METTL14 enhances the m6A modification level of lncRNA MSTRG.292666.16 to promote the progression of non-small cell lung cancer.

BACKGROUND: m6A modification has close connection with the occurrence, development, and prognosis of tumors. This study aimed to explore the roles of m6A modification and its related mechanisms in non-small cell lung cancer (NSCLC). METHODS: NSCLC tissues and their corresponding para-cancerous tissues were collected to determine the m6A levels of total RNA/lncRNAs and the expression of m6A modification-related genes/lncRNAs. Then, A549 cells were transfected with si-METTL14 or oe-METTL14, and the cell transfection efficiency was assessed. Subsequently, the viability, apoptosis, cell colony formation, migration and invasion of the different cells were determined. Finally, the nude mouse tumorigenicity experiments were performed to observe the effects of METTL14 in vivo. RESULTS: Compared to the para-NSCLC tissues, the m6A level and METTL14 expression were both significantly increased in the NSCLC tissues (P < 0.05). Based on the expression of METTL14 in the different cell lines, A549 cells were chosen for further experiments. Then, the A549 cells with METTL14 knockdown and overexpression were successfully established, as well as it was found that METTL14 knockdown could inhibit the viability, colony formation, migration, and invasion of A549 cells, while facilitate their apoptosis. In vivo experiments also showed that METTL14 knockdown could inhibit tumor formation and growth. Additionally, the m6A level of MSTRG.292666.16 was higher in the NSCLC tissues; and after METTL14 knockdown, the expression and m6A level of MSTRG.292666.16 were both significantly reduced in A549 cells, and vice versa. CONCLUSION: METTL14 may promote the progression of NSCLC through up-regulating MSTRG.292666.16 and enhance its m6A modification level.

A Phase 1b Study of Ivonescimab, a Programmed Cell Death Protein-1 and Vascular Endothelial Growth Factor Bispecific Antibody, as First- or Second-Line Therapy for Advanced or Metastatic Immunotherapy-Naive NSCLC.

INTRODUCTION: This study (HARMONi-5) aimed to evaluate the safety and efficacy of ivonescimab (a bispecific antibody against programmed cell death protein 1 and vascular endothelial growth factor) as first- or second-line monotherapy in patients with advanced immunotherapy-naive NSCLC. METHODS: Eligible patients received intravenous ivonescimab 10 mg/kg every 3 weeks (Q3W), 20 mg/kg every 2 weeks (Q2W), 20 mg/kg Q3W, or 30 mg/kg Q3W. The primary end points were safety and objective response rate (ORR) per Response Evaluation Criteria in Solid Tumors version 1.1. RESULTS: At data cutoff (October 5, 2022), 108 patients were enrolled and received ivonescimab. Programmed death ligand-1 tumor proportion score (TPS) was greater than or equal to 1% in 74 patients (68.5%), including 35 (32.4%) with TPS greater than or equal to 50%. The median follow-up was 10.4 months (range: 8.4-10.9 mo). For all patients, ORR and disease control rate were 39.8% and 86.1%, respectively. ORR by TPS was 14.7%, 51.4%, and 57.1% in patients with TPS less than 1%, greater than or equal to 1%, and greater than or equal to 50%, respectively. In the 67 programmed death ligand-1-positive patients receiving first-line ivonescimab, the ORR was 33.3%, 52.6%, 60.0%, and 75.0% at the doses of 10 mg/kg Q3W, 20 mg/kg Q2W, 20 mg/kg Q3W, and 30 mg/kg Q3W, respectively. Grade greater than or equal to 3 treatment-related adverse events (TRAEs) were observed in 24 patients (22.2%). TRAEs leading to treatment discontinuation occurred in one patient (0.9%). TRAEs leading to death occurred in three patients (2.8%) with squamous NSCLC. The occurrence of grade greater than or equal to 3 TRAEs and grade greater than or equal to 3 bleeding events in squamous versus nonsquamous NSCLC patients was 25.5% versus 18.9% and 0.0% versus 1.9%, respectively. CONCLUSIONS: Ivonescimab monotherapy was well tolerated and found to have a promising efficacy in patients with advanced or metastatic NSCLC. CLINICALTRIALS: gov identifier: NCT04900363.

Flotillin-1 enhances radioresistance through reducing radiation-induced DNA damage and promoting immune escape via STING signaling pathway in non-small cell lung cancer.

Radiation resistance results in the recurrence and metastasis of non-small cell lung cancer (NSCLC) after radiotherapy. A major cause of radiation resistance is subversion of immune surveillance and clearance. Although our previous research has demonstrated that programmed death-ligand 1 (PD-L1) is responsible for radiation resistance in NSCLC, PD-L1 alone was not a reliable predictor of radiotherapy efficacy. For further exploration of the predictors of radiotherapy efficacy, which could add accuracy to the single biomarker - PD-L1, immunoprecipitation followed by mass spectrometry assay was performed to identify proteins that interact with PD-L1, and flotillin-1 (FLOT1) was detected as a candidate. However, the role of FLOT1 in radiation resistance in NSCLC is largely unknown. Here, we defined FLOT1 as a positive regulator of PD-L1 at the cell level, and the expression of PD-L1 was reduced following FLOT1 depletion. Furthermore, we found that the knockdown of FLOT1 impeded radiation-mediated cell migration and epithelial-mesenchymal transition process. Moreover, FLOT1 depletion enhanced radiation-induced DNA damage, thereby increasing the radiation lethality for NSCLC cells and promoting radiation-mediated tumor regression in animal models and patients with NSCLC. Furthermore, FLOT1 depletion-boosted DNA damage activated STING signaling pathway and promoted the production of CCL5 and CXCL10 that can drive CD8+ T lymphocytes chemotaxis, thereby reprogramming tumor immune microenvironment and triggering the antitumor immune response. Indeed, FLOT1 expression correlated with infiltration of immune cells in NSCLC tumor tissue samples. Taken together, our findings reported an unexplored role of FLOT1 in radiotherapy and also provided an evidence base for FLOT1 as a promising biomarker to predict the response to radiotherapy and a potential therapeutic target for enhancing radiotherapy effects.

First-line continual EGFR-TKI plus local ablative therapy demonstrated survival benefit in EGFR-mutant NSCLC patients with oligoprogressive disease.

Introduction: The effect of local ablative therapy (LAT) for oligoprogressive epidermal growth factor receptor (EGFR) mutation non-small cell lung cancer (NSCLC) remains undetermined. This study aimed to investigate the survival benefit of addition of LAT to EGFR-TKIs in EGFR-mutant NSCLC patients with oligoprogression during TKI therapy. Materials and Methods: Patients with stage IIIB/IV EGFR mutant NSCLC who had oligoprogressive disease during the first-line EGFR-TKI therapy from March 2011 to February 2016 were identified. The primary research point were progression-free survival1 (PFS1), defined as time of initiation of TKI therapy to Response Evaluation Criteria in Solid Tumours (RECIST) 1.1 defined progress disease (PD) or death and PFS2, defined as time of initiation of TKI therapy to off-TKI PD. The second research piont inclued overal survival (OS) and safety. Results: A total of 206 patients were included. The median follow-up time was 42 months (20.0-69.6 months). The median PFS1, median PFS2 and median OS for the related cohort were 10.7 months (95% CI, 10.1-13.3 months), 18.3 months (95% CI, 17.4-19.2 months) and 37.4 months (95% CI, 35.9-38.9 months) respectively. Survival rates of 1 year, 2 years and 3 years were 94.1%, 78.9%, and 54.7%, respectively. Multivariate analysis revealed that female, EGFR exon 19 mutation, one metastatic lesion, partial or complete response to prior EGFR TKIs therapy were the independent prognostic factors. No unexpected toxicities were observed. Conclusion: The current study suggested that the addition of LAT to EGFR-TKI could provide satisfactory survival benefit for EGFR-mutant NSCLC patients with oligoprogression during first-line EGFR-TKI treatment.

Dual integrin αvß 3 and NRP-1-Targeting Paramagnetic Liposome for Tumor Early Detection in Magnetic Resonance Imaging.

Enhanced MRI (magnetic resonance imaging) plays a vital role in the early detection of tumor but with low specificity. Molecular imaging of angiogenesis could efficiently deliver contrast agents to the tumor site by specific targeted carriers. We designed and synthesized dual-targeted paramagnetic liposomes functionalized with two angiogenesis-targeting ligands, the αVß3 integrin-specific RGD (Arg-Gly-Asp) and the neuropilin-1 (NRP-1) receptor-specific ATWLPPR (Ala-Thr-Trp-Leu-Pro-Pro-Arg) (A7R). These liposomes were proved to be in the nanoparticle range and demonstrated to effectively encapsulate paramagnetic MRI contrast agents Gd-DTPA (gadolinium-diethylenetriamine pentaacetic acid). T1 relaxivity of various liposome formulations was lower than pure Gd-DTPA but with no statistically significant difference. In vitro cellular uptake and competitive inhibition assay showed the higher binding affinity of dual-targeted liposomes to HUVECs (human umbilical vein endothelial cells) and A549 cells compared with pure Gd-DTPA, non-targeted, and single-targeted liposomes, which was proved to be mediated by the binding of RGD/ανß3-integrin and A7R/NRP1. For MR imaging of mice bearing A549 cells in vivo, dual-targeted liposomes reached the highest SER (signal enhancement rate) value with a significant difference at all experimental time points. It was about threefold increase compared to pure Gd-DTPA and non-targeted liposomes and was 1.5-fold of single-targeted liposomes at 2 h post injection. The SER was lowered gradually and decreased only by 40% of the peak value in 6 h. Dual-targeted liposomes were likely to exert a synergistic effect and the specificity of delivering Gd-DTPA to the tumor site. Therefore, dual-ανß3-integrin-NRP1-targeting paramagnetic liposome with a RGD-ATWLPPR heterodimeric peptide might be a potent system for molecular imaging of tumor.

Functional cooperation between HIF-1α and c-Jun in mediating primary and acquired resistance to gefitinib in NSCLC cells with activating mutation of EGFR.

OBJECTIVE: Hypoxia-inducible factor 1 (HIF-1) and activator protein 1 (AP-1) are important transcription factors regulating expression of genes involved in cell survival. HIF-1α and c-Jun are key components of HIF-1 and AP-1, respectively, and are regulated by epidermal growth factor receptor (EGFR)-mediated cell signaling and tumor microenvironmental cues. The roles of HIF-1α and c-Jun in development of resistance to EGFR tyrosine kinase inhibitor (TKI) in non-small cell lung cancer (NSCLC) with activating mutation of EGFR have not been explored. In this study, we investigated the roles of HIF-1α and c-Jun in mediating primary and acquired resistance to gefitinib in NSCLC cells with activating mutation of EGFR. MATERIALS AND METHODS: Changes in HIF-1α protein and in total and phosphorylated c-Jun levels in relation to changes in total and phosphorylated EGFR levels before and after gefitinib treatment were measured using Western blot analysis in NSCLC cells sensitive or resistant to gefitinib. The impact of overexpression of a constitutively expressed HIF-1α (HIF-1α/ΔODD) or a constitutively active c-Jun upstream regulator (SEK1 S220E/T224D mutant) on cell response to gefitinib was also examined. The effect of pharmacological inhibition of SEK1-JNK-c-Jun pathway on cell response to gefitinib was evaluated. RESULTS: Downregulation of HIF-1α and total and phosphorylated c-Jun levels correlated with cell inhibitory response to gefitinib better than decrease in phosphorylated EGFR did in NSCLC cells with intrinsic or acquired resistance to gefitinib. Overexpression of HIF-1α/ΔODD or SEK1 S220E/T224D mutant conferred resistance to gefitinib. There exists a positive feed-forward regulation loop between HIF-1 and c-Jun. The JNK inhibitor SP600125 sensitized gefitinib-resistant NSCLC cells to gefitinib. CONCLUSIONS: HIF-1α and c-Jun functionally cooperate in development of resistance to gefitinib in NSCLC cells. The translational value of inhibiting HIF-1α/c-Jun cooperation in overcoming resistance to EGFR TKI treatment of NSCLC cells with activating mutation of EGFR deserves further investigation.

Knockdown of Long Noncoding RNA ENST457720 Inhibits Proliferation of Non-Small Cell Lung Cancer Cells In Vitro and In Vivo.

Non-small cell lung cancer (NSCLC) represents the leading cause of cancer-related mortality worldwide. More and more reports have identified important roles for long noncoding RNAs (lncRNAs) in cancer development. ENST457720 expression was upregulated in lung adenocarcinoma in a microarray-based lncRNA screen. We determined the expression levels of ENST457720 in NSCLC tissues with quantitative real-time PCR and then studied their clinical significance. We explored the biological significance of ENST457720 with gain- and loss-of-function analyses in vitro and in vivo. In this study, ENST457720 was expressed at higher levels in NSCLC tissues than in paired normal tissues. Higher ENST457720 expression was associated with larger tumor sizes, lymph node metastasis, and advanced TNM stage. ENST457720 silencing suppressed NSCLC cell proliferation in vitro and in vivo. Moreover, ENST457720 knockdown inhibited NSCLC invasion and reversed the epithelial-to-mesenchymal transition. ENST457720 promoted NSCLC proliferation and invasion, which may be a novel potential therapeutic target for NSCLC.

Treatment and prognostic analysis of patients with leptomeningeal metastases from non-small cell lung cancer.

BACKGROUND: Leptomeningeal metastases (LM) from non-small cell lung cancer (NSCLC) are associated with poor prognosis and optimal treatment for this subgroup of NSCLC patients is controversial. The purpose of this study is to evaluate treatment options and prognostic factors of NSCLC patients with LM. METHODS: We retrospectively analyzed data of 108 patients who had been diagnosed with LM from NSCLC between May 2006 and August 2013. RESULTS: The median survival time (MST) of the 108 patients was 5.3 months, and the one-year survival rate was 23.7%. Forty-nine patients received whole brain radiotherapy (WBRT) and the MST of patients who received WBRT and those who did not were 6.4 and 4.3 months, respectively. Forty-two patients were treated with epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) after being diagnosed with LM. These patients had prolonged survival (11.1 vs. 4.4 months). Patients who received concomitant WBRT and EGFR-TKIs had the longest MST (12.3 months). Eastern Cooperative Oncology Group performance status, whether patients received WBRT, and/or EGFR-TKIs were independent prognostic factors for patients with LM from NSCLC. CONCLUSION: WBRT, EGFR-TKIs or combined therapy, could lead to better clinical outcomes for NSCLC patients with LM. EGFR-TKIs plus WBRT has the potential to be the standard strategy for LM in NSCLC patients.

Translationally controlled tumor protein (TCTP) downregulates Oct4 expression in mouse pluripotent cells.

The present study aimed to investigate the function of translationally controlled tumor protein (TCTP) in the regulation of Oct4 in mouse embryonic carcinoma P19 cells and mouse J1 embryonic stem (ES) cells. The mRNA level of endogenous TCTP in somatic cells was 2-4 folds higher than that in pluripotent P19 and J1 ES cells. Overexpression of TCTP in mouse pluripotent cells not only reduced the level of Oct4 transcription, but also decreased the pluripotency of stem cells. The N-terminal end of TCTP (amino acids 1-60) played an important role in suppressing the Oct4 promoter. Moreover, overexpression of TCTP in P19 cells suppressed the Oct4 promoter activity in a dose- and a time-dependent manner. In addition, knockdown of TCTP by small interfering RNA increased the expression of Oct4. Our study indicates that TCTP downregulates the Oct4 expression by binding the Sf1 site of Oct4 promoter in mouse pluripotent cells.

Identification and characterization of the Oct4 extended transcriptional regulatory region in Guanzhong dairy goat.

The octamer-binding transcription factor 4 gene (Oct4) plays a critical role in maintaining pluripotency during early mammalian embryonic development and self-renewal of embryonic stem (ES) cells. In this study, we cloned the Oct4 cDNA and 2.8-kb regulatory region upstream of the start codon in Guanzhong dairy goat ( Capra hircus ). The comparative sequence analysis of Oct4 cDNA showed that it was highly conserved among six mammalian species. The goat Oct4 5' regulatory regions were homologous to the corresponding regions of Oct4 in other species and were functional in directing the expression of luciferase in mouse P19 embryonic carcinoma cells and mouse J1 ES cells. Furthermore, the methylation levels in the goat Oct4 minimal promoter and proximal enhancer in the fetal genital ridge were lower than those in the heart. Additionally, two processed pseudogenes that shared high homology with goat Oct4 cDNA were identified and characterized.

Magnetic resonance imaging contrast agent: cRGD-ferric oxide nanometer particle and its role in the diagnosis of tumor.

To construct tumor-targeted nanometer particles as a negative magnetic resonance imaging (MRI) contrast agent. Ultra-small superparamagnetic iron oxide (USPIO) nanometer particles were prepared by one-step chemical precipitation. The covalent bond between cyclic RGD (cRGD) containing an Arg-Gly-Asp sequence targeting integrin-alphavbeta3, and USPIO was conducted by chemical crosslinking. The physico-chemical property of cRGD-USPIO was detected. Prussian blue staining was applied to detect the specific binding capacity of cRGD-USPIO and USPIO to human pulmonary adenocarcinoma A549 cells and human umbilical vein endothelial cells. Subsequently, A549 xenografts in nude mice were established, and intravenous injections of USPIO and cRGD-USPIO into the vena caudalis were performed. The enhancement of cRGD-USPIO against tumor MRI signal was evaluated. The mean hydrodynamic diameter of cRGD-USPIO was 43.97 +/- 10.10 nm and the size of the ferric oxide core was 5-10 nm. The specific saturation magnetization was 59.94 A x m2 x Kg(-1). The cell conjugation assay results indicated that the positive staining of the cRGD-USPIO group was significantly enhanced. The in vivo MRI diagnosis indicated that the cRGD-USPIO tumor signal was significantly reduced compared to that of the USPIO group (P < 0.01). The targeted superparamagnetic iron oxide nanometer particle can be a novel MRI negative contrast agent for more specific tumor early diagnosis.

RGD-targeted paramagnetic liposomes for early detection of tumor: in vitro and in vivo studies.

Magnetic resonance molecular imaging has emerged as a potential approach for tumor diagnosis in the last few decades. This approach consists of the delivery of MR contrast agents to the tumor by specific targeted carriers. For this purpose, a lipopeptide was constructed by using a cyclic RGD peptide headgroup coupled to palmitic acid anchors via a KGG tripeptide spacer. Targeted paramagnetic liposomes were then prepared by the incorporation of RGD-coupled-lipopeptides into lipid bilayers for specific bounding to tumor. In vitro, study demonstrated that RGD-targeted liposomes exhibited a better binding affinity to targeted cells than non-targeted liposomes. MR imaging of mice bearing A549 tumors with the RGD-targeted paramagnetic liposomes also resulted in a greater signal enhancement of tumor compared to non-targeted liposomes and pure contrast agents groups. In addition, biodistribution study also showed specific tumor targeting of RGD-targeted paramagnetic liposomes in vivo. Therefore, RGD-targeted paramagnetic liposomes prepared in the present study may be a more promising method for early tumor diagnosis.

Integrin-targeted paclitaxel nanoliposomes for tumor therapy.

A neovessel-targeted PEGylated liposomal formulation of paclitaxel was prepared with the purpose of improving the solubility of paclitaxel and specific targeting ability of this drug to tumor vasculature. AlphaV integrins overexpressed on the surface of new formed tumor vessels were selected to be the targets and their specific ligand, a 12-mer peptide containing a cyclic RGD sequence was used to achieve the goal. After coupled with a KGG-Palmitic acid conjugate, the RGD containing peptide was successfully integrated to the lipid bilayers. Mean particle size of the liposomes was under 100 nm and the drug entrapment efficiency was greater than 95%. Release study showed a much lower release rate of paclitaxel from liposomal formulation than from Cremophor EL-based formulation which indicated that this drug was stable in an entrapped form in vitro. Plasma distribution study showed that liposomal paclitaxel-treated groups obtained higher paclitaxel concentration than Taxol-treated group after 6 h injection. Greater cellular uptake was also found in the integrin-targeted liposomal paclitaxel-treated group compared with Taxol-treated group. Treatment of mice bearing A549 tumors with the integrin-targeted paclitaxel liposomes resulted in a lower tumor microvessel density than Taxol-treated group. Therefore, RGD-based strategy could be used to enhance tumor-specific recognition of nanocarriers. Neovessel-targeted PEGylated paclitaxel liposomes developed in present study might be a more promising drug for cancer treatment.

Enhanced antitumor effect of novel dual-targeted paclitaxel liposomes.

A novel dual-targeted peptide containing an alpha V integrins specific ligand and a neuropilin-1 specific motif was developed which showed an increased specific targeting affinity to tumors. Active dual-targeted liposomes were then produced with this peptide and exhibited greater binding activity than single-targeted liposomes in vitro. Paclitaxel entrapped in this formulation greatly increased the uptake of paclitaxel in the targeting cells and significantly suppressed the growth of HUVEC and A549 cells compared with general paclitaxel injections (Taxol) and single-targeted paclitaxel liposomes. The treatment of tumor xenograft models with dual-targeted paclitaxel liposomes also resulted in better tumor growth inhibition than any other treatment groups. Therefore, the dual-targeted paclitaxel liposomes prepared in the present study might be a more promising drug for cancer treatment. Furthermore, the dual-targeting approach may produce synergistic effects that can be applied in the development of new targeted drug delivery systems.

[Drug resistance mechanism of non small cell lung cancer PC9/AB2 cell line with acquired drug resistance to gefitinib].

OBJECTIVE: To study the drug resistance mechanism of non-small cell lung cancer (NSCLC) cell line PC9/AB2 with acquired drug resistance to gefitinib. METHODS: The human lung adenocarcinoma cell line PC9 was cultured in vitro, and was induced by MNNG to obtain the cell line PC9/AB2 with acquired drug resistance to gefitinib. The sensitivity of the cell line PC9 and PC9/AB2 to gefitinib was determined by MTT assay. The effects of gefitinib on cell apoptosis of the 2 cell lines were determined by flow cytometry. The genomic DNA of the 2 cell lines were extracted, and then the exons 19-21 of EGFR gene were amplified by PCR and sequenced. The protein expression of c-MET and integrin beta1 in the 2 cell lines was determined by Western blot method. The adhesion ability and migration ability of the 2 cell lines were determined by adhesion test and scratch assay. RESULTS: (1) The data form MTT and apoptosis detection showed that the IC50 of PC9/AB2 cells was (24.2+/-5.5) micromol/L, 576 times higher than PC9 cells [IC50 (0.04+/-0.01) micromol/L]. Given the same concentration of gefitinib, the apoptosis rate of PC9 cells was 38.48%, while that of PC9/AB2 cells was 2.2%. (2) The results of gene sequencing showed that there was a deletion of 15 bp in both exon 19 of the 2 cell lines, while no T790M mutation occurred. (3) The results from Western blot showed that there was no significant difference in protein expression of c-MET between the 2 cell lines, while the protein expression of integrin beta1 in PC9/AB2 cells was significantly higher than that of the PC9 cells. (4) The result from adhesion test and scratch assay showed that the adhesion ability and migration ability of the PC9/AB2 cells was significantly higher that those of PC9 cells. CONCLUSION: The high expression of integrin beta1 may be associated with acquired drug resistance of NSCLC cell line PC9/AB2 to gefitinib.

[Quantitative analysis of telomerase reverse transcriptase gene expression in goat reprogramming cells].

Currently, animal somatic cell reprogramming into the induced pluripotent stem cell (iPS) is one of the hottest research target in the field of cell biology. We focused on the analysis of telomerase reverse transcriptase (TERT) gene expression during goat somatic fibroblasts reprogramming, and investigated the relationship between the expression of TERT and the pluripotency of reprogrammed cells. RNA samples of fetal tissues isolated from Guanzhong milk goat fetus, and the induced goat reprogramming cell clones were used to determine the relative expression levels of TERT by the real-time RT-PCR method. Goat embryonic fibroblasts (GEF) collected from the Guanzhong milk goat with normal karyotype were induced by 4 transcription factors to become reprogramming cells. The expression of TERT in reprogramming cells was detected by Real-time RT-PCR. The results showed that the expression of TERT in testis tissue was higher than that in epithelial tissues (P < 0.01). The expression level of TERT was higher in AP staining positive cells than that in AP staining negative cells (P < 0.01). This result indicated that TERT activity played an important role in cell reprogramming.

Fabrication and characterization of chitosan coated braided PLLA wire using aligned electrospun fibers.

The development of functionalized braided wires coated with chitosan that can be used for tissue suturing and tissue regeneration is the subject of this work. Poly(L: -lactic acid) (PLLA) braided wires were successfully fabricated by combining an electrospinning technique and alignment collection with a mini-type braiding method. The resulting PLLA wires with and without chitosan coating were characterized through a variety of methods including scanning electron microscopy (SEM), X-ray photoelectronic spectra (XPS) and tensile mechanical testing. Hemolytic property, kinetic hemostasis behavior, platelet adhesion, erythrocyte adhesion, and water uptake ability of the wires were explored. The results showed that a nearly comparable mechanical behavior of the braided wires with some commercial suture could be obtained with well-aligned fibers, and no significant difference in tensile performances were recognized with and without the introduction of chitosan. The PLLA wires coated with chitosan were found to have better prohemostatic activity than those without a chitosan coating.