嵌合型猪圆环病毒1-2型感染性DNA克隆的构建及其对小鼠的免疫原性

[目的]本研究旨在构建嵌合型猪圆环病毒1-2型感染性DNA克隆.[方法]利用PCR技术扩增PCV2 ORF2,克隆入缺失PCV1 ORF2的pSK-PCV1△ORF2中,得到pSK-sPCV1-2.该重组质粒中包含嵌合型PCV1-2全基因组,通过不完全酶切的方法,将嵌合型PCV1-2全基因组串联入pSK载体中,得到含串联双拷贝的嵌合型PCV1-2感染性DNA克隆.[结果]经序列测定,获得含串联双拷贝的嵌合型PCV1-2感染性DNA克隆.PCV1-2嵌合病毒接种BALB/c小鼠,用间接ELISA方法对接种后7、14、21、28、35、42 d的小鼠进行血清抗体检测.结果显示从接种后14 d开始,即有部分小鼠产生了针对PCV2 Cap蛋白的特异性抗体;至接种后42 d,几乎全部接种小鼠的血清均呈阳性.[结论]构建了PCV1-2型感染性DNA克隆,该嵌合病毒能够激发机体产生体液免疫应答.     

A chimeric porcine circovirus (PCV) with the immunogenic capsid gene of the pathogenic PCV type 2 (PCV2) cloned into the genomic backbone of the nonpathogenic PCV1 induces protective immunity against PCV2 infection in pigs

Porcine circovirus type 2 (PCV2) is associated with postweaning multisystemic wasting syndrome in pigs, whereas PCV1 is nonpathogenic. We previously demonstrated that a chimeric PCV1-2 virus (with the immunogenic capsid gene of PCV2 cloned into the backbone of PCV1) induces an antibody response to the PCV2 capsid protein and is attenuated in pigs. Here, we report that the attenuated chimeric PCV1-2 induces protective immunity to wild-type PCV2 challenge in pigs. A total of 48 specific-pathogen-free piglets were randomly and equally assigned to four groups of 12 pigs each. Pigs in group 1 were vaccinated by intramuscular injection with 200 microg of the chimeric PCV1-2 infectious DNA clone. Pigs in group 2 were vaccinated by intralymphoid injection with 200 microg of a chimeric PCV1-2 infectious DNA clone. Pigs in group 3 were vaccinated by intramuscular injection with 10(3.5) 50% tissue culture infective doses (TCID(50)) of the chimeric PCV1-2 live virus. Pigs in group 4 were not vaccinated and served as controls. By 42 days postvaccination (DPV), the majority of pigs had seroconverted to PCV2 capsid antibody. At 42 DPV, all pigs were challenged intranasally and intramuscularly with 2 x 10(4.5) TCID(50) of a wild-type pathogenic PCV2 virus. By 21 days postchallenge (DPC), 9 out of the 12 group 4 pigs were viremic for PCV2. Vaccinated animals in groups 1 to 3 had no detectable PCV2 viremia after challenge. At 21 DPC the lymph nodes in the nonvaccinated pigs were larger (P < 0.05) than those of vaccinated pigs. The PCV2 genomic copy loads in lymph nodes were reduced (P < 0.0001) in vaccinated pigs. Moderate amounts of PCV2 antigen were detected in most lymphoid tissues of nonvaccinated pigs but in only 1 of 36 vaccinated pigs. Mild-to-severe lymphoid depletion and histiocytic replacement were detected in lymphoid tissues in the majority of nonvaccinated group 4 pigs but in only a few vaccinated group 1 to 3 pigs. The data from this study indicated that when given intramuscularly in pigs, the attenuated chimeric PCV1-2 live virus, as well as the chimeric PCV1-2 infectious DNA clone, induces protective immunity against PCV2 infection and could potentially serve as an effective vaccine.     

Protective efficacy of a DNA vaccine encoding capsid protein of porcine circovirus‐like virus P1 against porcine circovirus 2 in mice

The capsid protein is the major immunogenic protein of porcine circovirus 2 (PCV2). The nucleotide sequence of porcine circovirus‐like virus P1 shares high homology with open reading frame (ORF) 2 of PCV2, and ORF1 of P1 encodes its structural protein. Mice were vaccinated twice intramuscularly with a plasmid expressing the P1 ORF1 protein (pcDNA3.1(+)‐ORF1) at 2‐week intervals. All animals vaccinated with pcDNA3.1(+)‐ORF1 developed higher specific anti‐P1 antibody levels, and had less PCV2 viremia and milder histopathological changes than PCV2‐challenged mice in the control group. Our results show that the P1 DNA vaccine elicited immune responses against PCV2 infection in a mouse model.

     

Construction of a fusion flagellin complex and evaluation of the protective immunity of it in red snapper (Lutjanus sanguineus)

Aims: The main aims of this study were to construct a bivalent subunit vaccine containing flagellin flaA gene and flagellin flaB gene from Vibrio alginolyticus strain HY9901 and to explore the potential application of the fusion protein FlaA‐(G₄S)₃‐FlaB as a vaccine candidate for red snapper (Lutjanus sanguineus). Methods and Results: Flagellin gene flaA and flaB of V. alginolyticus were linked by gene SOEing (gene splicing by overlap extension) technology. The expression of the fusion gene flaA‐(G₄S)₃‐flaB in Escherichia coli BL21(DE3) was confirmed by SDS‐PAGE. Western blot analysis showed that the fusion protein FlaA‐(G₄S)₃‐FlaB, which was purified by affinity chromatography on Ni‐NTA resin, had positive reaction with mouse anti‐FlaA serum and mouse anti‐FlaB serum, respectively. The immunoprotection of FlaA‐(G₄S)₃‐FlaB as a bivalent subunit vaccine was investigated in red snapper model by enzyme‐linked immunosorbent assay (ELISA) and challenge test. Red snapper vaccinated with FlaA‐(G₄S)₃‐FlaB produced specific antibodies and were highly resistant to infection by virulent V. alginolyticus. Conclusions: The fusion gene flaA‐(G₄S)₃‐flaB from V. alginolyticus strain HY9901 was cloned by gene SOEing and was expressed in E. coli. This fusion protein FlaA‐(G₄S)₃‐FlaB is a good protective antigen of V. alginolyticus and should be considered as an effective vaccine candidate against infection by V. alginolyticus in red snapper. Significance and Impact of the Study: Two flagellin genes, flaA and flaB, which are independent in structure and function, were first linked together by gene SOEing technology. The finding that red snapper did adequately respond to the fusion protein FlaA‐(G₄S)₃‐FlaB injection made it a promising candidate for vaccine treatment. To develop effective vaccine candidates against V. alginolyticus, more attention should be given to these immunogenic flagellins.     

Comparison of immune responses against FMD by a DNA vaccine encoding the FMDV/O/IRN/2007 VP1 gene and the conventional inactivated vaccine in an animal model

Foot-and-mouth disease virus (FMDV) is highly contagious and responsible for huge outbreaks among cloven hoofed animals. The aim of the present study is to evaluate a plasmid DNA immunization system that expresses the FMDV/O/IRN/2007 VP1 gene and compare it with the conventional inactivated vaccine in an animal model. The VP1 gene was sub-cloned into the unique Kpn I and BamH I cloning sites of the pcDNA3.1+ and pEGFP-N1 vectors to construct the VP₁ gene cassettes. The transfected BHKT7 cells with sub-cloned pEGFP-N1-VP1 vector expressed GFP-VP1 fusion protein and displayed more green fluorescence spots than the transfected BHKT7 cells with pEGFP-N1 vector, which solely expressed the GFP protein. Six mice groups were respectively immunized by the sub-cloned pcDNA3.1⁺-VP1 gene cassette as the DNA vaccine, DNA vaccine and PCMV-SPORT-GMCSF vector (as molecular adjuvant) together, conventional vaccine, PBS (as negative control), pcDNA3.1⁺ vector (as control group) and PCMV-SPORT vector that contained the GMCSF gene (as control group). Significant neutralizing antibody responses were induced in the mice which were immunized using plasmid vectors expressing the VP1 and GMCSF genes together, the DNA vaccine alone and the conventional inactivated vaccine (P<0.05). Co-administration of DNA vaccine and GMCSF gene improved neutralizing antibody response in comparison with administration of the DNA vaccine alone, but this response was the most for the conventional vaccine group. However, induction of humeral immunity response in the conventional vaccine group was more protective than for the DNA vaccine, but T-cell proliferation and IFN-γ concentration were the most in DNA vaccine with the GMCSF gene. Therefore the group that was vaccinated by DNA vaccine with the GMCSF gene, showed protective neutralizing antibody response and the most Th1 cellular immunity.     

UV and X‐ray structural studies of a 101‐residue long Tat protein from a HIV‐1 primary isolate and of its mutated,detoxified, vaccine candidate

The 101‐residue long Tat protein of primary isolate 133 of the human immunodeficiency virus type 1 (HIV‐1), wt‐Tat₁₃₃ displays a high transactivation activity in vitro, whereas the mutant thereof, STLA‐Tat₁₃₃, a vaccine candidate for HIV‐1, has none. These two proteins were chemically synthesized and their biological activity was validated. Their structural properties were characterized using circular dichroism (CD), fluorescence emission, gel filtration, dynamic light scattering, and small angle X‐ray scattering (SAXS) techniques. SAXS studies revealed that both proteins were extended and belong to the family of intrinsically unstructured proteins. CD measurements showed that wt‐Tat₁₃₃ or STLA‐Tat₁₃₃ underwent limited structural rearrangements when complexed with specific fragments of antibodies. Crystallization trials have been performed on the two forms, assuming that the Tat₁₃₃ proteins might have a better propensity to fold in supersaturated conditions, and small crystals have been obtained. These results suggest that biologically active Tat protein is natively unfolded and requires only a limited gain of structure for its function. Proteins 2010. © 2009 Wiley‐Liss, Inc     

Protective effect of a RSV subunit vaccine candidate G1F/M2 was enhanced by a HSP70-Like protein in mice

Respiratory syncytial virus (RSV) is a major respiratory pathogen in newborns. Neonate vaccine should induce strong protective immunity. We have engineered a subunit vaccine candidate G1F/M2. A major problem in developing subunit vaccines is their limited immunogenicity. Aluminium adjuvants with a long history of use with routine childhood vaccines have some limitations, especially inability to elicit CTL response. There is a need for alternative adjuvants. Heat shock proteins (HSPs) are characterized as potent immunoadjuvants. In this study, HSP70-like protein 1 (HSP70L1) gene was cloned. The recombinant protein HSP70L1 was expressed in E. coli, purified and renaturated. We evaluated the potential of HSP70L1 used as the adjuvant of G1F/M2. G1F/M2 was chemically cross-linked with HSP70L1 (HSP-G1F/M2). HSP70L1 enhanced significantly the immunogenicity and protective effect of G1F/M2. HSP-G1F/M2 induced significant higher levels of antibodies, neutralizing antibodies and CTL activity than unadjuvanted G1F/M2. The antibody titers induced by HSP-G1F/M2 were similar to that by G1F/M2 + Alum. RSV-specific CTL activity induced by HSP-G1F/M2 was stronger than that by G1F/M2 + Alum. Interestingly, the protective effect of HSP-G1F/M2 against RSV was significantly stronger than that of G1F/M2 + Alum. The results suggest that HSP70L1 is a potent adjuvant of G1F/M2.     

Immunogenicity and protective efficacy of recombinant M2e.Hsp70c（Hsp70359–610） fusion protein against influenza virus infection in mice

New strategies in vaccine development are urgently needed to combat emerging influenza viruses and to reduce the risk of pandemic disease surfacing. Being conserved, the M2 e protein, is a potential candidate for universal vaccine development against influenza A viruses. Mycobacterium tuberculosis Hsp70（mHsp70） is known to cultivate the function of immunogenic antigen-presenting cells, stimulate a strong cytotoxic T lymphocyte（CTL） response, and stop the induction of tolerance. Thus, in this study, a recombinant protein from the extracellular domain of influenza A virus matrix protein 2（M2e）, was fused to the C-terminus of Mycobacterium tuberculosis Hsp70（Hsp70c）, to generate a vaccine candidate. Humoral immune responses, IFN-γ-producing lymphocyte, and strong CTL activity were all induced to confirm the immunogenicity of M2 e.Hsp70c（Hsp70359–610）. And challenge tests showed protection against H1N1 and H9N2 strains in vaccinated groups. Finally these results demonstrates M2 e.Hsp70c fusion protein can be a candidate for a universal influenza A vaccine.     

A novel PINK1- and PARK2-dependent protective neuroimmune pathway in lethal sepsis

Although the PINK1-PARK2 pathway contributes to the pathogenesis of Parkinson disease, its roles in sepsis (a major challenge for critical care) were previously unknown. Here, we show that pink1^?/? and park2^?/? mice are more sensitive to polymicrobial sepsis-induced multiple organ failure and death. The decrease in the circulating level of the neurotransmitter dopamine in pink1^?/? and park2^?/? mice accelerates the release of a late sepsis mediator, HMGB1, via HIF1A-dependent anaerobic glycolysis and subsequent NLRP3-dependent inflammasome activation. Genetic depletion of Nlrp3 or Hif1a in pink1^?/? and park2^?/? mice confers protection against lethal polymicrobial sepsis. Moreover, pharmacological administration of dopamine agonist (e.g., pramipexole), HMGB1-inhibitor (e.g., neutralizing antibody or glycyrrhizin), or NLRP3-inhibitor (e.g., MCC950) reduces septic death in pink1^?/? and park2^?/? mice. The mRNA expression of HIF1A and NLRP3 is upregulated, whereas the mRNA expression of PINK1 and PARK2 is downregulated in peripheral blood mononuclear cells of patients with sepsis. Thus, an impaired PINK1-PARK2-mediated neuroimmunology pathway contributes to septic death and may represent a novel therapeutic target in critical care medicine.     

The mouse chorionic gonadotropin beta-subunit-like (muCG beta l) molecule produced by tumor cells elicits the switch of T-cell immunity response from TH2 to TH1 in mice immunized with DNA vaccine based on rhesus monkey homologous CG beta (rmCG beta)

BACKGROUND: CG beta is expressed not only in placenta, but also in a wide range of tumors. To study DNA vaccine based on xenogeneic CG beta for cancer immuno-therapy, we investigated whether rhesus monkey CG beta (rmCG beta) DNA vaccine could induce protective T-cell responses and humoral responses in mouse. METHODS: We constructed a plasmid containing the rmCG beta coding sequence. Two cloned syngeneic SP2/0 myeloma cell lines that stably express muCG beta l (SP2/0-muCG beta l) and HN (SP2/0-HN) protein were established. Inoculation of these cell lines was made into mice that had been immunized with DNA vaccine. Specific IgG and IgG type were measured by ELISA and the cytokine expression was detected with RT-PCR. To measure the lymphocyte metabolic activity, the MTS assay was used. RESULTS: After injection of SP2/0-muCG beta l into mice that had been immunized with DNA vaccine, a significant increase in the IgG2a specific to the antigen (p < 0.05) and a decrease in the specific IgG1 (p < 0.05) were measured. The expression of T(H)1 but not T(H)2 cytokines, including IFN-gamma and IL-2, were detected in the splenocytes. However, injection of tumor cells expressing irrelevant or mock molecules into immunized mice could not induce these changes. The survival rate of vaccine-immunized mice injected with SP2/0-muCG beta l was as high as 58.3% after 55 days. CONCLUSIONS: The rmCG beta DNA vaccine has proved to be a potential strategy for protection against tumors with homologous molecules. The muCG beta l produced by tumors is able to elicit an immunity switch from T(H)2 to T(H)1 in vaccinated mice.     

An experimental live chimeric porcine circovirus 1-2a vaccine decreases porcine circovirus 2b viremia when administered intramuscularly or orally in a porcine circovirus 2b and porcine reproductive and respiratory syndrome virus dual-challenge model

Commercially available inactivated vaccines against porcine circovirus type 2 (PCV2) have been shown to be effective in reducing PCV2 viremia. Live-attenuated, orally administered vaccines are widely used in the swine industry for several pathogens because of their ease of use yet they are not currently available for PCV2 and efficacy. The aims of this study were to determine the efficacy of a live-attenuated chimeric PCV2 vaccine in a dual-challenge model using PCV2b and porcine reproductive and respiratory syndrome virus (PRRSV) and to compare intramuscular (IM) and oral (PO) routes of vaccination. Eighty-three 2-week-old pigs were randomized into 12 treatment groups: four vaccinated IM, four vaccinated PO and four non-vaccinated (control) groups. Vaccination was performed at 3 weeks of age using a PCV1-2a live-attenuated vaccine followed by no challenge, or challenge with PCV2b, PRRSV or a combination of PCV2b and PRRSV at 7 weeks of age. IM administration of the vaccine elicited an anti-PCV2 antibody response between 14 and 28 days post vaccination, 21/28 of the pigs being seropositive prior to challenge. In contrast, the anti-PCV2 antibody response in PO vaccinated pigs was delayed, only 1/27 of the pigs being seropositive at challenge. At 21 days post challenge, PCV2 DNA loads were reduced by 80.4% in the IM vaccinated groups and by 29.6% in the PO vaccinated groups. PCV1-2a (vaccine) viremia was not identified in any of the pigs. Under the conditions of this study, the live attenuated PCV1-2a vaccine was safe and provided immune protection resulting in reduction of viremia. The IM route provided the most effective protection.     

The essentiality of α‐2‐macroglobulin in human salivary innate immunity against new H1N1 swine origin influenza A virus

A novel strain of influenza A H1N1 emerged in the spring of 2009 and has spread rapidly throughout the world. Although vaccines have recently been developed that are expected to be protective, their availability was delayed until well into the influenza season. Although anti‐influenza drugs such as neuraminidase inhibitors can be effective, resistance to these drugs has already been reported. Although human saliva was known to inhibit viral infection and may thus prevent viral transmission, the components responsible for this activity on influenza virus, in particular, influenza A swine origin influenza A virus (S‐OIV), have not yet been defined. By using a proteomic approach in conjunction with beads that bind α‐2,6‐sialylated glycoprotein, we determined that an α‐2‐macroglobulin (A2M) and an A2M‐like protein are essential components in salivary innate immunity against hemagglutination mediated by a clinical isolate of S‐OIV (San Diego/01/09 S‐OIV). A model of an A2M‐based “double‐edged sword” on competition of α‐2,6‐sialylated glycoprotein receptors and inactivation of host proteases is proposed. We emphasize that endogenous A2M in human innate immunity functions as a natural inhibitor against S‐OIV.     

Curcumin synergistically potentiates the protective effect of sitagliptin against chronic deltamethrin nephrotoxicity in rats: Impact on pro‐inflammatory cytokines and Nrf2/Ho‐1 pathway

Deltamethrin (DLM) is a synthesized organophosphorus acaricide and bug spray, broadly utilized for veterinary and farming purposes. Although its exposure to humans and animals causes toxicity in the kidney and other primary organs, our objective was to assess the defensive effects of sitagliptin (Sita) and additionally curcumin (Cur) in the DLM‐intoxicated rats’ kidney. DLM‐intoxicated rats revealed a huge increase of various biochemical parameters in serum identified with kidney damage: uric acid, urea, and creatinine. DLM intoxication altogether increased renal lipid peroxidation, and critically restrained antioxidative biomarkers including superoxide dismutase, glutathione, and glutathione peroxidase. Likewise, it increased the tumor necrosis factor‐α, interleukin 6 (IL‐6) and IL‐1β level in serum. Additionally, DLM intoxication diminished the outflow of the nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2)/heme oxygenase‐1 (HO‐1) pathway in rats. Both Sita and Cur act against DLM‐prompted serum along with renal tissue biochemical parameters when utilized alone or in a mix alongside DLM intoxication. Besides this, both Sita and Cur delivered synergetic nephroprotective, antioxidative, and anti‐inflammatory impacts. Consequently, it could be presumed that Sita as well as Cur administration can limit the poisonous impacts of DLM by their free radical‐scavenging, strong antioxidant, and Nrf2/HO‐1 pathway upregulation activity.     

Adenosine A1 and A2A receptors are involved on guanosine protective effects against oxidative burst and mitochondrial dysfunction induced by 6-OHDA in striatal slices

6-Hydroxydopamine (6-OHDA) is the most used toxin in experimental Parkinson’s disease (PD) models. 6-OHDA shows high affinity for the dopamine transporter and once inside the neuron, it accumulates and undergoes non-enzymatic auto-oxidation, promoting reactive oxygen species (ROS) formation and selective damage of catecholaminergic neurons. In this way, our group has established a 6-OHDA in vitro protocol with rat striatal slices as a rapid and effective model for screening of new drugs with protective effects against PD. We have shown that co-incubation with guanosine (GUO, 100 μM) prevented the 6-OHDA-induced damage in striatal slices. As the exact GUO mechanism of action remains unknown, the aim of this study was to investigate if adenosine A₁ (A₁R) and/or A_2A receptors (A_2AR) are involved on GUO protective effects on striatal slices. Pre-incubation with DPCPX, an A₁R antagonist prevented guanosine effects on 6-OHDA-induced ROS formation and mitochondrial membrane potential depolarization, while CCPA, an A₁R agonist, did not alter GUO effects. Regarding A_2AR, the antagonist SCH58261 had similar protective effect as GUO in ROS formation and mitochondrial membrane potential. Additionally, SCH58261 did not affect GUO protective effects. The A_2AR agonist CGS21680, although, completely blocked GUO effects. Finally, the A₁R antagonist DPCPX, and the A_2AR agonist CGS21680 also abolished the preventive guanosine effect on 6-OHDA-induced ATP levels decrease. These results reinforce previous evidence for a putative interaction of GUO with A₁R-A_2AR heteromer as its molecular target and clearly indicate a dependence on adenosine receptors modulation to GUO protective effect.

     

2-(2-Methylfuran-3-carboxamido)-3-phenylpropanoic acid,a potential CYP26A1 inhibitor to enhance all-trans retinoic acid-induced leukemia cell differentiation based on virtual screening and biological evaluation

To develop new CYP26A1 inhibitors, a three-cycle virtual screening was carried out based on the constructed homology model of human CYP26A1 using Dock, Fred, Gold and AutoDock. Twenty-two compounds exhibited high scores and reasonable binding modes in molecular docking were purchased from Specs Company. Eighteen compounds were tested their abilities to enhance ATRA-induced differentiation in human acute promyelocytic leukemia NB4 cells. Eight of them enhanced the ability of ATRA to induce differentiation at concentrations of 0.5 and 1 μM. Among these compounds, 2-(2-methylfuran-3-carboxamido)-3-phenylpropanoic acid (S8) is of most effective in blocking ATRA breaking down in NB4 cells based on the LC–MS/MS assay.     

Regulation of RAGE splicing by hnRNP A1 and Tra2β‐1 and its potential role in AD pathogenesis

The receptor for advanced glycation end products (RAGE) gene expresses two major alternative splicing isoforms, full‐length membrane‐bound RAGE (mRAGE) and secretory RAGE (esRAGE). Both isoforms play important roles in Alzheimer's disease (AD) pathogenesis, either via interaction of mRAGE with β‐amyloid peptide (Aβ) or inhibition of the mRAGE‐activated signaling pathway. In the present study, we showed that heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) and Transformer2β‐1 (Tra2β‐1) were involved in the alternative splicing of mRAGE and esRAGE. Functionally, two factors had an antagonistic effect on the regulation. Glucose deprivation induced an increased ratio of mRAGE/esRAGE via up‐regulation of hnRNP A1 and down‐regulation of Tra2β‐1. Moreover, the ratios of mRAGE/esRAGE and hnRNP A1/Tra2β‐1 were increased in peripheral blood mononuclear cells from AD patients. The results provide a molecular basis for altered splicing of mRAGE and esRAGE in AD pathogenesis.

     

A single-nucleotide polymorphism in lnc-LAMC2-1:1 interferes with its interaction with miR-128 to alter the expression of deleted in colorectal cancer and its effect on the survival rate of subjects with ovarian cancer

This study aimed to identify the association between lnc-LAMC2-1:1 polymorphism rs2147578 and the recurrence of ovary cancer, as well as to study the underlying mechanism of rs2147578 in ovary cancer. Real-time polymerase chain reaction, Western blot analysis, immunohistochemistry, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, Logrank test, and Kaplan-Meier analysis were carried out to explore the role of rs2147578 in ovary cancer. No obvious difference was observed concerning all clinical characteristics among 90 patients genotyped as CC (N = 28), CG (N = 38), and GG (N = 24) in their rs2147578 polymorphism. In addition, the subjects carrying the CC genotype had longer recurrence-free survival time and showed a lower level of malignancy compared with those carrying CG and GG genotypes. Lnc-LAMC2-1:1 and miR-128 were lowly expressed in the CC group, while deleted in colorectal cancer (DCC) was highly expressed in the CC group. Furthermore, DCC was identified as a target gene of miR-128, and miR-128 mimics decreased the luciferase activity of cells cotransfected with wild-type DCC 3′-untranslated region. Lnc-LAMC2:1-1 directly targeted and affected miR-128 expression, and the G allele in lnc-LAMC2-1:1 rs2147578 upregulated miR-128 expression. Transfection with a miR-128 precursor evidently downregulated the expression of lnc-LAMC2-1:1, miR-128, and DCC expression, but did not affect the expression of ABCC5 and body mass index. Finally, miR-128 precursor promoted cell proliferation and inhibited cell apoptosis. Compared with lnc-LAMC2-1:1 rs2147578C allele, the G allele increases the risk of ovarian cancer by reducing the binding between lnc-LAMC2-1:1 and miR-128-3p, which in turn further decreases the expression of DCC and inhibits cell apoptosis.