Metabolic hijacking disrupts tumor redox homeostasis and reprograms immune-metabolic crosstalk. Nevertheless, existing approaches lack integrated coordination between metabolic perturbation and immunogenic activation to achieve self-reinforcing photodynamic-immunotherapy synergy. Here, we designed an upconversion nanoparticle (UCNP)-bacteria hybrid system that depletes glycine while generating the photosensitizer protoporphyrin IX (PpIX) in tumors. We reprogrammed E. coli 1917 probiotics to express glutamyl-tRNA reductase A and malate synthase B to synthesize 5-aminolevulinic acid, which tumor cells convert into PpIX. Microfluidic-chip screening optimized bacteria to utilize glycine as their sole carbon source, while UCNP-DNA through G4-hairpin and bacterial aptamers binds to bacteria, responding to tumor miRNA-21 to form G-quadruplexes that trap PpIX and amplify PDT. This dual metabolic system disrupts tumor self-protection against ROS by glycine depletion and enriches photosensitizers by functionalized-UCNPs, enabling self-reinforcing PDT. Additionally, it promotes ROS-mediated immunogenic cell death, dendritic cell activation, and M1 macrophage polarization, exhibiting robust antitumor growth and metastasis.

AIMS:Comorbid anxiodepressive-like symptoms (CADS) in chronic pain are closely related to the overactivation of the lateral habenula (LHb). Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels have been implicated to play a key role in regulating neuronal excitability. However, the role of HCN channels in the LHb during CADS has not yet been characterized. This study aimed to investigate the effect of HCN channels in the LHb on CADS during chronic pain. METHODS:After chronic neuropathic pain induction by spared nerve injury (SNI), mice underwent a sucrose preference test, forced swimming test, tail suspension test, open-field test, and elevated plus maze test to evaluate their anxiodepressive-like behaviors. Electrophysiological recordings, immunohistochemistry, Western blotting, pharmacological experiments, and virus knockdown strategies were used to investigate the underlying mechanisms. RESULTS:Evident anxiodepressive-like behaviors were observed 6w after the SNI surgery, accompanied by increased neuronal excitability, enhanced HCN channel function, and increased expression of HCN2 isoforms in the LHb. Either pharmacological inhibition or virus knockdown of HCN2 channels significantly reduced LHb neuronal excitability and ameliorated both pain and depressive-like behaviors. CONCLUSION:Our results indicated that the LHb neurons were hyperactive under CADS in chronic pain, and this hyperactivation possibly resulted from the enhanced function of HCN channels and up-regulation of HCN2 isoforms.

Abstract The prevention and treatment of gastric cancer has been the focus and difficulty of medical research. We aimed to explore the mechanism of inhibiting migration and invasion of gastric cancer cells by methionine restriction (MR). The human gastric cancer cell lines AGS and MKN45 cultured with complete medium (CM) or medium without methionine were used for in vitro experiments. MKN45 cells were injected tail vein into BALB/c nude mice and then fed with normal diet or methionine diet for in vivo experiments. MR treatment decreased cell migration and invasion, increased E-cadherin expression, decreased N-cadherin and p-p65 expressions, and inhibited nuclear p65 translocation of AGS and MKN45 cells when compared with CM group. MR treatment increased IκBα protein expression and protein stability, and decreased IκBα protein ubiquitination level and TRIM47 expression. TRIM47 interacted with IκBα protein, and overexpression of TRIM47 reversed the regulatory effects of MR. TRIM47 promoted lung metastasis formation and partially attenuated the effect of MR on metastasis formation in vivo compared to normal diet group mice. MR reduces TRIM47 expression, leads to the degradation of IκBα, and then inhibits the translocation of nuclear p65 and the migration and invasion of gastric cancer cells.

This study explores the role of the long noncoding RNA (LncRNA) CRNDE in cisplatin (CDDP) resistance of gastric cancer (GC) cells. Here, we show that LncRNA CRNDE is upregulated in carcinoma tissues and tumor-associated macrophages (TAMs) of GC patients. In vitro experiments show that CRNDE is enriched in M2-polarized macrophage-derived exosomes (M2-exo) and is transferred from M2 macrophages to GC cells via exosomes. Silencing CRNDE in M2-exo reverses the promotional effect of M2-exo on cell proliferation in CDDP-treated GC cells and homograft tumor growth in CDDP-treated nude mice. Mechanistically, CRNDE facilitates neural precursor cell expressed developmentally downregulated protein 4-1 (NEDD4-1)-mediated phosphatase and tensin homolog (PTEN) ubiquitination. Silencing CRNDE in M2-exo enhances the CDDP sensitivity of GC cells treated with M2-exo, which is reduced by PTEN knockdown. Collectively, these data reveal a vital role for CRNDE in CDDP resistance of GC cells and suggest that the upregulation of CRNDE in GC cells may be attributed to the transfer of TAM-derived exosomes.

In order to explore new prediction methods and key genes for gastric cancer. Firstly, we downloaded the 6 original sequencing data of gastric cancer on the Illumina HumanHT-12 platform from Array Expression and Gene Expression Omnibus, and used bioinformatics methods to identify 109 up-regulated genes and 271 down-regulated genes. Further, we performed univariate Cox regression analysis of prognostic-related genes, then used Lasso regression to remove collinearity, and finally used multivariate Cox regression to analyze independent prognostic genes (MT1M, AKR1C2, HEYL, KLK11, EEF1A2, MMP7, THBS1, KRT17, RPESP, CMTM4, UGT2B17, CGNL1, TNFRSF17, REG1A). Based on these, we constructed a prognostic risk proportion signature, and found that patients with high-risk gastric cancer have a high degree of malignancy. Subsequently, we used the GSE15459 data set to verify the signature. By calculating the area under the recipient operator characteristic curve of 5-year survival rate, the test set and verification set are 0.739 and 0.681, respectively, suggesting that the prognostic signature has a moderate prognostic ability. The nomogram is used to visualize the prognostic sig-nature, and the calibration curve verification showed that the prediction accuracy is higher. Finally, we verified the expression and prognosis of the hub gene, and suggested that HEYL, MMP7, THBS1, and KRT17 may be potential prognostic biomarkers.

Background: The occurrence of recurrence and metastasis after treatment is a major challenge in the treatment of gastric cancer. This study was based on the methionine (Met)-dependent characteristics of gastric cancer cells to explore the effect of Met deficiency on the occurrence and development of gastric cancer. Methods: Human gastric cancer cell lines MKN45 and AGS and nude mice model were used to explore how Met affects gastric cancer by regulating lncRNA PVT1. Results: The levels of lncRNA PVT1 in gastric cancer cells and human gastric cancer xenografts of nude mice were down-regulated under the condition of Met deficiency. The cell viability and cell proliferation were declined after MKN45 and SGC-790 cells were cultured in Met-deficient medium. LncRNA PVT1 could affect BNIP3 promoter DNA methylation level through its interaction with DNMT1. Moreover, the silence of lncRNA PVT1 and the up-regulation of BNIP3 level inhibited the gastric cancer cell proliferation. Met deficiency could up-regulate BNIP3 expression by inhibiting the binding of lncRNA PVT1 to DNMT1, and activate mitophagy, thus inhibiting gastric cancer cell proliferation. Conclusion: Our study suggested that Met deficiency could down-regulate the expression of lncRNA PVT1, further demethylated the promoter of BNIP3, thus inhibiting the proliferation of gastric cancer cells by activating mitophagy.

Background: Gastric cancer (GC) derived exosomes (Exos) aggravate GC development by facilitating M2 macrophage polarization and long non-coding RNA (lncRNA) HCG18 was highly expressed in GC. This study aimed to investigate whether the exosomal lncRNA HCG18 regulated the M2 macrophage polarization in GC and the possible mechanism. Methods: The isolated GC cells (GCCs)-Exos were identified using transmission electron microscopy, Nanoparticle Tracking Analysis and Western blot. The GCCs-Exos function was verified by enzyme-linked immunosorbent assay and flow cytometry. Meanwhile, the exosomal lncRNA HCG18 function was determined using thein vitro assays. Furthermore, the underlying mechanism of the exosomal lncRNA HCG18 that regulated M2 macrophage polarization in GC was investigated using dual-luciferase reporter gene assay and RNA pull-down. Results: After the validation of GCCs-Exos, the GCCs-Exos facilitated the M2 macrophage polarization. The in vitro assays confirmed that the exosomal lncRNA HCG18 positively regulated the M2 macrophage polarization. Mechanistically, lncRNA HCG18 bound to miR-875-3p, miR-875-3p bound to KLF4. Furthermore, GCCs-exosomal lncRNA HCG18 elevated the KLF4 expression by decreasing miR-875-3p in macrophages to facilitate M2 macrophage polarization, thus alleviating GC. The in vivo assays clarified that the GCCs-exosomal lncRNA HCG18 restrained the tumor growth of GC induced by M2 macrophages. Conclusion: GCCs-exosomal lncRNA HCG18 elevated KLF4 expression by decreasing miR-875-3p in macrophages to facilitate the M2 macrophage polarization.

OBJECTIVE:Sine oculis homeobox homolog 2 (Six2), a developmental transcription factor, is known to be correlated with the development and prognosis of various cancers. In this study, we explored the prognostic value of Six2 in colon adenocarcinoma (COAD).METHODS:Wilcoxon signed-rank test and logistic regression were applied to identify relationship between clinical features and Six2 expression. The effect of Six2 expression and clinical features on the survival of COAD patients was explored using Kaplan-Meier and Cox regression analyses. Gene Set Enrichment Analysis (GSEA) was performed utilizing TCGA dataset.RESULTS:Compared to adjacent normal tissues, Six2 was highly expressed in COAD. Overexpression of Six2 in COAD was significantly associated with M classification (OR=2.557, positive vs. negative), N classification (OR=2.636, N2 vs. N0), and stage (OR=1.864, III vs. I) (all p-values<0.05). Patients with higher Six2 expression had significantly poor overall survival (OS, p=0.003). The univariate analysis showed that high expression of Six2 was significantly correlated with a poor OS (HR=1.135, 95%Cl 1.038-1.241; p=0.005). The multivariate analysis demonstrated that Six2 was an independent predictor of OS (HR=1.107, 95%Cl 1.007-1.216; p=0.036). According to GSEA, differentially enriched pathways in the Six2 high expression phenotype, included the TGF- β and Wnt signaling pathway.CONCLUSIONS:Six2 may be a valuable biomarker and potential therapeutic target for the treatment of COAD.

This study focused on the role of methionine (MET) in the autophagy of gastric cancer stem cells (GCSCs) and aims to elaborate its regulatory mechanism. In the present study, the GCSCs were isolated from human gastric cancer cell lines using an anti-CD44 antibody, and then cultured in MET+ homocysteine (HCY)- or MET-HCY+ medium. In MET+HCY-treated GCSCs, autophagy was suppressed, the methylation and phosphorylation of RAB37 were elevated, and miR-200b expression was down-regulated. Lentiviral vector (LV-) carrying methionine-γ lyase (an enzyme that could specifically lyse MET; Metase) promoted autophagy, reduced the methylation and phosphorylation of RAB37, and up-regulated miR-200b expression in MET+HCY--treated GCSCs. Then, we found that miR-200b suppressed the expression of protein kinase C α (PKCα), a protein that could inactivate RAB37 through promoting its phosphorylation. LV-Metase down-regulated RAB37 phosphorylation via miR-200b/PKCα, thus promoting the RAB37-mediated autophagy and suppressing cell viability in MET+HCY-treated GCSCs. Finally, the in vivo study proved that LV-Metase treatment inhibited tumor growth through up-regulating RAB37 expression. In conclusion, MET suppressed RAB37 expression via enhancing its methylation and suppressed RAB37 activity via miR-200b/PKCα axis, thus repressing RAB37-mediated autophagy in GCSCs. The supplementation of Metase lysed MET, thus inducing the autophagy of GCSCs and inhibiting tumor growth.

Background: Gastric cancer (GC) severely threatens human life, and METase seemed to inhibit tumor growth. However, the potential mechanism underlying it is still unclear. Methods: Both clinical tissues and cell lines were used in the present study. SNHG5 and miR-20a expressions were determined using real-time PCR. Western blot was performed to determine the expression of autophagy-related proteins. The interaction between miR-20a and SNHG5 was determined using luciferase reporter assay and RNA immunoprecipitation (RIP). Results: The expression of SNHG5 was decreased in GC tissues and cell lines. Overexpressed METase significantly promoted cell apoptosis and autophagy, as well as the expression of SNHG5. SNHG5 directly regulated the expression of miR-20a. GC cells transfected with pcDNA-SNHG5 significantly promoted cell apoptosis and autophagy, while the co-transfected with miR-20a mimic dramatically reversed the effects of pcDNA-SNHG5. Overexpressed METase significantly promoted cell autophagy, which was abolished by down-regulated SNHG5. Conclusion: Overexpressed METase promoted cell apoptosis and autophagy via up-regulating the expression of SNHG5 and down-regulating miR-20a in GC. (C) 2018 Elsevier B.V. All rights reserved.

Cancer susceptibility candidate 2 (CASC2), a recently discovered long non-coding RNA (lncRNA), was confirmed to play numerous roles in several human cancers. However, the involvement and concrete mechanism of CASC2 in hepatocellular carcinoma (HCC) still need to be further elucidated. The relative expressions of CASC2 and miR-24-3p in HCC tissue and cell lines were determined by quantitative real-time PCR (qRT-PCR). The effects of CASC2 and miR-24-3p on HCC cells were further assessed via cell viability and apoptosis. In vivo tumorigenesis assay was performed to verify the inhibition effect of CASC2 on the tumor growth and further clarify the important role of miR-24-3p in this mechanism. Compared with the paired normal tissues, the relative expression of CASC2 significantly reduced in the HCC tissues, while miR-24-3p as determined by qRT-PCR obviously increased in the HCC tissues. This observation was also found in HCC cell lines. Meanwhile, the expression of CASC2 was negatively related to miR-24-3p expression in the HCC tissues (r = -0.804, P < 0.001). CASC2 could negatively regulate the expression of miR-24-3p in vitro. Moreover, CASC2 overexpression resulted in the growth inhibitory and apoptosis-inducing effects on HCC cells, but the up-regulation of miR-24-3p greatly eliminated the CASC2-induced effects. The tumorigenesis of HCC cells was restrained significantly by CASC2 overexpression as shown by decreased tumor volume and growth rate. However, miR-24-3p up-regulation rescued the inhibition of CASC2 on the tumor growth in tumor-bearing mice. LncRNA CASC2 inhibited the viability and induced the apoptosis of HCC cells through regulating miR-24-3p.

RATIONALE:Colonic lipomas are rare benign tumours, usually without any symptoms, and most occur in the caecum and ascending colon. We describe a patient with upper rectal intussusception caused by a giant rectal lipoma; no similar report of this type of case has been published.PATIENT CONCERNS:We report the case of a patient who suffered from repeated bloody stools. A wide pedicle polyp (size, 6.5 × 4.5 × 3.5 cm) was detected at the 15th centimetre of the anal canal via an electronic colonoscope. At the initial part of the rectum, intussusception caused by a 6.5-cm fat-density mass was observed via abdominal contrast-enhanced computed tomography.DIAGNOSIS:Upper rectal intussusception caused by a giant rectal lipoma.INTERVENTIONS:Due to the large size of the polyp, an endoscopic polypectomy could not be performed. We performed laparoscopic segmental resection of the rectum (with preservation of the left colic artery [LCA]).OUTCOMES:The patient was discharged on the 7th postoperative day without any complications, was monitored on a regular basis at our outpatient department and was free of symptoms at a 3-month follow-up visit.LESSONS:Laparoscopic segmental resection of the rectum with LCA preservation is safe and feasible for the treatment of upper rectal intussusception caused by a giant rectal lipoma.

Objective: This study aimed to investigate the role of recombinant methioninase (rMETase) in the maintenance of gastric cancer stem cells (GCSCs) features and its molecular mechanism. Methods: GCSCs were isolated and enriched. GCSCs marker CD44 was detected by flow cytometry and immunofluorescence assay. The effect of rMETase on the GCSCs self-renewal was detected by the formation of the suspension cell spheres and the soft agar colony formation assay respectively. Cell survival rate was calculated with MMT assay. Cell apoptosis was analyzed by TUNEL method. The effect of silencing rMETase on the cancerigenicity of GCSCs in vivo was observed by subcutaneous transplantation cancer model in nude mice. The expression levels of stem cell associated genes Oct4, Nanog, bmi-1 and ttf-1 and PI3/Akt/mTOR signal pathway were detected by Real-time PCR method. Results: The number of suspended gastric cancer cells was significantly decreased in rMETase treatment group (P<0.01). The results of soft agar colony formation test showed that the number of colons in rMETase treatment group was lower than that of control group (36.8 +/- 9.0 vs 48.8 +/- 10.5, P<0.05). The proportion of S phase GCSCs was significantly increased while G2 phase GCSCs was significantly decreased after rMETase treatment (P<0.05). TUNEL results showed that rMETase treatment increased cell apoptosis. The expression levels of Oct4, Nanog, bmi-1 and ttf-1 decreased after rMETase treatment (P<0.05). rMETase treatment also inhibited the expression of Akt, m-TOR and PI3K (P<0.05). Conclusions: rMETase can inhibit the self renewal and proliferation of GCSCs, which maybe through PI3/Akt/mTOR signal pathway.

Background: Stem cells isolated from peripheral blood of gastric adenocarcinoma patients have noninvasive advantages. However, at present, there is no simple and effective separation technique. Purpose: In this study, CD133+ cells were isolated from peripheral blood of patients with gastric adenocarcinoma by using specific immunomagnetic particles, and the immunology of subcultured cells was identified to evaluate whether the immune magnetic particle separation had any effect on the cells themselves. Methods: Immune magnetic particles, made by a specific technique, are used to sort out the cells whose membrane could express CD133 from peripheral blood of gastric adenocarcinoma patients. By observing the sorted cells within serum-free culturing, we compare the differences in morphology and proliferation ability between the collected cells and cells from a standard tumor cell line. At the same time, an immunofluorescence method is used to detect the expression of the CD133 antibody. Moreover, this study explores the inhibition effect on gastric adenocarcinoma stem cell growth when combining 5-fluorouracil and methionine enzymes. Results and Conclusions: The specific immunomagnetic particles have a small diameter and strong sorting characteristics. In the experiment, there were 20 patients with gastric adenocarcinoma. CD133+ cells were separated successfully from peripheral blood of 13 patients (65%), among which subcultured cells of 9 cases (69.2%) were found to express CD44+ antigens. The sorted cells grew vigorously with a variety of morphologies in non-inducing culture, while the cells induced by β transforming growth factor presented slow growth and uniform morphology. There was a significant difference (P < 0.05) in cell proliferation between these two groups and the standard tumor cell line. In addition, 5-fluorouracil combined with methionine enzyme inhibited the growth of gastric adenocarcinoma stem cells significantly (P < 0.05). Accordingly, the CD133+/CD44+ cells from peripheral blood of gastric adenocarcinoma patients, sorted by specific immune magnetic particles, had clear stem cell properties as determined by cell function and structure. This lays a foundation for gastric adenocarcinoma stem cell extraction, culture and further research on stem cell characteristics.

PEGylated and folate-targeted chitosan polymeric nanoparticles (FPNs) for the treatment of gastric carcinoma were prepared successfully. OQC-anchored folate conjugates were synthesized and used in assembling FPNs nano-system for enhancing intracellular uptake against folate receptor overexpressing cancer cells. The results indicated that folate-targeted chitosan polymeric nanoparticles (CPNs) can reverse drug-resistant SGC-7901 cells of 5-fluorouracil (5-FU) compared with non-targeted CPNs. Increased therapeutic efficiency of 5-FU/METHFR shRNA co-loaded PNs were also tested in SGC-7901 cells and compaed with 5-FU or METHFR shRNA in solution, which was associated with increased cell inhibition function for single drug group and synergistic effects of 5-FU and METHFR shRNA at 2.0 µg/mL FPNs concentration. In addition, the cell accumulation levels of 5-FU in SGC-7901 cells was time dependent for these nanoparticles. FPNs (effective diameter: 83.2 ± 1.1 nm; polydispersity index: 0.193) could significantly boost cellular accumulation of 5-FU and overcome the drug efflux mechanism of MDR than 5-FU-loaded NPNs and 5-FU in solution. In conclusion, ligand-targeted PNs can be used as a potentially effective drug delivery system.

Stealth PLGA/Liposome nanoparticles (NPs) modified with tumor-targeting single-chain antibody fragment (scFV-P/L) for systemic delivery of recombinant methioninase (rMETase) for gastric cancer were prepared. The morphologies and therapeutic effects of rMETase-loaded scFV-P/L (scFV-rMETase-P/L) in vitro were analyzed. Functional scFV-P/L NPs composed of PLGA, DOPC and DSPE-PEG display low cell cytoxicity in SGC-7901 cells, and has more cell uptake ability than P/L NPs. scFV-rMETase-P/L was more effective in inhibiting tumor growth in the subcutaneous gastric carcinoma tumor model than free rMETase in solution (p < 0.05) and rMETase-loaded P/L (rMETase-P/L) (p < 0.05). Our findings collectively support the utility of scFV-targeted P/L NPs as a potentially effective drug delivery system.

OBJECTIVE:To observe the effects of miR-224 antisense oligonucleotide (ASO) on the proliferation and apoptosis of gastric cancer cells in vitro and vivo.METHODS:The expression of miR-224 in the cancer tissues and their adjacent tissues in 120 gastric cancer patients were detected by real-time quantitative PCR. The biological effects of miR-224 ASO on human gastric cancer SGC7901 cells was assessed by MTT assay, clone formation assay, flow cytometry and in vivo experiment in nude mice.RESULTS:Compared with the control group (0.50 ± 0.07), miR-224 ASO significantly reduced the miR-224 mRNA expression in the cancer patients (0.09 ± 0.01, P < 0.05). MTT assay results showed that the survival rate of gastric cells at 24 h, 48 h and 72 h was 53.6%, 59.1% and 70.1% in the miR-224 ASO group, and 12.3%, 17.4% and 24.7%, respectively, in the control group (P < 0.05 for all). Clone formation assay revealed that clone formation rate in the miR-224 ASO group was (5.33 ± 0.74)%, significantly lower than the (33.33 ± 8.38)% in the control group (P < 0.05). Flow cytometry indicated that the apoptotic index was (15.68 ± 1.46)% in the miR-224 ASO group and (3.36 ± 0.88)% in the control group (P < 0.01). In addition, the expressions of Bcl2 mRNA and protein were 1.05 ± 0.04 and 0.21 ± 0.03 in the miR-224 ASO group, significantly lower than that in the control group (4.87 ± 0.96 and 0.88 ± 0.09, P < 0.01). The in vivo study further showed that the tumor volume in the experimental group is significantly smaller than that in the control group (P = 0.01).CONCLUSIONS:MiR-224 is overexpressed in human gastric cancer. Reducing the expression of miR-224 can effectively inhibit the growth and promote apoptosis of gastric cancer cells. miR-224 may become a new target for the regulation of gene expression in gastric cancer.

In the last decade, phage-display technology for the generation of monoclonal antibodies (mAbs) has improved significantly. Several novel human mAbs directed to a wide range of targets have been generated for the treatment of common malignancies. These targets include antigens associated with apoptosis, angiogenesis and solid tumors, as well as tumor growth-related antigens, insulin-like growth factor I receptor and hepatocyte growth factor. The safety, pharmacokinetics, and pharmacodynamics of several human mAbs have been evaluated in patients with advanced solid tumors. In conclusion, significant advances in the generation and application of human mAbs in cancer therapy have been made in the last decade.

The aim of this study was to construct a human single-chain variable fragment (scFv) gene library for gastric cancer, from which human anti-cancer-associated gene (CAGE) scFvs are selected. Human lymphocytes were isolated from the peripheral blood of 10 gastric cancer patients and whole human heavy and light chain genes were cloned by reverse transcription-polymerase chain reaction (RT-PCR). VH and VL were rearranged randomly by splicing by overlap extension PCR. The ribosome complexes were enriched against the recombinant CAGE protein conjugated to magnetic beads. scFv antibodies were evaluated by western blot analysis, and affinity constants in a solution of antigen-antibody complexes were determined by enzyme-linked immunosorbent assay. An scFv library was constructed using the peripheral blood lymphocytes. The expressed scFv proteins from the ternary ribosome complexes were analyzed by western blot analysis and the affinity [equilibrium dissociation constant (KD)] of scFv for CAGE was determined to be 7.6x10-8 M. The ribosome display technique is efficient for selecting a fully human antibody fragment from a patient-derived gene pool.

Stealth cationic liposomes (SCLs) modified with tumor-targeting single-chain fragment variable (scFV) antibody for systemic delivery of recombinant methioninase (rMETase) for gastric cancer were prepared successfully. These functional SCL nanoparticles are composed of cationic lipids, dioleoylphosphatidylethanolamine, and distearoylphosphatidylethanolamine-polyethylene glycol, which have lower gene transfection efficiencies compared with Lipofectamine 2000, and can also be used as effective gene delivery vectors. Increased therapeutic efficiency of rMETase-loaded scFV-SCLs were tested in SGC-7901 cells and compared with free rMETase in solution and rMETase-loaded SCLs. In addition, scFV-SCLs (effective diameter: 185.7 nm; polydispersity index: 0.236) can significantly boost rhodamine 123 cellular accumulation in the cytoplasm. The scFV-targeted SCLs can be used as a potentially effective drug delivery system.