 were matched cohort studies, 2 were unmatched cohort, and 3 were database studies. Methodological quality was high in ten studies and moderate in thirteen studies. Our analysis demonstrated that patients with TKA who had undergone prior bariatric surgery were associated with increased risks of long-term revision, long-term infection, long-term stiffness or MUA and blood transfusions, whereas prior bariatric surgery did not increase the risk of short-term complications and short-term revision. CONCLUSION: This meta-analysis highlights the risks of bariatric surgery prior to TKA and suggests that prior bariatric surgery may increase the risk of perioperative blood transfusion and also the risk of revision and infection in long-term follow-up. Surgeons can use this information to help counsel patients undergoing bariatric surgery before primary TKA.

miR-17-5p/HOXA7 Is a Potential Driver for Brain Metastasis of Lung Adenocarcinoma Related to Ferroptosis Revealed by Bioinformatic Analysis.

Objectives: Present study aims to identify the essential mRNAs responsible for the development of brain neurovascular-related metastases (BNM) among lung adenocarcinoma (LUAD) patients. Further, we attempted to predict brain metastases more accurately and prevent their development in LUAD patients. Methods: Transcriptome data analysis was used to identify differentially expressed mRNAs (DEMs) associated with brain metastasis, and thereby the ferroptosis index (FPI) is calculated using a computational model. Meanwhile, the DEmRNAs linked with FPI, and brain metastasis were derived by the intersection of these two groups of DEMs. We also constructed a ceRNA network containing these DEmRNAs, identifying the HCP5 /hsa-miR-17-5p/HOXA7 axis for analysis. Further, a clinical cohort was employed to validate the regulatory roles of molecules involved in the ceRNA regulatory axis. Results: Here we report the development of a ceRNA network based on BNM-associated DEMs and FPI-associated DEmRNAs which includes three core miRNAs (hsa-miR-338-3p, hsa-miR-429, and hsa-miR-17-5p), three mRNAs (HOXA7, TBX5, and TCF21), and five lncRNAs (HCP5, LINC00460, TP53TG1). Using gene set enrichment analysis (GSEA) and survival analysis, the potential axis of HCP5 /hsa-miR-17-5p/HOXA7 was further investigated. It is found that HOXA7 and ferroptosis index are positively correlated while inhibiting tumor brain metastasis. It may be that HCP5 binds competitively with miR-17-5p and upregulates HOXA7 to increase iron death limiting brain cancer metastases. Conclusions: The expression of both HOXA7 and HCP5 is positively correlated with FPI, indicating a possible link between ferroptosis and BNM. According to the results of our study, the ferroptosis-related ceRNA HCP5 /hsa-miR-17-5p/HOXA7 axis may contribute to the development of BNM in LUAD patients.

Quercetin attenuates the proliferation, inflammation, and oxidative stress of high glucose-induced human mesangial cells by regulating the miR-485-5p/YAP1 pathway.

BACKGROUND: Diabetic nephropathy (DN) is a kidney damage caused by diabetes and the main cause of end-stage renal disease. However, the current treatment of DN has many limitations. Quercetin is a bioflavonoid compound with therapeutic benefits in metabolic diseases. This study aims to determine the therapeutic potentials and underlying mechanism of quercetin on DN. METHODS: We collected blood samples from DN patients and healthy controls and treated human mesangial cells (HMCs) with high glucose (HG) to establish an in vitro model of DN. Then we assessed the expression difference of miR-485-5p as well as YAP1 in serum of DN patients and healthy controls and between HG-induced HMCs and control cells. qRT-PCR and western blot were performed to assess miR-485-5p and YAP1 expression levels; CCK-8 and ELISAs were used to examine cell proliferation, inflammation, and oxidative stress. Dual luciferase reporter assay was implemented to detect the binding of miR-485-5p and YAP1 mRNA sequence. RESULTS: Quercetin suppressed proliferation, inflammation, and oxidative stress of HMCs induced by HG. As for mechanism, miR-485-5p directly bound to YAP1 and inhibited YAP1 expression. The downregulation of miR-485-5p and upregulation of YAP1 were also observed in the serum of DN patients. Quercetin modulated miR-485-5p/YAP1 axis to regulate HG-induced inflammation and oxidative stress. CONCLUSION: Quercetin inhibits the proliferation, inflammation, and oxidative stress of HMCs induced by HG through miR-485-5p/YAP1 axis, which might provide a novel treatment strategy for DN.

Impact of KMN network genes on progression and prognosis of non-small cell lung cancer.

The Knl1-Mis12-Ndc80 (KMN) network genes (including KNL, MIS12 and NDC80 complexes) encode a highly conserved network of protein complexes that act in cell mitosis. In recent years, multiple studies revealed that KMN network genes also play a vital role in tumor appearance and growth. However, the role of the KMN gene network in non-small cell lung cancer (NSCLC) remains unknown. In this study, we analyzed the effects of KMN genes expression and clinical phenotype in patients with lung adenocarcinoma (LUAD). The expression of KMN network genes and related clinical information was extracted from The Cancer Genome Atlas. The samples were classified into cluster I and II by consistent clustering. We analyzed the gene distribution by principal component analysis, and the potential risk characteristics were analyzed using the least absolute shrinkage and selection operator Cox regression algorithm. Univariate and multivariate Cox regression analyses were used to analyze the clinical information. The Database for Annotation, Visualization, and Integrated Discovery, Gene MANIA and gene set enrichment analysis were used to analyze function and correlation among genes of the KMN network. The expression levels of nine out of ten KMN genes were significantly up-regulated in LUAD and were associated with poor overall survival (OS). Higher expression of NDC80 and KNL1 was related to low OS in both univariate and multivariate analyses. According to two independent prognostic KMN network genes (KNL1 and NDC80), a risk signature was established to predict the prognosis of patients with LUAD. Additionally, the genes NDC80 and KNL1 were considerably enriched in pathways associated with signaling pathways, biological processes, and the cell cycle. The results indicate that KMN network genes are intimately related to lung adenocarcinoma. KMN network genes are involved in the malignant process of LUAD. Assessment of NDC80 and KNL1 might be helpful for prognostic stratification and treatment strategy development.

Analysis at the single-cell level indicates an important role of heterogeneous global DNA methylation status on the progression of lung adenocarcinoma.

Aberrant DNA modifications affect the tumorigenesis and progression of lung cancer. However, the global methylation status of tumor cells and the heterogeneous methylation status of cells within the same tumor need further study. We used publicly available single-cell RNAseq data to investigate the impact and diversity of global methylation status on lung adenocarcinoma. Clustering cells into subgroups and cell differentiation pseudotime analysis, based on expression profile, demonstrated that the global methylation status was crucial to lung adenocarcinoma function and progression. Hypermethylated tumor cells had increased activity related to the hypoxia response. Hyper- and hypomethylated cells indicated upregulation in pathways involving focal adhesion and cell junctions. Pseudotime analysis showed that cell clusters with unique methylation activities were located at the ends of the putative trajectories, suggesting that DNA methylation and demethylation activities were essential to tumor cell progression. Expression of SPP1 was associated with the global methylation status of tumor cells and with patient prognosis. Our study identified the importance and diversity of global DNA methylation status by analysis at the single-cell level. Our findings provide new information about the global DNA methylation status of tumor cells and suggest new approaches for precision medical treatments for lung adenocarcinoma.

LncRNA ACTA2-AS1 suppress colon adenocarcinoma progression by sponging miR-4428 upregulation BCL2L11.

BACKGROUND: Long non-coding RNA is considered to be essential to modulate the development and progression of human malignant cancers. And long non-coding RNA can act as crucial modulators by sponging the corresponding microRNA in tumorigenesis. We aimed to elucidate the function of ACTA2-AS1 and its molecular mechanism in colon adenocarcinoma. MATERIALS AND METHODS: The expression of ACTA2-AS1, miR-4428 and BCL2L11 in colon adenocarcinoma tissues were detected via qRT-PCR. SW480 and HT29 cells were transfected with shRNA ACTA2-AS1, OE ACTA2-AS1, miRNA mimics of miR-4428, miR-4428 inhibitor, si-BCL2L11 and over-expression of si-BCL2L11. Cell proliferation, colony formation and apoptosis were respectively assessed using CCK-8 assay, colony assay and flow cytometry. Luciferase reporter assay was performed to verify the targets of ACTA2-AS1 and miR-4428. Tumor subcutaneous xenograft mode was constructed to explore tumor growth in vivo. RESULTS: ACTA2-AS1 was obviously downregulated in human colon adenocarcinoma tissues and colon adenocarcinoma cell lines. Silence or over-expression of ACTA2-AS1 promoted or inhibited cell proliferation and colony formation abilities, and regulated apoptosis. The silence of ACTA2-AS1 resulted in the decrease of Bax and increase of Bal2, while restored in OE ACTA2-AS1 group when compared with the control transfected cells. In addition, luciferase reporter assay revealed that ACTA2-AS1 interacted with miR-4428 and suppressed its expression. miR-4428 could bind to 3' untranslated region of BCL2L11 and modulated the expression of BCL2L11 negatively. Knockdown of ACTA2-AS1 and over-expression of BCL2L11 reversed the biological function that ACTA2-AS1 mediated by knockdown ACTA2-AS1 alone. CONCLUSION: Our data demonstrated that ACTA2-AS1 could suppress colon adenocarcinoma progression via sponging miR-4428 to regulate BCL2L11 expression.

Columbamine suppresses the proliferation and malignization of colon cancer cells via abolishing Wnt/ß-catenin signaling pathway.

BACKGROUND: Colon cancer is one of the most common malignancies worldwide. Because of the side effects and defects in tolerance of chemotherapy, it is necessary to discover new drugs for colon cancer treatment. Columbamine has been identified as an effective anti-osteosarcoma compound with only minor side effects. In this study, we analyzed the anticancer effect of columbamine on colon cancer. METHODS: Human colon cancer cell lines were treatment with columbamine. MTT assay, colony formation assay, apoptosis detection and tumorigenicity assay were performed to detect the protective effect of columbamine on colon cancer development. Western blot assay and luciferase reporter assay were conducted to investigate the potential mechanism of the columbamine treatment. RESULTS: Columbamine significantly inhibited the proliferation, migration, invasion process of colon cancer cells, and dramatically promoted the apoptosis rate of colon cancer cells to further suppress the development of colon cancer to tumor. Both the signaling transducing and key factors expression of Wnt/ß-catenin signaling pathway were obviously repressed by columbamine treatment in a dose-dependent manner. CONCLUSION: The present study indicated that columbamine exerts its anti-tumor effect in colon cancer cells through abolishing Wnt/ß-catenin signaling pathway. Columbamine may be a new therapy compound for colon cancer.

Curative effect of endostar combined with oxaliplatin in the treatment of primary hepatic carcinoma and its influence on immune cells.

Curative effect and adverse reactions of oxaliplatin combined with endostar in the interventional treatment of primary hepatic carcinoma (PHC) were investigated. A total of 101 PHC patients from October 2012 to December 2014 in The First Affiliated Hospital of Xi'an Jiaotong University were retrospectively collected. Fifty patients in combined therapy group were treated with oxaliplatin combined with endostar, while the remaining 51 patients in oxaliplatin group were treated with oxaliplatin alone. The treatment lasted for a total of 4 cycles (20 days as 1 cycle). The ratios of cluster of differentiation 3 (CD3)+, CD4+ and CD8+ were detected via enzyme-linked immunosorbent assay (ELISA). The objective response rate in combined therapy group was 92.00%, which was significantly higher than that in oxaliplatin group (74.51%). The main adverse reactions showed no statistical difference between the two groups (P>0.05). The median progression-free survival (PFS) was 8.6 months in combined therapy group and 6.3 months in oxaliplatin group, while the median overall survival (OS) was 12.9 months in combined therapy group and 10.6 months in oxaliplatin group. After treatment, CD4+ and CD3+ levels in the peripheral blood in both groups were obviously lower than those before treatment, but the CD8+ level was obviously higher than that before treatment. At the same time, changes in the ratio of T lymphocyte subsets in combined therapy group were superior to those in oxaliplatin group, displaying statistically significant differences (P<0.05). Oxaliplatin combined with endostar has a good curative effect in the treatment of PHC with mild adverse reactions, which can prolong the survival time of patients, improve the levels of T lymphocyte subsets and increase the immunity of patients, so it is worthy of promotion and application in clinic.

Hsa-miR-132 inhibits proliferation of hepatic carcinoma cells by targeting YAP.

MicroRNAs and Yes-associated protein (YAP) play an important role in the occurrence and development of hepatic carcinomas. However, the interaction between microRNAs and YAP was seldom elucidated. In this study, we showed that miR-132 could target YAP gene by using dual-luciferase reporter system. Further quantitative polymerase chain reaction analysis and western blotting showed that miR-132 could significantly reduce the expression of YAP at mRNA and protein levels. Results of annexin V-fluorescein isothiocyanate, 5-ethynyl-2'-deoxyuridine staining and transwell assays showed that miR-132 significantly promoted the cell apoptosis and effectively inhibited the proliferation and invasion of hepatoma cells. These results indicated that miR-132 could inhibit the growth of hepatoma cells by targeting YAP gene and reducing its expression level. Taken together, results from this study would help us to understand the mechanisms for occurrence and development of hepatic carcinoma and provide new targets for diagnosis and treatment of liver cancer.

Lentivirus vectors construction of SiRNA targeting interference GPC3 gene and its biological effects on liver cancer cell lines Huh-7.

OBJECTIVES: To build GPC3 gene short hairpin interference RNA (shRNA) slow virus vector, observe expression of Huh-7 GPC3 gene in human liver cell line proliferation apoptosis and the effect of GPC3 gene influencing on liver cancer cell growth, and provide theoretical basis for gene therapy of liver cancer. METHODS: Hepatocellular carcinoma cell line Huh-7 was transfected by a RNA interference technique. GPC3 gene expression in a variety of liver cancer cell lines was detected by fluorescence quantitative PCR. Targeted GPC3 gene sequences of small interfering RNA (siRNA) PGC-shRNA-GPC3 were restructured. Stable expression cell lines of siRNA were screened and established with the help of liposomes (lipofectamine(TM2000)) as carrier transfection of human liver cell lines. In order to validate siRNA interference efficiency, GPC3 siRNA mRNA expression was detected after transfection by using RT-PCR and Western blot. The absorbance value of the cells of blank group, untransfection group and transfection group, the cell cycle and cell apoptosis were calculated, and effects of GPC3 gene on Huh-7 cell proliferation and apoptosis were observed. RESULTS: In the liver cancer cell lines Huh-7, GPC3 gene showed high expression. PGC-shRNA-GPC3 recombinant plasmid was constructed successfully via sequencing validation. Stable recombinant plasmid transfected into liver cancer cell lines Huh-7 can obviously inhibit GPC3 mRNA expression level. CONCLUSIONS: The targeted GPC3 siRNA can effectively inhibit the expression of GPC3.