Single-cell analysis reveals one cancer-associated fibroblasts subtype linked to metastasis in breast cancer: MXRA5 as a potential novel marker for prognosis.

Cancer-associated fibroblasts (CAFs) are prevalent in the tumor microenvironment of breast cancer, comprising a group of cell subpopulations with spatial, phenotypic, and functional heterogeneity. Due to the lack of specific markers for CAF subpopulations, their specific mechanisms in breast cancer remain unclear. We identified eight distinct CAF phenotypes in breast cancer using multiple single-cell RNA sequencing datasets and determined distinct transcription factors (TFs) of CAFs through SCENIC analysis. Our study highlights one CAF subtype in breast cancer, FN1+CAF2, associated with metastasis and macrophage polarization. We observed elevated FN1 expression in the stromal tissue of breast cancer patients. Furthermore, FN1 knockdown in CAFs reduced the migration ability of breast cancer cells. We identified a regulatory gene, MXRA5, in CAF2, which may play crucial roles in breast cancer. Our results indicated upregulated MXRA5 expression in breast cancer tissues and CAFs from patients with lymph node metastasis in the following experiment. Overall, our study reveals that the FN1+CAF2 subtype is associated with metastasis and suggests that MXRA5 may be a novel marker mediating the effects of CAF2 on breast cancer metastasis. This study enriches our understanding of CAF heterogeneity and offers new insights for treating breast cancer metastasis.

LRPPRC promotes glycolysis by stabilising LDHA mRNA and its knockdown plus glutamine inhibitor induces synthetic lethality via m6 A modification in triple-negative breast cancer.

BACKGROUND: Targeted therapy for triple-negative breast cancer (TNBC) remains a challenge. N6-methyladenosine (m6 A) is the most abundant internal mRNA modification in eukaryotes, and it regulates the homeostasis and function of modified RNA transcripts in cancer. However, the role of leucine-rich pentatricopeptide repeat containing protein (LRPPRC) as an m6 A reader in TNBC remains poorly understood. METHODS: Western blotting, reverse transcription-polymerase chain reaction (RT-qPCR) and immunohistochemistry were used to investigate LRPPRC expression levels. Dot blotting and colorimetric enzyme linked immunosorbent assay (ELISA) were employed to detect m6 A levels. In vitro functional assays and in vivo xenograft mouse model were utilised to examine the role of LRPPRC in TNBC progression. Liquid chromatography-mass spectrometry/mass spectrometry and Seahorse assays were conducted to verify the effect of LRPPRC on glycolysis. MeRIP-sequencing, RNA-sequencing, MeRIP assays, RNA immunoprecipitation assays, RNA pull-down assays and RNA stability assays were used to identify the target genes of LRPPRC. Patient-derived xenografts and organoids were employed to substantiate the synthetic lethality induced by LRPPRC knockdown plus glutaminase inhibition. RESULTS: The expressions of LRPPRC and m6 A RNA were elevated in TNBC, and the m6 A modification site could be recognised by LRPPRC. LRPPRC promoted the proliferation, metastasis and glycolysis of TNBC cells both in vivo and in vitro. We identified lactate dehydrogenase A (LDHA) as a novel direct target of LRPPRC, which recognised the m6 A site of LDHA mRNA and enhanced the stability of LDHA mRNA to promote glycolysis. Furthermore, while LRPPRC knockdown reduced glycolysis, glutaminolysis was enhanced. Moreover, the effect of LRPPRC on WD40 repeat domain-containing protein 76 (WDR76) mRNA stability was impaired in an m6 A-dependent manner. Then, LRPPRC knockdown plus a glutaminase inhibition led to synthetic lethality. CONCLUSIONS: Our study demonstrated that LRPPRC promoted TNBC progression by regulating metabolic reprogramming via m6 A modification. These characteristics shed light on the novel combination targeted therapy strategies to combat TNBC.

LINC00571 drives tricarboxylic acid cycle metabolism in triple-negative breast cancer through HNRNPK/ILF2/IDH2 axis.

BACKGROUND: Triple-negative breast cancer is a complex breast malignancy subtype characterized by poor prognosis. The pursuit of effective therapeutic approaches for this subtype is considerably challenging. Notably, recent research has illuminated the key role of the tricarboxylic acid cycle in cancer metabolism and the complex landscape of tumor development. Concurrently, an emerging body of evidence underscores the noteworthy role that long non-coding RNAs play in the trajectory of breast cancer development. Despite this growing recognition, the exploration of whether long non-coding RNAs can influence breast cancer progression by modulating the tricarboxylic acid cycle has been limited. Moreover, the underlying mechanisms orchestrating these interactions have not been identified. METHODS: The expression levels of LINC00571 and IDH2 were determined through the analysis of the public TCGA dataset, transcriptome sequencing, qRT‒PCR, and Western blotting. The distribution of LINC00571 was assessed using RNA fluorescence in situ hybridization. Alterations in biological effects were evaluated using CCK-8, colony formation, EdU, cell cycle, and apoptosis assays and a tumor xenograft model. To elucidate the interaction between LINC00571, HNRNPK, and ILF2, RNA pull-down, mass spectrometry, coimmunoprecipitation, and RNA immunoprecipitation assays were performed. The impacts of LINC00571 and IDH2 on tricarboxylic acid cycle metabolites were investigated through measurements of the oxygen consumption rate and metabolite levels. RESULTS: This study revealed the complex interactions between a novel long non-coding RNA (LINC00571) and tricarboxylic acid cycle metabolism. We validated the tumor-promoting role of LINC00571. Mechanistically, LINC00571 facilitated the interaction between HNRNPK and ILF2, leading to reduced ubiquitination and degradation of ILF2, thereby stabilizing its expression. Furthermore, ILF2 acted as a transcription factor to enhance the expression of its downstream target gene IDH2. CONCLUSIONS: Our study revealed that the LINC00571/HNRNPK/ILF2/IDH2 axis promoted the progression of triple-negative breast cancer by regulating tricarboxylic acid cycle metabolites. This discovery provides a novel theoretical foundation and new potential targets for the clinical treatment of triple-negative breast cancer.

LncRNA CARMN suppresses EMT through inhibiting transcription of MMP2 activated by DHX9 in breast cancer.

Long non-coding RNAs (lncRNAs) have been shown to drive cancer progression. However, the function of lncRNAs and the underlying mechanism in early-stage breast cancer(BC) have rarely been investigated. Datasets of pre-invasive ductal carcinoma in situ (DCIS), invasive ductal BC (IDC) and normal breast tissue from TCGA and GEO databases were used to conduct bioinformatics analysis. LncRNA CARMN was identified as a tumor suppressor in early-stage BC and related to a better prognosis. CARMN over-expression inhibited MMP2 mediated migration and EMT in BC. Further analysis showed that CARMN was located in the nucleus and functioned as an enhancer RNA (eRNA) in mammary epithelial cell. Mechanically, CARMN binding protein DHX9 was identified by RNA pull-down and mass spectrometry (MS) assays and it also bound to the MMP2 promoter to activate its transcription. As a decoy, CARMN competitively bound to DHX9 and blocked MMP2 transcriptional activation, thereby inhibiting metastasis and EMT of BC cells. These findings reveal the important role of CARMN as a tumor suppressor in the metastasis and a potential biomarker for progression in early-stage BC.

Advanced Electrode Technologies for Noninvasive Brain-Computer Interfaces.

Brain-computer interfaces (BCIs) have garnered significant attention in recent years due to their potential applications in medical, assistive, and communication technologies. Building on this, noninvasive BCIs stand out as they provide a safe and user-friendly method for interacting with the human brain. In this work, we provide a comprehensive overview of the latest developments and advancements in material, design, and application of noninvasive BCIs electrode technology. We also explore the challenges and limitations currently faced by noninvasive BCI electrode technology and sketch out the technological roadmap from three dimensions: Materials and Design; Performances; Mode and Function. We aim to unite research efforts within the field of noninvasive BCI electrode technology, focusing on the consolidation of shared goals and fostering integrated development strategies among a diverse array of multidisciplinary researchers.

Transcriptionally regulated miR-26a-5p may act as BRCAness in Triple-Negative Breast Cancer.

BACKGROUND: DNA damage and DNA damage repair (DDR) are important therapeutic targets for triple-negative breast cancer (TNBC), a subtype with limited chemotherapy efficiency and poor outcome. However, the role of microRNAs in the therapy is emerging. In this study, we explored whether miR-26a-5p could act as BRCAness and enhance chemotherapy sensitivity in TNBC. METHODS: Quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-26a-5p in breast cancer tissues and cell lines. CCK-8 was used to measure drug sensitivity in concentration gradient and time gradient. Comet assay was used to detect DNA damage. Flow cytometry was performed to examine apoptosis. Moreover, we used western blot and immunofluorescence to detect biomarkers. Luciferase reporter assay was performed to verify the combination of miR-26a-5p and 3'UTR of target gene. Hormone deprivation and stimulation assay were used to validate the effect of hormone receptors on the expression of miR-26a-5p. Chromatin immunoprecipitation (ChIP) assays were used to verify the binding sites of ER-a or PR with the promoter of miR-26a-5p. Animal experiments were performed to the effect of miR-26a-5p on Cisplatin treatment. RESULTS: The expression of miR-26a-5p was significantly downregulated in TNBC. Overexpressing miR-26a-5p enhanced the Cisplatin-induced DNA damage and following apoptosis. Interestingly, miR-26a-5p promoted the expression of Fas without Cisplatin stimulating. It suggested that miR-26a-5p provided a hypersensitivity state of death receptor apoptosis and promoted the Cisplatin sensitivity of TNBC cells in vitro and in vivo. Besides, miR-26a-5p negatively regulated the expression of BARD1 and NABP1 and resulted in homologous recombination repair defect (HRD). Notably, overexpressing miR-26a-5p not only facilitated the Olaparib sensitivity of TNBC cells but also the combination of Cisplatin and Olaparib. Furthermore, hormone receptors functioned as transcription factors in the expression of miR-26a-5p, which explained the reasons that miR-26a-5p expressed lowest in TNBC. CONCLUSIONS: Taken together, we reveal the important role of miR-26a-5p in Cisplatin sensitivity and highlight its new mechanism in DNA damage and synthetic lethal.

m6A reader HNRNPA2B1 destabilization of ATG4B regulates autophagic activity, proliferation and olaparib sensitivity in breast cancer.

N6-methyladenosine RNA (m6A) is the most extensive epigenetic modification in mRNA and influences tumor progression. However, the role of m6A regulators and specific mechanisms in breast cancer still need further study. Here, we investigated the significance of the m6A reader HNRNPA2B1 and explored its influence on autophagy and drug sensitivity in breast cancer. HNRNPA2B1 was selected by bioinformatics analysis, and its high expression level was identified in breast cancer tissues and cell lines. HNRNPA2B1 was related to poor prognosis. Downregulation of HNRNPA2B1 reduced proliferation, enhanced autophagic flux, and partially reversed de novo resistance to olaparib in breast cancer. ATG4B was determined by RIP and MeRIP assays as a downstream gene of HNRNPA2B1, by which recognized the m6A site in the 3'UTR. Overexpression of ATG4B rescued the malignancy driven by HNRNPA2B1 in breast cancer cells and increased the olaparib sensitivity. Our study revealed that the m6A reader HNRNPA2B1 mediated proliferation and autophagy in breast cancer cell lines by facilitating ATG4B mRNA decay and targeting HNRNPA2B1/m6A/ATG4B might enhance the olaparib sensitivity of breast cancer cells.

MXene-Reinforced Liquid Metal/Polymer Fibers via Interface Engineering for Wearable Multifunctional Textiles.

Stretchable conductive fibers are an important component of wearable electronic textiles, but often suffer from a decrease in conductivity upon stretching. The use of liquid metal (LM) droplets as conductive fillers in elastic fibers is a promising solution. However, there is an urgent need to develop effective strategies to achieve high adhesion of LM droplets to substrates and establish efficient electron transport paths between droplets. Here, we use large-sized MXene two-dimensional conductive materials to modify magnetic LM droplets and prepare MXene/magnetic LM/poly(styrene-butadiene-styrene) composite fibers (MLMS fibers). The MXene sheets decorated on the surface of magnetic LM droplets not only enhance the droplet adhesion to substrate but also bridge adjacent droplets to establish efficient conductive paths. MLMS fibers show several-fold improvements in tensile strength and elongation and a 30-fold increase in conductivity compared with pure LM-filled fibers. These conductive fibers can be easily woven into multifunctional textiles, which exhibit strong electromagnetic interference shielding and stable Joule heating performances even under large tensile deformation. In addition, other advantages of MLMS textiles, such as high gas/liquid permeability, strong chemical resistance (acid and alkaline conditions), high/low-temperature tolerance (-40-150 °C) and water washability, make them particularly suitable for wearable applications.

Environmentally Tough and Stretchable MXene Organohydrogel with Exceptionally Enhanced Electromagnetic Interference Shielding Performances.

Conductive hydrogels have potential applications in shielding electromagnetic (EM) radiation interference in deformable and wearable electronic devices, but usually suffer from poor environmental stability and stretching-induced shielding performance degradation. Although organohydrogels can improve the environmental stability of materials, their development is at the expense of reducing electrical conductivity and thus weakening EM interference shielding ability. Here, a MXene organohydrogel is prepared which is composed of MXene network for electron conduction, binary solvent channels for ion conduction, and abundant solvent-polymer-MXene interfaces for EM wave scattering. This organohydrogel possesses excellent anti-drying ability, low-temperature tolerance, stretchability, shape adaptability, adhesion and rapid self-healing ability. Two effective strategies have been proposed to solve the problems of current organohydrogel shielding materials. By reasonably controlling the MXene content and the glycerol-water ratio in the gel, MXene organohydrogel can exhibit exceptionally enhanced EM interference shielding performances compared to MXene hydrogel due to the increased physical cross-linking density of the gel. Moreover, MXene organohydrogel shows attractive stretching-enhanced interference effectiveness, caused by the connection and parallel arrangement of MXene nanosheets. This well-designed MXene organohydrogel has potential applications in shielding EM interference in deformable and wearable electronic devices.

YTHDF1 promotes breast cancer progression by facilitating FOXM1 translation in an m6A-dependent manner.

BACKGROUND: N6-methyladenosine (m6A) is the most common post-transcriptional modification at the RNA level. However, the exact molecular mechanisms of m6A epigenetic regulation in breast cancer remain largely unknown and need to be fully elucidated. METHODS:  The integrating bioinformatics analyses were used to screen clinical relevance and dysregulated m6A "reader" protein YTHDF1 in breast cancer from TCGA databases, which was further validated in a cohort of clinical specimens. Furthermore, functional experiments such as the CCK-8 assay, EdU assay, wound healing assay, transwell invasion assay and cell cycle assay were used to determine the biological role of YTHDF1 in breast cancer. RIP, m6A-IP, and CLIP assays were used to find the target of YTHDF1 and further verification by RT-qPCR, western blot, polysome profiling assay. The protein-protein interaction between YTHDF1 and FOXM1 was detected via co-immunoprecipitation. RESULTS: Our study showed that YTHDF1 was overexpressed in breast cancer cells and clinical tissues specimens. At the same time, the high expression level of YTHDF1 was positively correlated with tumor size, lymph node invasion, and distant metastasis in breast cancer patients. YTHDF1 depletion repressed the proliferation, invasion and epithelial-mesenchymal transformation (EMT) and induced G0/G1 phase cell cycle arrest of breast cancer cells in vitro and in vivo. We also demonstrated that FOXM1 is a target of YTHDF1. Through recognizing and binding to the m6A-modified mRNA of FOXM1, YTHDF1 accelerated the translation process of FOXM1 and promoted breast cancer metastasis. Whereas overexpression of FOXM1 in breast cancer cells partially counteracted the tumor suppressed effects caused by YTHDF1 silence, which further verified the regulatory relationship between YTHDF1 and FOXM1. CONCLUSION: Our study reveals a novel YTHDF1/FOXM1 regulatory pathway that contributes to metastasis and progression of breast cancer, suggesting that YTHDF1 might be applied as a potential biomarker and therapeutic target. That also advances our understanding of the tumorigenesis for breast cancer from m6A epigenetic regulation.

A Metabolic-associated Nomogram Predicts Recurrence Survival of Thyroid Cancer.

OBJECTIVE: Various studies have suggested that metabolic genes play a significant role in papillary thyroid cancer (PTC). The current study aimed to identify a metabolic signature related biomarker to predict the prognosis of patients with PTC. METHODS: We conducted a comprehensive analysis on the data obtained from the Cancer Genome Atlas (TCGA) database. The correlation between survival result and metabolic genes was evaluated based on the univariate Cox analyses, least absolute shrinkage and selection operator (LASSO) and multivariate Cox analyses. The performance of a 7-gene signature was assessed according to Kaplan-Meier and receiver operating characteristic (ROC) analysis. Multivariate Cox regression analysis was adopted to unearth clinical factors related to the recurrence free survival (RFS) of patients with PTC. Finally, a prognostic nomogram was developed based on risk score, cancer status and cancer width to improve the prediction for RFS of PTC patients. RESULTS: Seven metabolic genes were used to establish the prognostic model. The ROC curve and C-index exhibited high value in training, testing and the whole TCGA datasets. The established nomogram, incorporating the 7-metabolic gene signature and clinical factors, was able to predict the RFS with high effectiveness. The 7-metabolic gene signature-based nomogram had a good performance to predict the RFS of patients with PTC. CONCLUSION: Our study identified a 7-metabolic gene signature and established a prognostic nomogram, which were useful in predicting the RFS of PTC.

Overexpression of miRNA-3613-3p Enhances the Sensitivity of Triple Negative Breast Cancer to CDK4/6 Inhibitor Palbociclib.

Triple negative breast cancer (TNBC) is characterized by lack of expression of the estrogen and progesterone receptors and HER2, which are common therapeutic targets. CDK4/6 inhibitor Palbociclib has been approved as an anti-cancer agent for breast cancer. However, identifying biomarkers that predict the response to Palbociclib has always been a challenge for molecular targeted therapy. In this study, we identify microRNA as a hallmark in TNBC patients and explore if miR-3613-3p might serve as a tumor suppressor biomarker for triple negative breast cancer patients and if overexpression of miR-3613-3p could enhance the sensitivity of TNBC cells to Palbociclib. We show that the expression of miR3613-3p was down-regulated in TNBC tumors and cells, and the overexpression of miR-3613-3p in patients' tumor tissues was clinically and pathologically correlated with favorable prognosis, such as smaller tumor size and the lower Ki-67. In vitro, overexpression of miR-3613-3p inhibited cell proliferation, induced G1 cell-cycle arrest, and enhanced the sensitivity of TNBC cells to Palbociclib treatment. In vivo study revealed that overexpression of miR-3613-3p inhibited TNBC tumorigenesis and exerted a significant inhibitory effect of Palbociclib on MDA-MB-231 cells. Mechanically, SMAD2 and EZH2 were found to be two direct targets of miR-3613-3p and mediate the proliferation of TNBC cells and the sensitivity of the cells to Palbociclib through inducing cellular senescence. Our findings suggested that miR-3613-3p acts as a cancer-suppressor miRNA in TNBC. Moreover, our study showed that miR-3613-3p might be used as a predictive biomarker for the response of TNBC to Palbociclib.

Prognostic Value of Pro-Inflammatory Neutrophils and C-Reactive Protein in Cancer Patient With Coronavirus Disease 2019: A Multi-Center, Retrospective Study.

Background: At present, the epidemic of the novel coronavirus disease 2019 (COVID-19) has quickly engulfed the world. Inflammatory cytokines are associated with the severity and outcomes of patients with COVID-19. However, the prognostic value of pro-inflammatory factors in cancer patients with COVID-19 are unknown. Methods: A multi-center, retrospective, cross-sectional study, based on five designated tertiary hospitals for the treatment of COVID-19 in Hubei Province, China. 112 cancer patients with COVID-19, and 105 COVID-19 patients without cancer were enrolled in the study between January 1st, 2020 and April 30th, 2020. The risk assessment of pro-inflammatory factors for disease severity and clinical adverse outcomes was identified by univariable and multivariable logistic regression models. Results: Of the 112 cancer patients with COVID-19, 40 (35.7%) patients were in critical condition and 18 (16.1%) patients died unfortunately. Univariate and multivariate analysis demonstrated that hemoglobin level and pro-inflammatory neutrophils and C-reactive protein (CRP), can be used as independent factors affecting the severity of COVID-19; Meanwhile, pro-inflammatory neutrophils and CRP can be used as an independent influencing factor for adverse clinical outcome of death. Moreover, the dynamic changes of neutrophils and CRP were also presented, and compared with COVID-19 patients without cancer, cancer patients with COVID-19 showed higher neutrophil counts and CRP levels. Conclusion: In cancer patients with COVID-19, the significant increase in pro-inflammatory neutrophils and CRP indicated a more critical illness and adverse clinical outcome, and pro-inflammatory neutrophils and CRP played a greater adverse role compare with COVID-19 patients without cancer, which may be the cause of critical illness and adverse clinical outcomes of cancer patients with COVID-19.

Characteristics and Outcomes of 35 Breast Cancer Patients Infected With COVID-19.

Since December 2019, a novel coronavirus disease (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly engulfed the world. Cancer patients infected with COVID-19 are considered to carry higher severity of the disease and higher mortality rate than common COVID-19 patients in previous studies. However, due to the poor clinical information on COVID-19 patients with cancer, the evidences that supported this conclusion are insufficient. At present, rather limited reports have analyzed the clinical data of breast cancer patients infected with COVID-19. Therefore, in this retrospective study, we described the clinical characteristics and the outcomes of 35 COVID-19 patients with breast cancer and compared 55 COVID-19 patients without cancer and 81 COVID-19 patients with other types of cancer as controls. Our data showed that there were no differences in disease severity and outcomes between the COVID-19 patients with breast cancer and the common COVID-19 patients, which was in contrast to previous studies. In addition, compared with other types of cancer patients, asymptomatic infections and mild cases among breast cancer patients made up a substantially larger proportion. Our results indicated that the clinical characteristics of breast cancer patients were milder than those of other types of cancer patients, but there were no significant differences in outcomes between the two groups.

Coupling hydrophilic interaction chromatography materials with immobilized Fe3+ for phosphopeptide and glycopeptide enrichment and separation.

Simultaneous profiling of protein phosphorylation and glycosylation is very important to elucidate the bio-functions of these proteins. However, simultaneous enrichment of glyco- and phosphopeptides is the bottleneck in proteomics because of the low abundance of these species and ion suppression from non-modified peptides in mass spectrometry (MS). In this study, Fe3+ immobilized hydrophilic interaction chromatography (HILIC) materials (termed polySD-SiO2, recently reported in our lab) and polySD-SiO2 in the HILIC mode were employed for the simultaneous enrichment and subsequent separation of glyco- and phosphopeptides. The Fe3+ immobilized polySD-SiO2 could selectively enrich glycopeptides and phosphopeptides and the co-enriched peptides were further fractionated with polySD-SiO2 in the HILIC mode. With the established method, glyco- and phosphopeptides were well enriched and divided into two fractions even from tryptic digests of a-casein, fetuin and BSA at a molar ratio of 1 : 2 : 400. Application of the established method to HeLa cell lysate resulted in a total of 1903 phosphopeptides and 141 glycosylation sites. These results demonstrate that the established method could selectively and simultaneously enrich and fractionate glyco- and phosphopeptides from complex peptide mixtures.

LncRNA GASL1 inhibits tumor growth in gastric carcinoma by inactivating the Wnt/ß-catenin signaling pathway.

Growth arrest associated lncRNA 1 (GASL1) is a newly discovered tumor suppressor long non-coding RNA (lncRNA) in osteosarcoma; however its role in other malignancies remains unknown. The aim of the present study was to investigate the involvement of GASL1 in gastric cancer. In the current study, gastric cancer tissue and adjacent healthy tissue samples were collected from patients with gastric carcinoma, and blood samples were collected from patients with gastric carcinoma and healthy controls to detect the expression of serum GASL1. All patients were followed up for 5 years and the diagnostic and prognostic value of GASL1 for gastric carcinoma was evaluated by ROC and survival curve analyses, respectively. The chi-square test was used to analyze the correlation between serum levels of GASL1 and the clinicopathological features of patients with gastric carcinoma. A GASL1 expression vector and GASL1 small interfering RNA were transfected into gastric cancer cell lines and the effects on ß-catenin expression and cell proliferation were examined by western blot and cell proliferation assays, respectively. The expression level of lncRNA GASL1 was significantly downregulated in gastric cancer tissues compared with adjacent normal tissues from patients with gastric carcinoma. In addition, serum levels of GASL1 were significantly decreased in patients with gastric carcinoma when compared with healthy controls. Serum GASL1 levels distinguished patients with gastric carcinoma from healthy controls, and low expression levels of GASL1 were associated with decreased postoperative survival time. GASL1 overexpression downregulated, while GASL1 knockdown upregulated ß-catenin expression. GASL1 overexpression inhibited, and GASL1 knockdown promoted gastric cancer cell proliferation. In addition, treatment with a Wnt agonist demonstrated no significant effect on GASL1 expression, however the inhibitory effect of GASL1 overexpression on cell proliferation was reduced following treatment with the Wnt agonist. In conclusion, the GASL1 lncRNA may inhibit tumor growth in patients with gastric carcinoma by inactivating the Wnt/ß-catenin signaling pathway.