Floridean Starch and Floridoside Metabolic Pathways of Neoporphyra haitanensis and Their Regulatory Mechanism under Continuous Darkness.

Floridean starch and floridoside are the main storage carbohydrates of red algae. However, their complete metabolic pathways and the origin, function, and regulatory mechanism of their pathway genes have not been fully elucidated. In this study, we identified their metabolic pathway genes and analyzed the changes in related gene expression and metabolite content in Neoporphyra haitanensis under continuous dark conditions. Our results showed that genes from different sources, including eukaryotic hosts, cyanobacteria, and bacteria, were combined to construct floridean starch and floridoside metabolic pathways in N. haitanensis. Moreover, compared with those in the control, under continuous dark conditions, floridean starch biosynthesis genes and some degradation genes were significantly upregulated with no significant change in floridean starch content, whereas floridoside degradation genes were significantly upregulated with a significant decrease in floridoside content. This implies that floridean starch content is maintained but floridoside is consumed in N. haitanensis under dark conditions. This study elucidates the "floridean starch-floridoside" metabolic network and its gene origins in N. haitanensis for the first time.

[Retracted] Effects of cyclooxygenase­2 gene silencing on the biological behavior of SKOV3 ovarian cancer cells.

Following the publication of the above article, the authors have requested that it be retracted. They alerted the Editorial Office to the fact that the same data, albeit with a different view, had been selected to show the 'CON' and 'NC' experiments for the colony­formation assays featured in Fig. 6. The Editor has agreed to the authors' request that the paper be retracted. All the authors agree to this retraction, and apologize for any inconvenience caused. [the original article was published in Molecular Medicine Reports 11: 59­66, 2015; DOI: 10.3892/mmr.2014.2732].

Integrated effects of Ulva prolifera bloom and decay on nutrients inventory and cycling in marginal sea of China.

Ulva prolifera blooms occur annually in the Yellow Sea. Most studies focus on how U. prolifera blooming is influenced by nitrogen chemical forms and concentrations, while little concern goes to how U. prolifera bloom-decay cycle would impact local seawater nutrients structure. Therefore, we use 15N-labeled NO3 tracers and transcriptome analysis to determine N uptake, metabolism, and interconversion during U. prolifera growth and decay, so that we can quantify the conversions rate and fluxes of different nitrogen chemical forms. U. prolifera absorbes 17.37 µmol g-1·d-1 NO3-N during growth. NO3-N predominates (73.75-92.15%) in the dissolved inorganic nitrogen (DIN) in U. prolifera. During decay, NH4-N accountes for 60.87-92.13% of the in-cell DIN. The decomposing U. prolifera releases considerable amounts of NH4-N and dissolved organic nitrogen (DON) (63.8-98.2% < 1 kDa fraction and 1.8-36.2% is > 1 kDa fraction) into the ambient environment. The high DON release rate (59.57 µmol g-1 d-1) indicates active DON biosynthesis in U. prolifera. The isotope 15NO3-N tracer showes that 73.6% of the 15NO3-N is transformed to DON. The <1 kDa and the >1 kDa fractions account for 67.46-90.86% and 9.14-32.54% of the DON, respectively. The high efficiency of U. prolifera in utilizing NO3-N is explained by the responsive nitrate/nitrite transporter in cell membrane, and the DON biosynthesized capability is attributed to the up-regulated glutamine synthetase. Our study highlights the unique role of U. prolifera as a "Nitrogen-Pump" in converting nitrogen chemical forms during its bloom-decay cycle and quantifies its impacts on local N-nutrients inventory.

Emissions of biogenic sulfur compounds and their regulation by nutrients during an Ulva prolifera bloom in the Yellow Sea.

Three cruises were conducted during an Ulva prolifera bloom in 2018 off the Qingdao coast to observe early-, late-, and after-bloom characteristics. Spatio-temporal changes in dimethylsulfide (DMS), dimethylsulphoniopropionate (DMSP), and acrylic acid (AA) and their relationships with environmental parameters were examined. Mesocosm experiments tested the effect of nutrient on the release of biogenic sulfur compounds during the decline period. Biogenic sulfur concentrations contrasted with those in non-bloom regions and reached their highest values during the late-bloom period. The average sea-to-air DMS flux was about 5 times higher than those of non-bloom regions. The mean concentrations of DMS and DMSP in the enclosures were 3-5 times those of in-situ seawater. Biogenic sulfur release was promoted by the addition of high concentrations of nutrients as U. prolifera was declining. The contribution of the U. prolifera bloom to atmospheric DMS was estimated to be 125 kg S d-1.

The complete plastid genome and phylogenetic analysis of Codium fragile.

Codium fragile, a nutrient-rich green algae that is both edible and medicinal, it is called a 'rat tail' because of its unique shape, it can reach up to a metre in length and has the functions of clearing heat and detoxifying, detumescence and water, and repelling insects. The plastid genome sequence of C. fragile is 83,422 bp. A total of 105 genes were determined, including 77 protein-encoding genes, 3 rRNA genes, and 25 tRNA genes. Phylogenetic analysis showed that C. fragile clustered together into a single branch with C. simulans and Codium sp. 'arenicola' as sister branches. The plastid genome analysis will help the understanding of Chlorophyta evolution.

Transcriptomic and Proteomic Analysis of Mannitol-metabolism-associated Genes in Saccharina japonica.

As a carbon-storage compound and osmoprotectant in brown algae, mannitol is synthesized and then accumulated at high levels in Saccharina japonica (Sja); however, the underlying control mechanisms have not been studied. Our analysis of genomic and transcriptomic data from Sja shows that mannitol metabolism is a cyclic pathway composed of four distinct steps. A mannitol-1-phosphate dehydrogenase (M1PDH2) and two mannitol-1-phosphatases (M1Pase1 and MIPase2) work together or in combination to exhibit full enzymatic properties. Based on comprehensive transcriptomic data from different tissues, generations, and sexes as well as under different stress conditions, coupled with droplet digital PCR (ddPCR) and proteomic confirmation, we suggest that SjaM1Pase1 plays a major role in mannitol biosynthesis and that the basic mannitol anabolism and the carbohydrate pool dynamics are responsible for carbon storage and anti-stress mechanism. Our proteomic data indicate that mannitol metabolism remains constant during diurnal cycle in Sja. In addition, we discover that mannitol-metabolism-associated (MMA) genes show differential expression between the multicellular filamentous (gametophyte) and large parenchymal thallus (sporophyte) generations and respond differentially to environmental stresses, such as hyposaline and hyperthermia conditions. Our results indicate that the ecophysiological significance of such differentially expressed genes may be attributable to the evolution of heteromorphic generations (filamentous and thallus) and environmental adaptation of Laminariales.

HDAC11: a rising star in epigenetics.

Epigenetic mechanisms, such as acetylation, methylation, and succinylation, play pivotal roles in the regulation of multiple normal biological processes, including neuron regulation, hematopoiesis, bone cell maturation, and metabolism. In addition, epigenetic mechanisms are closely associated with the pathological processes of various diseases, such as metabolic diseases, autoimmune diseases and cancers. Epigenetic changes may precede genetic mutation, so research on epigenetic changes and regulation may be important for the early detection and diagnosis of disease. Histone deacetylase11 (HDAC11) is the newest member of the histone deacetylase (HDAC) family and the only class IV histone deacetylase. HDAC11 has different expression levels and biological functions in different systems of the human body and is among the top 1 to 4% of genes overexpressed in cancers, such as breast cancer, hepatocellular carcinoma and renal pelvis urothelial carcinoma. This article analyzes the role and mechanism of HDAC11 in disease, especially in tumorigenesis, in an attempt to provide new ideas for clinical and basic research.

Role of lncRNAHCP5/microRNA-525-5p/PRC1 crosstalk in the malignant behaviors of ovarian cancer cells.

PURPOSE: Owing to the late diagnosis and frequent metastasis, ovarian cancer (OC) exhibits a high mortality rate. The study was intended to figure out the function of long non-coding RNA (lncRNA) HCP5 in OC metastasis. METHODS: Microarray analysis was conducted to probe aberrantly expressed lncRNAs in OC tissues. Artificial silencing of lncRNA HCP5 was introduced in OC cells to identify its role in cell viability, invasion, migration, and epithelial-mesenchymal transition (EMT). The potential downstream targets of lncRNA HCP5 were predicted by bio-information system and validated through dual luciferase reporter gene assays. Silencing of microRNA-525-5p (miR-525-5p) was introduced in cells to probe its role in cell behaviors. Xenograft tumors were induced in nude mice for in vivo experiments. RESULTS: High expression of lncRNA HCP5 was found in OC tissues and cells. Silencing of lncRNA HCP5 led to a decrease in cell proliferation, invasion, migration and EMT process. LncRNA HCP5 is mainly sub-localized in cytoplasm. LncRNA HCP5 could act as a sponge for miR-525-5p, which could further bind to polycomb repressive complex 1 (PRC1). Knockdown of miR-525-5p partly recovered the biological behaviors of OC cells inhibited by HCP5 silencing. In addition, HCP5 promoted Wnt/ß-catenin signaling pathway activity. Silencing of lncRNA HCP5 also impeded growth and metastasis of tumor in mice. CONCLUSION: The study suggested that lncRNA HCP5 might promote malignant behaviors of OC cells through the miR-525-5p/PRC1 crosstalk and the Wnt/ß-catenin pathway. Silencing of HCP5 might serve as a novel option for OC treatment.

Exosomal release of microRNA-454 by breast cancer cells sustains biological properties of cancer stem cells via the PRRT2/Wnt axis in ovarian cancer.

AIMS: Cancer-derived exosomes carrying tumor-derived molecules such as miRNAs and proteins related to various phenotypes have been detected in both the bloodstream and other biofluids of patients with different cancers. Thus, our main purpose here was to determine the role of the exosomal microRNA-454 (miR-454) derived by MDA-MB-231 in self-renewal of cancer stem cells (CSCs) in ovarian cancer (OC). MATERIALS AND METHODS: Extraction of MDA-MB-231 cells-derived exosomes (231-derived exosomes) was conducted to treat CD44+/CD133+ SKOV3 and CoC1 cells to observe cell growth and stemness. Next, the differentially expressed miRNAs in SKOV3 cells after exosome treatment were filtered using microarray analysis. Subsequently, the cell viability was detected after reducing the exosomal miR-454 and the addition of a Wnt pathway inhibitor C59. Finally, the pro-tumorigenic function of exosomes on OC cells in vivo was investigated. KEY FINDINGS: After co-culture with 231-derived exosomes, the stemness of CSCs were promoted. Subsequently, the reduction of exosomal miR-454 weakened the roles of exosomes on cell stemness. Proline-rich transmembrane protein 2 (PRRT2) was substantiated as a target gene of miR-454 in SKOV3 and CoC1 cells. C59 reversed the repressive role of exosomes in stemness of CSCs. When being evaluated in a mouse model, exosomal miR-454 led to an efficacious effect in suppressing the tumor weight and volume in vivo. SIGNIFICANCE: Altogether, 231-derived exosomes carrying miR-454 disrupted the Wnt pathway by targeting PRRT2, thereby promoting CSC stemness in vitro and OC cell growth in vivo.

Progress and Clinical Application of Single-Cell Transcriptional Sequencing Technology in Cancer Research.

Cancer has been a daunting challenge for human beings because of its clonal heterogeneity and compositional complexity. Tumors are composed of cancer cells and a variety of non-cancer cells, which together with the extracellular matrix form the tumor microenvironment. These cancer-related cells and components and immune mechanisms can affect the development and progression of cancer and are associated with patient diagnosis, treatment and prognosis. As the first choice for the study of complex biological systems, single-cell transcriptional sequencing (scRNA-seq) has been widely used in cancer research. ScRNA-seq has made breakthrough discoveries in tumor heterogeneity, tumor evolution, metastasis and spread, development of chemoresistance, and the relationship between the tumor microenvironment and the immune system. These results will guide clinical cancer treatment and promote personalized and highly accurate cancer treatment. In this paper, we summarize the latest research progress of scRNA-seq and its guiding significance for clinical treatment.

Long noncoding RNA H19 regulates HIF-1α/AXL signaling through inhibiting miR-20b-5p in endometrial cancer.

In a variety of cancers, long non-coding RNAs (lncRNAs) were believed to play important roles. Nevertheless, H19's possible molecular mechanism related to miR-20b-5p has not yet been explored in endometrial cancer. Differential lncRNAs in endometrial cancer were identified based on microarray analysis (GSE23339). In this research, in the first place, H19 expression was detected to be increased but miR-20b-5p to be decreased in endometrial cancer tissues and cells. Besides, H19 expression displayed a negative relationship to miR-20b-5p expression in endometrial cancer tissues. According to gain- and loss-of-function experiments of H19, like a ceRNA, H19 elevated AXL level and HIF-1α expression so as to stimulate the migration, proliferation and EMT process of endometrial cancer. Additionally, the knockdown of H19 slowed down tumor growth, promoted apoptosis and upregulated miR-20b-5p expression but lowered the expressions of HIF-1α, PCNA and AXL in vivo. Furthermore, H19 was also verified to stimulate the activity of endometrial cancer with AXL inhibitor BGB324 in vitro and in vivo. To sum up, H19 accelerates the tumor formation of endometrial cancer through the miR-20b-5p/AXL/HIF-1α signaling pathway, thereby providing a novel target for diagnosing and treating endometrial cancer.

LncRNA HAND2-AS1 exerts anti-oncogenic effects on ovarian cancer via restoration of BCL2L11 as a sponge of microRNA-340-5p.

In the early stage of ovarian cancer (OC), molecular biomarkers are critical for its diagnosis and treatment. Nevertheless, there is little research on the mechanism underlying tumorigenesis in OC. Herein, we aimed to explore whether long noncoding RNA (lncRNA) HAND2-AS1 participated in the regulation of the cell proliferation, migration, and apoptosis of OC by regulating B-cell lymphoma 2 like 11 (BCL2L11) and microRNA-340-5p (miR-340-5p). Differentially expressed lncRNAs in OC were screened by microarray-based analysis. HAND2-AS1, BCL2L11, and miR-340-5p expression was assessed in normal ovarian and OC tissues and human OC cell lines. Then, the relationships among HAND2-AS1, BCL2L11, and miR-340-5p were explored. Ectopic expression and depletion experiments were applied to analyze the effects of HAND2-AS1, miR-340-5p and BCL2L11 on migration, invasion, and proliferation of OC cells, as well as apoptosis. Lastly, the tumor xenograft in nude mice was conducted to test the tumorigenesis in vivo. In silico analysis displayed poor expression of HAND2-AS1 in OC. HAND2-AS1 specifically sponged with miR-340-5p which was found to directly target BCL2L11. Importantly, HAND2-AS1 or BCL2L11 overexpression or miR-340-5p downregulation resulted in reduction of cell invasion and migration, together with decrease of cell proliferation and increase of cell apoptosis in OC. Besides, high-expressed HAND2-AS1 inhibited the tumorigenesis in nude mice. To sum up, these data suggests HAND2-AS1 as an anti-oncogene in OC through upregulation of BCL2L11 by competitively binding to miR-340-5p, which demonstrates that there are potential diagnosis and therapy values of HAND2-AS1 in OC.

The function of histone acetylation in cervical cancer development.

Cervical cancer is the fourth most common female cancer in the world. It is well known that cervical cancer is closely related to high-risk human papillomavirus (HPV) infection. However, epigenetics has increasingly been recognized for its role in tumorigenesis. Epigenetics refers to changes in gene expression levels based on non-gene sequence changes, primarily through transcription or translation of genes regulation, thus affecting its function and characteristics. Typical post-translational modifications (PTMs) include acetylation, propionylation, butyrylation, malonylation and succinylation, among which the acetylation modification of lysine sites has been studied more clearly so far. The acetylation modification of lysine residues in proteins is involved in many aspects of cellular life activities, including carbon metabolism, transcriptional regulation, amino acid metabolism and so on. In this review, we summarize the latest discoveries on cervical cancer development arising from the aspect of acetylation, especially histone acetylation.

Impaired Th17 cell proliferation and decreased pro-inflammatory cytokine production in CXCR3/CXCR4 double-deficient mice of vulvovaginal candidiasis.

Vulvovaginal candidiasis (VVC) is a common observed infection, affecting approximately 75% of women of reproductive age. Drug resistance represents a troublesome stumbling block associated with VVC therapy. Thus the aim of the present study was to provide information regarding the selection of potential drug targets for VVC. CXCR3-, CXCR4-, or CXCR/CXCR4 double-deficient mouse models of VVC were subsequently established, with changes to the load of Candida Albicans evaluated accordingly. The biological behaviors of the vaginal epithelial cells were characterized in response to the CXCR3-, CXCR4-, or CXCR3/CXCR4 double-knockout in vivo. Our initial observations revealed that in mice with VVC, CXCR3-, CXCR4-, or CXCR3 - CXCR4 double-knockout resulted in a decreased load of C. Albicans as well as reduced levels and proportion of Th17 cells. Proinflammatory cytokine production was found to be inhibited by CXCR3-, CXCR4-, or CXCR3/CXCR4 double-knockout whereby the mRNA and protein expressions CXCR3, CXCR4, IL-17, IL-6, and TNF-α exhibited decreased levels. CXCR3-, CXCR4-, or CXCR3/CXCR4 double-knockout appeared to function as positive proliferation factors, while playing a negative role in the processes of apoptosis and the cell cycle of vaginal epithelial cells. Taken together, the key findings of the study suggested that CXCR3/CXCR4 double-knockout could act to hinder the progression of VVC, highlighting its promise as a novel therapeutic target in the treatment of VVC. CXCR3 and CXCR4 genes may regulate Th17/IL-17 immune inflammatory pathways to participate in antifungal immunity.

The complete mitogenome of Caulerpa lentillifera and its phylogenetic analysis.

Caulerpa lentillifera is a marine nutrient-rich edible green algae, with its external shape similar to 'sea grape', it has functions of purifying blood, anti-oxidation, anti-cancer, and anti-tumor. The mitogenome sequence of C. lentillifera is 209,894 bp long. A total of 67 genes were determined, including 17 protein-encoding genes, 3 rRNA genes, 27 tRNA genes, and 20 unidentified open reading frame (ORF). Phylogenetic analysis showed that C. lentillifera clustered together into a single branch. The mitogenome analysis will help the understanding of Ulvophyceae evolution.

Silencing the expression of MTDH increases the radiation sensitivity of SKOV3 ovarian cancer cells and reduces their proliferation and metastasis.

Ovarian cancer has a high mortality rate among women worldwide. Radiotherapy is considered an effective method of ovarian cancer treatment, however, radioresistance presents a challenge. It is necessary to develop techniques that can increase radiosensitivity in ovarian cancer, and gene therapy is a promising option. The aim of the present study was to investigate the effects of metadherin (MTDH) silencing on the radiosensitivity of ovarian cancer. Ovarian cancer tissues (n=273) and normal ovarian tissues (n=277) were used, as were SKOV3 ovarian cancer cells and the immortalized human ovarian epidermal HOSEpiC cell line. MTT, Transwell and wound-healing assays were performed to assess the proliferation, invasion and migration abilities of the SKOV3 cells. Colony-forming assays and flow cytometry were applied to detect the radiosensitivity and apoptosis of the SKOV3 cells. Nude mouse xenograft models were established to evaluate the effect of MTDH gene silencing on tumor growth and the efficacy of radiotherapy. Ovarian cancer, in tissues and cells, was demonstrated to have a high level of MTDH. Additionally, MTDH silencing was found to significantly inhibit proliferation, migration and invasion, and induce apoptosis in SKOV3 cells, and it was suggested that MTDH depletion significantly increased the sensitivity of the SKOV3 cells to X-ray radiation. MTDH silencing enhanced radiosensitivity and delayed tumor growth in the nude mouse xenograft model. Collectively, the results obtained in the present study suggest the potential role of MTDH silencing as a technique for ameliorating radioresistance in ovarian cancer. The present study provides a promising experimental basis for the improvement of ovarian cancer radiotherapy treatment.

Robotic radical hysterectomy is superior to laparoscopic radical hysterectomy and open radical hysterectomy in the treatment of cervical cancer.

OBJECTIVE: Cervical cancer (CC) continues to be a global burden for women, with higher incidence and mortality rates reported annually. Many countries have witnessed a dramatic reduction in the prevalence of CC due to widely accessed robotic radical hysterectomy (RRH). This network meta-analysis aims to compare intraoperative and postoperative outcomes in way of RRH, laparoscopic radical hysterectomy (LTH) and open radical hysterectomy (ORH) in the treatment of early-stage CC. METHODS: A comprehensive search of PubMed, Cochrane Library and EMBASE databases was performed from inception to June 2016. Clinical controlled trials (CCTs) of above three hysterectomies in the treatment of early-stage CC were included in this study. Direct and indirect evidence were incorporated for calculating values of weighted mean difference (WMD) or odds ratio (OR), and drawing the surface under the cumulative ranking curve (SUCRA). RESULTS: Seventeen 17 CCTs were ultimately enrolled in this network meta-analysis. The network meta-analysis showed that patients treated by RRH and LRH had lower estimated blood loss compared to patients treated by ORH (WMD = -399.52, 95% CI = -600.64~-204.78; WMD = -277.86, 95%CI = -430.84 ~ -126.07, respectively). Patients treated by RRH and LRH had less hospital stay (days) than those by ORH (WMD = -3.49, 95% CI = -5.79~-1.24; WMD = -3.26, 95% CI = -5.04~-1.44, respectively). Compared with ORH, patients treated with RRH had lower postoperative complications (OR = 0.21, 95%CI = 0.08~0.65). Furthermore, the SUCRA value of three radical hysterectomies showed that patients receiving RRH illustrated better conditions on intraoperative blood loss, operation time, the number of resected lymph nodes, length of hospital stay and intraoperative and postoperative complications, while patients receiving ORH demonstrated relatively poorer conditions. CONCLUSION: The results of this meta-analysis confirmed that early-stage CC patients treated by RRH were superior to patients treated by LRH and ORH in intraoperative blood loss, length of hospital stay and intraoperative and postoperative complications, and RRH might be regarded as a safe and effective therapeutic procedure for the management of CC.

Complete sequences of the mitochondrial DNA of the Petalonia binghamiae.

Here, the complete mitogenome of Petalonia binghamiae (J. Agardh) K. L. Vinogradova was determined and analyzed. The length of the complete P. binghamiae mitogenome was determined to be 37,460 bp. The mitogenome contains a set of 68 genes, including 35 protein-coding genes, 3 rRNA genes, 24 tRNA genes, 1 tRNA pseudogene, and 5 unidentified open reading frames (ORFs). The noncoding sequence constitutes 7.03% of the P. binghamiae mtDNA. Twenty-seven of the 35 (77.14%) protein-coding genes ended with a TAA stop codon, 6 (17.14%) with TAG, and 2 (5.71%) with TGA. All protein-coding genes in P. binghamiae were inferred to use the start codon ATG, except for nad11. The mitogenome phylogenetic analysis, based on 35 protein-coding genes, reveals that P. binghamia showed that P. binghamiae was clustered together with P. fascia. The complete mitochondrial genome sequence provided here would be useful for further understanding the evolution of Petalonia.

Long Noncoding RNA LINC00261 Suppresses Cell Proliferation and Invasion and Promotes Cell Apoptosis in Human Choriocarcinoma.

Choriocarcinoma is one of the gestational trophoblastic neoplasias (GTNs) that originate in the chorionic villi and the extravillous trophoblast. Long noncoding RNAs (lncRNAs) are a type of non-protein-coding RNAs that have recently been implicated in human tumorigenesis. The present study investigated the role of the lncRNA LINC00261 in cell proliferation, metastasis, and apoptosis in choriocarcinoma cell lines. The transcription level of LINC00261 was significantly lower in choriocarcinoma tissues and in choriocarcinoma cell lines. Overexpression of LINC00261 caused a decrease in cell proliferation and arrested the cell cycle at the G0/G1 phase. Furthermore, overexpression of LINC00261 inhibited cell migration and invasion. Meanwhile, it promoted cell apoptosis and the relative activities of caspase 3 and caspase 9 in choriocarcinoma JEG-3 and JAR cells. These data suggested that LINC00261 promotes cell proliferation and metastasis in choriocarcinoma. Our data might provide novel insight into the early diagnosis and treatment of choriocarcinoma in clinics.

Effects of cyclooxygenase-2 gene silencing on the biological behavior of SKOV3 ovarian cancer cells.

The aim of the present study was to investigate the effects of plasmid-mediated RNA interference targeting of cyclooxygenase-2 (COX-2) on the biological behaviors of SKOV3 human ovarian cancer cells and to analyze the function of COX-2 in carcinogenesis and development of ovarian cancer. A COX-2 small hairpin (sh)RNA sequence was designed and synthesized and pGPU6-COX-2-shRNA plasmids were constructed. The recombinant vector plasmids were stably transfected into SKOV3 cells. The mRNA and protein expression of COX-2 was subsequently analyzed by quantitative polymerase chain reaction and western blot analysis, respectively. MTT and colony formation assays were used to detect the cellular proliferation ability and flow cytometry was performed to detect phase changes in the cell cycle. Finally, a Transwell assay was used to detect cell invasion. The SKOV3 cells, transfected with recombinant vector plasmids, and control cells, were injected into nude mice and the tumor emergence time, volume and weight were measured. The impact of COX-2 gene silencing on the growth of xenograft tumors in nude mice was analyzed. Following transfection of the pGPU6-COX-2-shRNA plasmid, in vitro analyses indicated that the shRNA efficiently suppressed the mRNA and protein expression of COX-2. COX-2 gene silencing significantly inhibited the proliferation and invasion ability of SKOV3 cells, leading to cell cycle arrest in G1. The tumor formation time in the interference group was significantly prolonged, and the tumor volume and weight were significantly decreased, as compared with the control group. Plasmid-mediated shRNA was shown to effectively silence COX-2 expression in SKOV3 ovarian cancer cells. It was identified that COX-2 functioned in regulating proliferation, cell cycle and invasion of ovarian cancer cells. These findings provided a theoretical basis for determining the function of COX-2 in the development of ovarian cancer and suggested that COX-2 may be an effective target for gene therapy and clinical applications.