Single-Cell Diagnosis of Cancer Drug Resistance through the Differential Endocytosis of Nanoparticles between Drug-Resistant and Drug-Sensitive Cancer Cells.

Single-cell diagnosis of cancer drug resistance is highly relevant for cancer treatment, as it can be used to identify the subpopulations of drug-resistant cancer cells, reveal the sensitivity of cancer cells to treatment, and monitor the progress of cancer drug resistance. However, simple and effective methods for cancer drug resistance detection at the single-cell level are still lacking in laboratory and clinical studies. Inspired by the fact that nanoparticles with diverse physicochemical properties would generate distinct and specific interactions with drug-resistant and drug-sensitive cancer cells, which have distinctive molecular signatures, here, we have synthesized a library of fluorescent nanoparticles with various sizes, surface charges, and compositions (SiO2 nanoparticles (SNPs), organic PS-co-PAA nanoparticles (ONPs), and ZIF-8 nanoparticles (ZNPs)), thus demonstrating that the composition has a critical influence on the interaction of nanoparticles with drug-resistant cancer cells. Furthermore, the clathrin/caveolae-independent endocytosis of ZNPs together with the P-glycoprotein-related decreased cell membrane fluidity resulted in a lower cellular accumulation of ZNPs in drug-resistant cancer cells, consequently causing the distinct cellular accumulation of ZNPs between the drug-resistant and drug-sensitive cancer cells. This difference was further quantified by detecting the fluorescence signals generated by the accumulation of nanoparticles at the single-cell level via flow cytometry. Our findings provide another insight into the nanoparticle-cell interactions and offer a promising platform for the diagnosis of cancer drug resistance of various cancer cells and clinical cancer samples at the single-cell level.

Investigation with ESI FT-ICR MS on sorbent selectivity and comprehensive molecular composition of landfill leachate dissolved organic matter.

Molecular characterization of landfill leachate dissolved organic matter (LDOM) is essential for developing effective processing techniques. However, the molecular selectivity of extraction method and ionization modes often leads to the bias of molecular characterization of LDOM. Here, seven representative sorbents were selected and electrospray ionization negative ion mode (ESI (-)) and positive ion mode (ESI (+)) Fourier-transform ion cyclotron resonance mass spectrometry (FT-ICR MS) were used to investigate the molecular composition of different LDOM samples. Obvious sorbent selectivity during extraction procedure was observed, resulting in the underestimation of molecular diversity of LDOM from 32.7% to 69.3%. Totally, 14,000-18,000 unique molecules were obtained in a single sample, indicating the unprecedented molecular diversity of LDOM. Lignins, proteins and lipids are three major molecular groups in LDOM, and N or S containing molecules occupied 83%. Although much of total organic carbon was removed during biochemical treatment process, the molecular diversity of LDOM was not reduced because a considerable of bio-recalcitrant molecules was produced. The results uncover the sorbents selectivity and ionization modes selectivity in LDOM analysis and provided a comprehensive change of LDOM molecular composition during biochemical treatment, which benefits the development of accurate methods to remove organic carbon in landfill leachate.

Chronic obstructive pulmonary disease alters the genetic landscape and tumor immune microenvironment in lung cancer patients.

Background: Chronic obstructive pulmonary disease (COPD) and lung cancer are leading causes of morbidity and mortality worldwide. Studies have reported molecular alterations in patients with lung cancer and in patients with COPD. However, few investigation has been conducted on the molecular characteristics of lung cancer patients with COPD. Materials and methods: We performed a retrospective cohort study that included 435 patients with pathologically confirmed lung cancer at the Ruijin Hospital. For patients with documented spirometry, Global Initiative for Chronic Obstructive Lung Disease criteria were used to define COPD. For patients without documented spirometry, chest computed tomography and other clinical information were used to define COPD. Tumor tissue DNA was extracted from formalin-fixed paraffin-embedded samples. DNA mutation analysis, multiplex immunohistochemistry (mIHC), calculation of tumor mutational burden (TMB), mutant-allele tumor heterogeneity (MATH), and predication of neoantigens were performed. Results: Although SNV mutations in lung cancer patients with COPD (G1 group) were generally higher than those in lung cancer patients without COPD (G2 group), the difference in the number of mutations was insignificant between the two groups. Of the 35 mutated genes, the number of them was higher in G1 than in G2, except that of EGFR. PI3K-Akt signaling pathway was enriched from significantly different genes. While TMB and MATH levels were not significantly different, the tumor neoantigen burdenwas markedly higher in G1 than that in G2. The level of CD68+ macrophages was significant higher in the stroma and total areas in the G1 group than in G2 group. The level of CD8+ lymphocytes was markedly higher in the stroma and showed a clear tendency forhigher expression in the G1 group than inthe G2 group. No significant differences were observed for the level of programmed death-ligand 1+ (PD-L1+), programmed death 1+ (PD-1+), and CD68PD-L1 in the stroma, tumor and total areas. Conclusion: Our study revealed different genetic aberrations and pathways, higher neoantigen burden, and higher level of CD68+ macrophages and CD8+ T lymphocytes in lung cancer patients with COPD. Our investigation implies that the existence of COPD should be considered and immunotherapy is a potential choice when treating lung cancer patients with COPD.

Eosinophil and IFN-γ associated with immune-related adverse events as prognostic markers in patients with non-small cell lung cancer treated with immunotherapy.

Objectives: Immune checkpoint inhibitors (ICIs) alone or combined with other antitumor agents are largely used in lung cancer patients, which show both positive effects and side effects in particular subjects. Our study aims to identify biomarkers that can predict response to immunotherapy or risk of side effects, which may help us play a positive role and minimize the risk of adverse effects in clinical practice. Methods: We retrospectively collected data from patients with advanced non-small cell lung cancer (NSCLC) treated with ICIs at our center. Patients who received initial ICI therapy for >1 year without progression of disease were classified as long-term treatment (LT) group, while others were classified as the non-long-term treatment (NLT) group. Multivariate logistic analysis was performed to identify independent risk factors of progression-free survival (PFS) and immune-related adverse events (irAEs). Results: A total of 83 patients (55.7%) had irAEs. The median PFS for patients in grades 1-2 of irAEs vs. grades 3-4 vs non-irAEs groups was (undefined vs. 12 vs. 8 months; p = 0.0025). The 1-year PFS rate for multisystem vs. single vs. non-irAE groups was 63%, 56%, and 31%, respectively. Signal transduction of inflammatory cytokines improves clinical prognosis through immunomodulatory function, but the benefit is also limited by the resulting organ damage, making it a complex immune balance. Serum biomarkers including EOS% of ≥ 1.15 (HR: 8.30 (95% CI, 2.06 to 33.42); p = 0.003) and IFN-γ of ≥ 3.75 (HR: 5.10 (95% CI, 1.29 to 20.15), p = 0.02) were found to be predictive for irAEs. Conclusion: EOS% of ≥1.15% and IFN-γ of ≥3.75 ng/L were considered peripheral-blood markers for irAEs and associated with improved clinical outcomes for immunotherapy in patients with advanced NSCLC.

Risk of reactive cutaneous capillary endothelial proliferation induced by camrelizumab in patients with non-small cell lung cancer: a retrospective study.

Background: Reactive cutaneous capillary endothelial proliferation (RCCEP) is a common immune-related adverse event (irAE) related to camrelizumab. This study aimed to investigate the risk factors of RCCEP and its association with patients' survival. Methods: This retrospective study collected the data of consecutive patients with non-small cell lung cancer (NSCLC) who received camrelizumab between January 2019 and December 2021. Baseline characteristics and peripheral blood biomarkers were collected. The outcomes were the occurrence of RCCEP and progression-free survival (PFS). The factors associated with RCCEP were analyzed using univariable and multivariable logistic regression. The association between PFS and RCCEP occurrence was analyzed by the log-rank test. Results: Among the 80 patients included, 24 (30.0%) developed RCCEP, and 56 did not. Among the patients with RCCEP, only four reported the occurrence of grade 3-4 RCCEP. The multivariable analysis revealed that a percentage of eosinophil (EOS%) >1.75% was significantly associated with a higher risk of RCCEP [odds ratio (OR) =4.484; 95% confidence interval (CI): 1.139-17.651] and camrelizumab combined with an anti-angiogenic agent was significantly associated with a lower risk of RCCEP (OR =0.188; 95% CI: 0.055-0.639). The median PFS was numerically longer in patients with RCCEP than in those who did not (17 vs. 9 months, P=0.069). Patients who had baseline EOS% >1.75% and received camrelizumab without an anti-angiogenic agent had a longer median PFS than those who did not (17 vs. 9 months, P=0.011). Conclusions: Baseline EOS% >1.75% and camrelizumab without an anti-angiogenic agent were risk factors of RCCEP and might be associated with better survival in patients with NSCLC.

Increased Antimicrobial Resistance among Sputum Pathogens from Patients with Hyperglycemia.

BACKGROUND: Glucose management is of great significance. Infection and hyperglycemia are a vicious circle. This study was conducted to describe distribution and antimicrobial resistance of bacteria isolated from patients with normoglycemia, hyperglycemia, or diabetes on admission. METHODS: A retrospective study was conducted in a teaching hospital from January 2015 to March 2017. Bacteria were identified by the Vitek 2 automated system and antimicrobial susceptibility determined. RESULTS: A total of 1,163 patients were included: 582 with normoglycemia, 292 with hyperglycemia and 289 with diabetes. Enterobacter, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterococcus faecium were the main species isolated from these patients, with 1,616 unduplicated isolates from sputum samples. Patients with hyperglycemia were more prone to carry more than one species, and the rate of multidrug-resistant K. pneumoniae and methicillin-resistant S. aureus was higher in this group. K. pneumoniae from hyperglycemia patients demonstrated increased resistance to carbapenems, especially imipenem (p=0.002) and meropenem (p=0.003), than those isolated from patients with normoglycemia or diabetes. No significance was detected for K. pneumoniae, A. baumannii, or P. aeruginosa between nondiabetes and diabetes patients. In addition, hyperglycemia patients had a higher rate of ICU admission (p=0.035) and a lower survival rate (p<0.001). CONCLUSION: Patients with hyperglycemia were more prone to carry bacteria, especially multidrug-resistant K. pneumoniae and methicillin-resistant S. aureus. Assessing glucose on admission is of great significance in predicting bacterial carriage and antimicrobial resistance.

Carbonized Bark by Laser Treatment for Efficient Solar-Driven Interface Evaporation.

Interfacial localization of solar thermal energy conversion to drive evaporation is a promising water treatment technology, especially for gaining pure water in freshwater-deficient areas. Phoenix tree bark is chosen as the raw material mainly because of its low cost and renewability. The carbonized bark with broadened pore sizes possess efficient steam escape channels and light absorption structure. The film with a double-layer structure is constructed through converting the surface of the bark into the carbonized structure under controllable laser treatment. The evaporation efficiency is calculated to be 74% under 1 sun by enhancing the photothermal conversion ability and efficiently opening the surface water transport channels simultaneously. The distillation water exhibits large resistance values (9.65 MΩ) and low concentrations of four primary ions (Na+, K+, Mg2+, and Ca2+), which achieves international standard for drinking water. In addition, the carbonized bark also exhibits all-right purified performance toward water evaporation from dye wastewater. The low cost and clean technology provides new inspiration for the future development of applicable solar thermal energy-driven water treatment systems.

Methicillin-resistant Staphylococcus aureus pneumonia in diabetics: a single-center, retrospective analysis.

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) pneumonia is an important issue with significant morbidity and mortality in clinical practice, especially in diabetes mellitus (DM). Studies focusing on S. aureus pneumonia in DM is limited, we sought to make a relatively comprehensive exploration of clinical characteristics, antimicrobial resistance, and risk factors for mortality of S. aureus pneumonia in DM and non-diabetics mellitus (non-DM). METHODS: A retrospective study was conducted in Ruijin Hospital from 2014 to 2017. The characteristics of DM and non-DM patients were assessed, including demographics, comorbidities, using of invasive mechanical ventilation, Hemoglobin A1c (HbA1C), confusion, urea, respiratory rate, blood pressure, age ≥65 years (CURB-65) score, length of hospital stay, clinical outcomes, antimicrobial susceptibility. Independent risk factors for mortality were identified by univariate and multivariate logistic regression analysis. RESULTS: A total of 365 patients with S. aureus pneumonia were included in our study, including 144 with DM and 221 non-DM. DM patients were more susceptible to MRSA infection (65.3% vs. 56.1%, P > 0.05), suffered from much severer pneumonia with a higher CURB-65 score, invasive mechanical ventilation rate (46.5% vs. 28.1%, P < 0.01) and mortality rates (30.6% vs. 23.1%, P > 0.05); almost all DM patients had higher antimicrobial resistance than non-DM patients, the DM group had a higher co-infection rate (47.2% vs. 45.7%, P > 0.05), and Acinetobacter baumannii was the most common bacterium in DM, while Klebsiella pneumoniae ranked first in patients with non-DM. Independent risk factors for pneumonia-related mortality were MRSA and CURB-65. Higher HbA1c levels were linked to a higher MRSA infection and co-infection rate and more severe pneumonia, leading to an increase in mortality. CONCLUSIONS: DM patients with poor glucose control are more susceptible to MRSA infection. They suffer from higher antimicrobial resistance, a higher co-infection rate, and much severer pneumonia than non-DM. MRSA itself is an independent risk factor for mortality in all patients.

In-situ synthesized and pattern Ag/Bi2Se3 composite structure by LDW and photothermal conversion.

Bi2Se3 nanofilm has exhibited many promising potentials application in the field of photo-to-heat conversion. A highly-efficient photo-to-heat conversion system of Ag/Bi2Se3 composite nanofilm is successfully fabricated through laser direct writing (LDW) technique. The localized heat induced by laser simultaneously achieve Ag particles synthesis, transfer and patterning in a single processing step. The thermal reaction process includes the forming of nanoparticles based on the process of the thermal reduction, laser ablation, sputtering deposition and so on. The thermal storage capability and photothermal conversion stability have been greatly improved through preventing the heat from loss and efficient LSPR enhancing. The photothermal conversion mechanism of composition film is discussed in detail. This work suggests that the laser-assisted transfer technique give rise to a new expectation of functional composite nanofilm application for energy conversion.

Bimetallic Aluminum 5,6-Dihydro-7,7-dimethyl quinolin-8-olates as Pro-Initiators for the ROP of ε-CL; Probing the Nuclearity of the Active Initiator.

Six examples of aluminum 5,6-dihydro-7,7-dimethylquinolin-8-olates, [{2-R¹-7,7-Me2-8-R²C9H6N-8-O}AlR³2]2 (R¹ = R² = H, R³ = Me C1; R¹ = R² = H, R³ = Et C2; R¹ = R² = H, R³ = i-Bu C3; R¹ = Cl, R² = H, R³ = Me C4; R¹ = H, R² = R³ = Me C5; R¹ = Cl, R² = R³ = Me C6), have been prepared by treating the corresponding pro-ligand (L1⁻L4) with either AlMe3, AlEt3 or Al(i-Bu)3. All complexes have been characterized by ¹H and 13C NMR spectroscopy and in the case of C1 and C4 by single crystal X-ray diffraction; dimeric species are a feature of their molecular structures. In the presence of PhCH2OH (BnOH), C1⁻C6 displayed good control and efficiency for the ROP of ε-CL with almost 100% conversion achievable in 10 min at 90 °C; the chloro-substituted C4 and C6 notably exhibited the lowest activity of the series. However, in the absence of BnOH, C1 showed only low activity with 15% conversion achieved in 30 min forming a linear polymer capped with either a methyl or a L1 group. By contrast, when one or more equivalents of BnOH was employed in combination with C1, the resulting catalyst was not only more active but gave linear polymers capped with BnO end-groups. By using ¹H and 27Al NMR spectroscopy to monitor solutions of C1, C1/BnOH and C1/BnOH/10 ε-CL over a range of temperatures, some support for a monomeric species being the active initiator at the operational temperature is presented.

Thermo-enhanced ring-opening polymerization of ε-caprolactone: the synthesis, characterization, and catalytic behavior of aluminum hydroquinolin-8-olates.

A series of highly sensitive aluminum hydroquinolin-8-olates (C1-C8) was synthesized and characterized by 1H/13C NMR spectroscopy. The molecular structures of compounds C1, C3, C4, and C5 were confirmed by single crystal X-ray crystallography and demonstrated the binuclear form. In the presence of BnOH, all the aluminum complexes exhibited moderate to high activities towards the ring-opening polymerization of ε-CL at high temperatures, but quite low activities at ambient temperature. Microstructure analysis of the resultant polycaprolactones showed that the polymers were linear in nature with a BnO- end group. In addition, the mechanism was investigated by monitoring the 1H NMR and 27Al NMR of C1 and these results suggested that the complexes existed as dimeric species at low temperature and partly converted into active mononuclear species at higher temperatures, which was easily coordinated by BnOH to afford the active species for the ring-opening polymerization of ε-caprolactone.

Cigarette smoke-induced lung inflammation in COPD mediated via LTB4/BLT1/SOCS1 pathway.

BACKGROUND: Evidence suggests that suppressor of cytokine signaling 1 (SOCS1) is crucial for the negative regulation of inflammation. We investigated the relationship between smoking, SOCS1, and leukotriene B4 (LTB4) in vitro and in clinical samples of COPD; besides which we detected the impact of LTB4 receptor 1 (BLT1) antagonist on inflammation. METHODS: SOCS1 expression in bronchial mucosa was determined by immunohistochemistry and real-time polymerase chain reaction. We also detect SOCS1 and BLT1 expression in alveolar macrophages from bronchoalveolar lavage fluid (BALF) by real time-PCR, in addition to measuring the level of cytokines in BALF using enzyme-linked immunosorbent assay. In vitro, we investigated the expression of SOCS1 in cigarette smoke extract-induced mouse macrophage cell line RAW264.7 by real-time polymerase chain reaction and Western blot, and detected the level of cytokines in the supernatant by enzyme-linked immunosorbent assay. Then, we investigated the effects of BLT1 antagonist U-75302 on SOCS1 expression in these cells. RESULTS: We obtained endobronchial biopsies (15 COPD patients and 12 non-COPD control subjects) and BALF (20 COPD patients and 20 non-COPD control subjects), and our results showed that SOCS1 expression significantly decreased in lung tissues from COPD patients. Inflammatory cytokines in BALF were higher in COPD and these inflammatory cytokines negatively correlate with SOCS1 levels. Further, the BLT1 antagonist restored SOCS1 expression and in turn inhibited inflammatory cytokine secretion in vitro. CONCLUSION: Long-term cigarette smoke exposure induced SOCS1 degradation and LTB4 accumulation, which was associated with emphysema and inflammation. A BLT1 antagonist might be a potential therapeutic candidate for the treatment of COPD.

Critical role of RIG-I-like receptors in inflammation in chronic obstructive pulmonary disease.

INTRODUCTION: Viral infection is a significant cause of chronic obstructive pulmonary disease (COPD) and acute exacerbation of COPD. Retinoic acid inducible gene I (RIG-I)-like receptors (RLRs), including RIG-I and melanoma differentiation associated gene 5 (MDA-5), are important pattern recognition receptors for viral elimination. OBJECTIVE: The study aims to investigate the role of RIG-I and MDA-5 in COPD pathogenesis. METHODS: We examined the expression of RIG-I and MDA-5 by immunohistochemistry, real-time PCR and Western blots in COPD patients and control subjects. RESULTS: Our results showed that MDA-5 expression was upregulated in lung tissues and peripheral blood mononuclear cells of COPD patients and there was a negative correlation between MDA-5 mRNA levels and forced expiratory volume in 1 s %pred. COPD patients had higher interleukin (IL)-1 and IL-8 mRNA expression levels, and these inflammatory cytokines positively correlate with MDA-5 levels. However, there was no difference in the expression of RIG-I between COPD patients and control subjects. CONCLUSION: Our results suggested that MDA-5, but not RIG-I, may play a critical role in airway inflammation in COPD.

Suppressor of cytokine signaling 1-modulated metalloproteinases and tissue inhibitor of metalloproteinase in pulmonary fibrosis.

An imbalance between metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) affects the synthesis and degradation of extracellular matrix molecules, which have an important role in the pathogenesis of pulmonary fibrosis. Lower mRNA expression levels of suppressor of cytokine signaling 1 (SOCS1) are present in fibroblasts from the lungs of pulmonary fibrosis. However, little is currently known regarding the precise role of SOCS1 has in idiopathic pulmonary fibrosis (IPF). The present study examined the expression levels of MMPs and TIMPs in A549 human epithelial lung carcinoma cells and human embryonic lung fibroblasts (HLFs) stimulated with transforming growth factor­ß1 (TGF­ß1) in conditions of deficiency and over­expression of SOCS1, by transfection with a lentivirus. Overexpression of SOCS1 in A549 cells and HLFs significantly inhibited the mRNA expression levels of MMP­1, MMP­2 and MMP­9 (P<0.05). In the A549 cells lacking SOCS1 expression, the mRNA expression levels of TIMP­1 were significantly higher compared with the control groups (P<0.01). Overexpression of SOCS1 partially reversed these changes. The expression levels of TIMP­1 in the HLFs with an overexpression of SOCS1 were decreased, as compared with the SOCS1­deficient HLFs following TGF­ß1 stimulation; however, this finding was not significant (0.24±0.01 vs. 0.53±0.02, P>0.05). The expression levels of TIMP­2 were significantly lower in the cells overexpressing SOCS1. Conversely, the mRNA expression levels of TIMP­2 were significantly higher in the SOCS1­deficient A549 cells, as compared with all of the other groups (P<0.05). TIMP­4 expression levels were elevated in the A549 cells and HLFs transfected with the SOCS1­deficient lentivirus. The expression levels of TIMP­4 were significantly lower in the groups overexpressing SOCS1, as compared with the other groups. These results suggest that SOCS1 may act as a suppressor of pulmonary fibrosis, by reducing the expression of MMPs and TIMPs. Therefore, SOCS1 may be a target for IPF treatment.

Expression of suppressor of cytokine signaling 1 in the peripheral blood of patients with idiopathic pulmonary fibrosis.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive diffuse parenchymal disease with a poor prognosis. A variety of cytokines and chemokines are involved in its pathophysiology. The aim of this study was to evaluate the clinical features in IPF patients with the expression of suppressor of cytokine signaling 1 (SOCS-1), which acts as a negative regulator of cytokine signaling. METHODS: IPF patients (n = 20) and healthy controls (n = 16) were included in this study. The expression of SOCS-1 was analyzed in peripheral blood mononuclear cells (PBMC) of subjects using RT-PCR. Interleukin 4 (IL-4), transforming growth factor ß1 (TGF-ß1) and type I collagen expression were also analyzed in each individual using enzyme-linked immunosorbent assay (ELISA). The clinical characteristics of IPF patients were delineated. These results were analyzed by SPSS13.0 statistics software. RESULTS: SOCS-1 mRNA expression was significantly decreased in the PBMC of IPF patients compared with healthy controls; serum levels of IL-4 and TGF-ß1 were higher in IPF patients. The patients with lower expression of SOCS-1 developed lower percentage of forced vital capacity (FVC%) and DLCO/VA. A patients' SOCS-1 mRNA level was negatively correlated with serum levels of IL-4, and negatively correlated with their high-resolution computed tomography (HRCT) scores. CONCLUSIONS: SOCS-1 mRNA can be detected in PBMC, and it is down-regulated in IPF patients. The expression of SOCS-1 is associated with the severity of IPF patients' symptoms, so it might be the predictor of disease severity. SOCS-1 might play an important role in IPF by reducing the expression of the T helper type 2 (Th2) cell-related cytokine IL-4.

RNA interference-mediated silencing of SOCS-1 via lentiviral vector promotes apoptosis of alveolar epithelial cells in vitro.

Suppressor of cytokine signaling-1 (SOCS1) is a protein that negatively regulates cytokine and growth factor signaling. However, little is known regarding the precise role it plays in idiopathic pulmonary fibrosis. The aim of the present study was to construct a recombinant lentiviral vector for RNA interference targeting the SOCS1 gene and to detect the expression in human alveolar epithelial cells. A lentiviral vector-mediated RNA interference method was used to establish a SOCS1-negative cell line of alveolar origin (A549). Three pairs of complementary small hairpin RNA (shRNA) oligonucleotides targeting the SOCS1 gene were designed, synthesized and inserted into the pPll3.7 vector. Packaged lentivirus particles were obtained after 48 h, and the supernatant was used to transfect the human alveolar epithelial cell line A549. The expression of the SOCS1 protein was detected by Western blotting. MTT assay was used to detect the cell proliferation of alveolar epithelial cells with SOCS1 knockdown. The recombinant plasmids were confirmed by sequencing. The lentivirus-containing supernatant effectively infected the A549 cell line, and the expression of SOCS1 protein was inhibited, which was confirmed by Western blotting in the target cells. MTT assay indicated the inhibition effect for cell proliferation of A549 cells in the SOCS1-RNA interference group, compared to the control group with no interference-mediated silencing of the SOCS1 gene. A lentiviral vector for RNA interference targeting the SOCS1 gene was successfully constructed, and cell survival tests showed that knockdown of the SOCS1 gene promotes the apoptosis of alveolar cells.