ObjectiveThis study aims to explore the potential of different orders of magnitude single-nucleotide polymorphism (SNP) locus combinations for predicting distant kinship relationships. A high-density SNP locus set was constructed, and a comprehensive assessment of its inference capability was conducted. MethodsFirstly, we selected three commercial chip panels, CGA (Chinese genotyping array, Illumina), GSA (Global screening array, Illumina), Affy (23MF_V2 high-density SNP array, Affymetrix) and merged them after quality control, forming a high-density SNP locus panel(1 180 k). Secondly, we selected 161 samples and collected their peripheral blood samples by using whole-genome sequencing technology. Within this sample population, the levels of kinship relationships fully covered the range from level 1 to level 9, and the number of kinship pairs at each level was consistently maintained at over 50 pairs. From 161 samples data of whole-genome sequencing, the 1 180 k locus set was extracted, which is referred to as the high-density SNP locus set in the following text. The kinship inference was conducted using the identity-by-descent (IBD) algorithm with the selected optimal parameters. To comprehensively evaluate the performance of the high-density SNP locus set in kinship inference, we compared it with the three commercial chip panels, the intersection of these three chip loci, and the control sets constructed by randomly reducing the number of the high-density SNP locus set. Based on the changes in the IBD lengths, as well as the dynamic trends in prediction accuracy, we conducted a scientific assessment of the kinship inference capability of the high-density SNP locus set. ResultsAfter screening, a set of 1 184 334 autosomal SNPs was obtained. During the process of screening the optimal IBD length threshold, the result revealed that 0 cM, 1 cM, and 2 cM all demonstrated good applicability. However, to avoid the issue of a large amount of redundant information caused by setting a too low IBD length threshold, this study ultimately selected 2 cM as the optimal threshold. Compared with the average results of three chip panels, the high-density SNP locus set increased the total IBD length and the average IBD length across levels 1-9; the accuracy of the confidence interval for level 8 was 70.97%, which represented a 3.50% improvement; the average confidence interval accuracy for levels 1-8 was 91.39%, representing a 1.00% increase; and the false negative rates at levels 8 and 9 were reduced by 2.42% and 6.76%, respectively. The system efficacy of the high-density SNP locus set for kinship inference of first to eighth degree relationships reached 98.91%. Through random reduction of the high-density SNP locus set results, it is found that increasing the number of SNPs with the panel, the detection efficiency of IBD length showed a significant upward trend. At the same time, the overall trend in the accuracy of kinship relationship prediction as well as the confidence interval accuracy also indicated that both metrics steadily increased with the addition of more loci. ConclusionThe results show that the high-density SNPs panel significantly enhances the efficacy of distant kinship inference, accurately covering kinship degrees, with the average confidence interval accuracy for first to eighth degree relationships stably above 90%. The study finds that increasing the number of SNPs panel can improve the ability to predict distant kinship.

Objective To investigate the temporal changes in pathological damage and macrophage polarization in liver and spleen tissues of mice infected with Angiostrongylus cantonensis, and to preliminarily unravel the peripheral immune responses during the early stage of A. cantonensis infection. Methods Forty female BALB/c mice at ages of 6 to 8 weeks were randomly divided into four groups, including the control group and 7-, 14-, and 21-day infection groups, with 10 mice in each group. Each mouse in the infection groups was inoculated with 30 third-stage (L3) larvae of A. cantonensis by oral gavage, and five mice were randomly selected from each infection group on days 7, 14, and 21 post-infection, while mice in the control group were given the same volume of physiological saline and five mice were randomly selected from the control group on the day of oral gavage. Mouse liver and spleen tissues were sampled. The histopathological changes of mouse liver and spleen tissues were observed using hematoxylin and eosin (HE) staining, and the percentage of positive staining area and the co-localization positive rates of the macrophage surface antigens F4/80, CD86, and CD206 were quantified in mouse liver and spleen tissues using immunohistochemical and immunofluorescence staining. In addition, five mice were collected from each infection group on days 7, 14, and 21 post-infection, and five mice were collected from the control group on the day of oral gavage. Mouse liver and spleen tissues were sampled for detection of macrophage markers CD86 and CD206 and macrophage phenotyping using flow cytometry, and the expression of M1 macrophage markers, including inducible nitric oxide synthase (Nos2), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and M2 markers, including arginase 1 (Arg1), mannose receptor C-type 1 (Mrc1) and chitinase-like protein 3 (Chil3) was quantified in mouse liver and spleen tissues using real-time quantitative PCR (RT-qPCR) assay. Results Proliferative lesions of the hepatocyte were observed in mouse liver tissues and the follicular structures of the mouse spleen white pulp were disrupted 21 days post-infection with A. cantonensis. Immunohistochemical staining showed that there were significant differences in the percentages of F4/80, CD86 and CD206 positive staining areas in the liver and spleen tissues among the four groups of mice (F = 242.40, 197.14, 183.19, 157.65, 242.35 and 146.24; all P values < 0.001), and the percentages of positive staining in the liver and spleen tissues of mice in the 14-day infection group [(4.45 ± 0.51)%, (3.74 ± 0.67)%, (8.32 ± 0.72)%, (16.56 ± 1.14)%, (11.62 ± 0.52)%, and (8.29 ± 0.72)%, respectively] and the 21-day infection group [(3.70 ± 0.11)%, (3.22 ± 0.43)%, (11.53 ± 1.03)%, (12.59 ± 1.05)%, (9.02 ± 0.83)%, and (11.67 ± 1.10)%, respectively] were higher than in the control group [(0.35 ± 0.16)%, (0.40 ± 0.02)%, (0.93 ± 0.05)%, (2.78 ± 0.26)%, (2.33 ± 0.20)%, and (1.85 ± 0.20)%, respectively] (all P values < 0.05). Immunofluorescence staining showed significant differences in the positive rates of F4/80 co-localization with CD86 and CD206 in mouse liver and spleen tissues among the four groups (F = 24.42, 25.28, 54.51 and 130.55; all P values < 0.001). Flow cytometry detected significant differences in the proportions of CD86⁺ and CD206⁺ macrophages in mouse liver and spleen tissues among the four groups (F = 67.98, 18.41, 29.77, 172.80; all P values < 0.001), and the proportions of CD206⁺ macrophages in the liver and spleen of the 21-day infection group were significantly higher than those in the control group [(9.25 ± 2.55)% vs (3.83 ± 0.72)%, and (4.22 ± 0.56)% vs (0.47 ± 0.18)%, respectively] (both P values < 0.05). In addition, RT-qPCR assay quantified significant differences in the relative mRNA expression of M1 macrophage markers (IL-1β, TNF-α and Nos2) and M2 macrophage markers (Arg1, Chil3 and Mrc1) in mouse liver and spleen tissues among the four groups (F = 41.30, 31.82, 199.33, 19.96, 62.01, 119.76, 23.67, 95.90, 72.27, 82.59, 123.41 and 29.75; all P values < 0.05). Conclusions A. cantonensis infection may cause progressive pathological damage in mouse liver and spleen tissues, accompanied by dynamic temporal changes in macrophage polarization. M1 macrophage polarization predominates at the early stage of A. cantonensis infection and shifts towards M2 polarization at the later stages, suggesting that M2 polarization may participate in immune regulation at late stages of A. cantonensis infection by suppressing excessive inflammatory responses and promoting tissue repair.

Objective: To compare the effects of eccentric cycling (ECC), concentric cycling (CON), and standard care (CTL) on cardiopulmonary capacity, respiratory health, and quality of life (QoL) in patients with chronic kidney disease (CKD). Methods: Thirty-one CKD patients were divided into the CTL, CON, and ECC groups. The CON and ECC groups participated in 8-week, 24-session cycling programs. Outcomes were assessed through cardiopulmonary exercise tests, respiratory function tests, and the 36-Item Short Form Survey Instrument questionnaire. Results: The ECC group achieved significant improvements in maximal oxygen uptake, while the CTL group showed a decline. For oxygen uptake efficiency slope, significant changes were observed only in the ECC group, with a group-by-time interaction effect compared to CTL. Furthermore, the ECC group demonstrated the most significant increase in diaphragm movement and a significant increase in diaphragm thickness, with comparisons indicating that ECC outperformed both CTL and CON. Regarding QoL, the ECC group exhibited significantly greater improvements in Physical Component Summary and Mental Component Summary, with statistically significant differences compared with the CTL and CON groups. Conclusion ECC is a low-effort, high-benefit exercise modality that significantly enhances cardiopulmonary fitness, respiratory function, and QoL in patients with CKD.

Receptor tyrosine kinases (RTKs) are a class of transmembrane cell surface enzyme-linked receptors that play essential roles in various cellular life processes under normal physiological conditions. Dysregulation of RTKs and their signaling pathways is closely associated with multiple human diseases, including cancer. RON is a member of the RTK family. When RON is abnormally expressed, it can actively drive the proliferation, metastasis, and epithelial-mesenchymal transition of cancer cells through complex downstream signal transduction pathways, thereby contributing to the occurrence and subsequent development process of various types of cancers. Consequently, RON is regarded as a potent target for cancer targeted therapy. In recent years, as RTKs have gradually become popular candidate targets for antibody-drug conjugates (ADCs), a variety of ADCs targeting RON have been successfully developed and studied. To highlight the therapeutic potential of anti-RON ADCs in cancer treatment and to provide a foundation for further development and clinical research of them, this article summarized the selected components and construction strategies of existing anti-RON ADCs, and systematically reviewed their in vitro and in vivo anticancer efficacy, as well as their pharmacological and toxicological characteristics. Anti-RON ADCs demonstrated favorable stability both in vitro and in vivo. In cellular models, anti-RON ADCs carrying different payloads all exhibited potent cytotoxic effects. In animal models, anti-RON ADCs have convincingly demonstrated significant anti-cancer activity, with stable pharmacological properties and manageable toxicity at therapeutic doses. Anti-RON ADCs have a number of distinct therapeutic advantages. Compared with ADCs targeting other RTKs, anti-RON ADCs have unique effects in regulating the immune microenvironment and can potentially provide additional therapeutic options for overcoming drug resistance. Compared with RON antibodies and small molecule inhibitors, anti-RON ADCs do not rely on the RON signaling pathways, thereby significantly enhancing therapeutic efficacy. Moreover, anti-RON ADCs show therapeutic potential for targeting RON variants. In summary, the results of basic researches indicated that anti-RON ADCs have favorable anti-cancer effects and show promising clinical translation prospects. In addition, this article analyzed the current limitations of anti-RON ADCs and emphatically discussed their future development directions. The payloads of the existing anti-RON ADCs are relatively limited, and the drug-to-antibody ratio (DAR) of each ADC is not uniform. There also remains considerable room for improvement in terms of endocytosis efficiency and drug combination strategies. Therefore, the development of the next-generation anti-RON ADCs should focus on the diversification of the payloads, and explore new types of ADCs, dual-load ADCs, etc. Additionally, the structure of antibodies or ADCs could be optimized to enhance the endocytosis efficiency and progressively overcome current limitations. At present, anti-RON ADCs are limited to basic research, and the current research outcomes and observations indicated their potential for clinical application. Therefore, the clinical translation of anti-RON ADCs will be an important objective for future development. To this end, it is necessary to carefully devise a rational clinical translation pathway for anti-RON ADCs, and comprehensively evaluate the potential challenges that may arise during the implementation, so as to accelerate the initiation of clinical trials. Ultimately, clinical application of anti-RON ADCs will be realized, providing more treatment options for cancer patients.

AIM: To predict diabetic retinopathy(DR)progression through macular layer thickness in diabetic patients detected by optical coherence tomography(OCT).METHODS: Retrospective study. The clinical data of 100 cases(200 eyes)of diabetic patients admitted to our hospital from January 2023 to September 2024 were collected. According to the international clinical DR classification, they were divided into the non-diabetic retinopathy(NDR)group with 32 cases(64 eyes), the non-proliferative diabetic retinopathy(NPDR)group with 38 cases(76 eyes), and the proliferative diabetic retinopathy(PDR)group with 30 cases(60 eyes). At the same time, 49 cases(98 eyes)of healthy controls whose age and gender were matched with those of the diabetic patients were collected as the normal group. All patients underwent OCT examination. The thickness changes of the retinal nerve fiber layer(RNFL), ganglion cell layer(GCL), inner plexiform layer(IPL), outer nuclear layer(ONL), photoreceptor cell layer and total retinal thickness(RT)in the subregions of the macular area were compared among the groups. The Eta coefficient was used to analyze the correlation between them and the severity of DR.RESULTS: The thickness of RNFL, GCL, IPL, ONL and photoreceptor cell layer in each sub-region and the average of macular area in the PDR group was significantly lower than that in the NDR and normal groups, while the average RT thickness was significantly higher than that in the NPDR, NDR and normal groups(all P<0.05). The thickness of RNFL(central area, upper inner and outer rings and lower inner and outer rings and average), GCL(upper inner and outer rings and lower inner and outer rings and average), IPL(upper inner ring), ONL(central, upper inner ring and lower inner ring)and photoreceptor cell layer(upper inner and outer rings and lower inner and outer rings and average)in macular area of the PDR group was significantly thicker than that in the NPDR group(all P<0.05). The thickness of RNFL, GCL, IPL, ONL and photoreceptor cell layer in each sub-region and the average of macular area in the NPDR group was significantly lower than that in the NDR and normal groups, while the average RT thickness was significantly thicker than that in the NDR and normal groups(all P<0.05). There was no statistically significant difference in the above indicators between the NDR group and the normal group(all P>0.05). The severity of DR was significantly correlated with the average thickness of RNFL, GCL, IPL, ONL, photoreceptor cell layer and RT in macular area(all P<0.001).CONCLUSION: OCT measurement of the thickness of RNFL, GCL, IPL, ONL, photoreceptor cell layer and RT in the macular area in the diabetic patients can evaluate the progression of DR.

ObjectiveThe aim of this study was to investigate the prophylactic effects of caloric restriction (CR) on lipopolysaccharide (LPS)-induced septic cardiomyopathy (SCM) and to elucidate the mechanisms underlying the cardioprotective actions of CR. This research aims to provide innovative strategies and theoretical support for the prevention of SCM. MethodsA total of forty-eight 8-week-old male C57BL/6 mice, weighing between 20-25 g, were randomly assigned to 4 distinct groups, each consisting of 12 mice. The groups were designated as follows: CON (control), LPS, CR, and CR+LPS. Prior to the initiation of the CR protocol, the CR and CR+LPS groups underwent a 2-week acclimatization period during which individual food consumption was measured. The initial week of CR intervention was set at 80% of the baseline intake, followed by a reduction to 60% for the subsequent 5 weeks. After 6-week CR intervention, all 4 groups received an intraperitoneal injection of either normal saline or LPS (10 mg/kg). Twelve hours post-injection, heart function was assessed, and subsequently, heart and blood samples were collected. Serum inflammatory markers were quantified using enzyme-linked immunosorbent assay (ELISA). The serum myocardial enzyme spectrum was analyzed using an automated biochemical instrument. Myocardial tissue sections underwent hematoxylin and eosin (HE) staining and immunofluorescence (IF) staining. Western blot analysis was used to detect the expression of protein in myocardial tissue, including inflammatory markers (TNF-α, IL-9, IL-18), oxidative stress markers (iNOS, SOD2), pro-apoptotic markers (Bax/Bcl-2 ratio, CASP3), and SIRT3/SIRT6. ResultsTwelve hours after LPS injection, there was a significant decrease in ejection fraction (EF) and fractional shortening (FS) ratios, along with a notable increase in left ventricular end-systolic diameter (LVESD). Morphological and serum indicators (AST, LDH, CK, and CK-MB) indicated that LPS injection could induce myocardial structural disorders and myocardial injury. Furthermore, 6-week CR effectively prevented the myocardial injury. LPS injection also significantly increased the circulating inflammatory levels (IL-1β, TNF-α) in mice. IF and Western blot analyses revealed that LPS injection significantly up-regulating the expression of inflammatory-related proteins (TNF-α, IL-9, IL-18), oxidative stress-related proteins (iNOS, SOD2) and apoptotic proteins (Bax/Bcl-2 ratio, CASP3) in myocardial tissue. 6-week CR intervention significantly reduced circulating inflammatory levels and downregulated the expression of inflammatory, oxidative stress-related proteins and pro-apoptotic level in myocardial tissue. Additionally, LPS injection significantly downregulated the expression of SIRT3 and SIRT6 proteins in myocardial tissue, and CR intervention could restore the expression of SIRT3 proteins. ConclusionA 6-week CR could prevent LPS-induced septic cardiomyopathy, including cardiac function decline, myocardial structural damage, inflammation, oxidative stress, and apoptosis. The mechanism may be associated with the regulation of SIRT3 expression in myocardial tissue.

Background The association between occupational physical activity (OPA) and cardiometabolic risk factors remains controversial, potentially due to differences in the associations between OPA and various cardiometabolic indicators, as well as the lack of a clearly defined optimal OPA range for multiple-indicator synergistic benefits. Objective To investigate the relationship between OPA and cardiometabolic risk factors in individuals at high risk of cardiovascular disease (CVD) in Hubei Province, and to explore an optimal OPA range for multi-indicator improvements. Methods Data were derived from the Hubei Province dataset of the China Health Evaluation And Risk Reduction Through Nationwide Teamwork from 2015 to 2023, including 19028 high-risk CVD individuals. OPA (metabolic equivalent·h·d⁻¹, MET·h·d⁻¹) was assessed using the China Kadoorie Biobank physical activity questionnaire, anthropometric measurements (height, weight, waist circumference) and cardiometabolic indicators (blood pressure, fasting blood glucose, lipid profiles) were measured. Multivariate logistic regression was used to analyze the association between logOPA quartiles (Q1-Q4) and abnormal cardiometabolic indicators, while restricted cubic spline (RCS) models were employed to explore their dose-response relationships. Subgroup and interaction analyses were also conducted by gender. Results The median OPA of all participants was 12.86 MET·h·d⁻¹ (male: 14.40 MET·h·d⁻¹, female: 11.14 MET·h·d⁻¹). After adjusting for confounders, compared with the Q1 group, logOPA in the Q4 group was associated with 20% (OR=0.80, 95%CI: 0.72, 0.89), 14% (OR=0.86, 95%CI: 0.78, 0.96), and 13% (OR=0.87, 95%CI: 0.79, 0.95) reduction in the risk of abdominal obesity, low high-density lipoprotein cholesterol (HDL-C), and metabolic syndrome (MS), respectively, and 33% (OR=1.33, 95%CI: 1.18, 1.49), 33% (OR=1.33, 95%CI: 1.18, 1.50), and 38% (OR=1.38, 95%CI: 1.21, 1.57) increase in the risk of high total cholesterol (TC), high low-density lipoprotein cholesterol (LDL-C), and high non-HDL-C, respectively. Similar trends were observed in males and females, with significant positive associations of logOPA with high TC and high non-HDL-C in males (P_interaction<0.05). The risk of low HDL-C decreased rapidly when logOPA was more than 2.213 (OPA>9.14 MET·h·d⁻¹), showing an inverted L-shaped trend. The risk of high TC, high LDL-C, and high non-HDL-C increased beyond logOPA thresholds of 3.244, 2.476, and 3.377 (OPA >25.64, 11.89, and 29.28 MET·h·d⁻¹), respectively, showing a J-shaped trend. However, logOPA exhibited a U-shaped nonlinear dose-response relationship with blood pressure and fasting blood glucose abnormalities (P_non-linear<0.05) , with minimal risks at logOPA 2.969 and 2.372 (OPA of 19.47 and 10.72 MET·h·d⁻¹). Conclusion OPA exhibits heterogeneous dose-response patterns across cardiometabolic indicators. Integrating the inverted L-, J-, and U-shaped association patterns, we suggest an optimal OPA range of 9.14−25.64 MET·h·d⁻¹ for multiple cardiometabolic indicators in total individuals at high-risk of CVD, with ranges of 9.61−31.34 MET·h·d⁻¹ for males and 8.97−22.87 MET·h·d⁻¹ for females. These findings provide critical evidence for developing OPA interventions strategies targeting high-risk population for CVD.

Objective: To investigate the reciprocal causal relationships between periodontitis and hepatobiliary diseases through Mendelian randomization (MR) analyses, to provide evidence for joint prevention and clinical decision-making in patients with concurrent periodontitis and hepatobiliary diseases. Methods: Single nucleotide polymorphisms (SNPs) were extracted from the largest genome-wide association study on periodontitis (17 353 cases, 28 210 controls) and hepatobiliary diseases within the European ancestry and used as instrumental variables (IVs). The strength of the associations was examined by calculating the F-statistic. The SNPs significantly associated with the outcome were removed by scanning on Phenoscanner platform. Bidirectional causal associations between periodontitis and hepatobiliary diseases were estimated using inverse variance weighted (IVW), MR-Egger, and Weighted Median methods. The robustness of the findings was further verified through additional sensitive MR approaches, including Cochran’s Q statistic （IVW）, Rucker’s Q statistic （MR-Egger）, MR-PRESSO and Leave-one-out analysis. Further MR analyses, utilizing other available genome-wide association studies (GWAS) on hepatobiliary diseases, were conducted to validate the results. Results: The IVW method found that periodontitis had a causal impact on acalculous cholecystitis (odds ratio = 1.277, 95% CI 1.097-1.485, P=0.002), implying an increased risk of acalculous cholecystitis associated with periodontitis, while the MR-Egger regression and Weighted Median failed to observe significant causal effects of periodontitis on acalculous cholecystitis. However, no bidirectional causal associations between periodontitis and nonalcoholic fatty liver disease, cirrhosis or liver cancer were observed using IVW, MR-Egger regression and Weighted Median. The bidirectional causal relationships were deemed unlikely to be influenced by horizontal pleiotropy. Further, the validation analysis based on alternative GWAS data suggested parallel results. Conclusions The MR analyses suggest that periodontitis may elevate the risk of acalculous cholecystitis. Further investigations, including clinical studies and mechanistic explorations, are warranted to validate these findings. However, the MR analyses do not support bidirectional causal associations between periodontitis and nonalcoholic fatty liver disease, cirrhosis or liver cancer.

Objective To conduct a quantitative risk assessment of Listeria monocytogenes(LM)in prepackaged,non-vacuum sealed,short shelf-life,ready-to-eat meat products in Chengdu using the@Risk software.Methods Based on monitoring data of LM contamination in pre-packaged,non-vacuum sealed,refrigerated ready-to-eat meat products in Chengdu obtained from a previous study,a risk assessment model was established.The risk of LM infection caused by consuming cooked meat products in different groups of people was quantitatively assessed.In addition,the growth of LM in cooked meat products,from retail to consumption,was also taken into consideration in the assessment.Results In Chengdu,the numbers of potential cases of listeriosis caused by consumption of prepackaged,non-vacuum sealed,refrigerated ready-to-eat meat products were 0.01(95％confidence interval[CI]:0-1.71 × 10-2)per year per million in healthy individuals aged 5-＜65 years old,0.22(95％CI:0-2.67 × 10-1)in healthy individuals aged 65 and above,and 2.88(95％CI:3.85 × 10-8-4.35)in pregnant women.According to the results of the sensitivity analysis,the initial pollution level of LM in the retail stage was the most important factor affecting the prevalence(R=0.25),followed by retail temperature(R=0.08),retail time(R=0.07),and amount of consumption per meal(R=0.07).Conclusions For pre-packaged,non-vacuum sealed,cooked meat products,the most important measure to reduce the prevalence of listeriosis is to control the initial contamination level,which requires food processing plants to regularly clean and strictly disinfect the processing environment and equipment to minimize LM contamination at the source.Retail delicatessens should strictly maintain a storage temperature below 5.0℃ and strictly adhere to product shelf-life recommendations.As for consumers,they should consume these meat products as soon as possible after purchase or store them under refrigerated conditions and shorten the storage time.Pregnant women should thoroughly heat the meat products before eating to reduce the risk of listeriosis.

Objective To investigate the inhibitory effect of β-elemonic acid(β-EA)on the proliferation and inva-sion of colon cancer cells and the underlying mechanisms through PI3K/AKT/mTOR signaling pathway.Methods The effects of β-EA on colon cancer cell proliferation were evaluated using the MTT assay and colony formation as-say.Transwell invasion assay were used to assess the impact of β-EA on invasion.Western blot analysis was con-ducted to detect changes in PI3K/AKT/mTOR pathway proteins after treatment.Results MTT assay showed thatβ-EA effectively inhibited the proliferation of colon cancer HCT8 and HCT116 cells in a dose-dependent manner.The colony formation assay confirmed its inhibitory effect on cell proliferation.Transwell invasion assays demonstra-ted that β-elemonic acid reduced the invasion abilities of the cells.Western blot analysis revealed increased expression of apoptosis-related proteins cleaved-caspase 3,cleaved-caspase 9,and Bax,while Bcl-2 expression was decreased.Invasion-related proteins vimentin,snail,MMP2,and MMP9 were downregulated after treatment.Addi-tionally,β-EAA reduced the levels of p-PI3K,p-Akt,and p-mTOR,and these reductions were more pronounced af-ter the addition of the PI3K inhibitor LY294002.Conclusions β-EA may inhibit proliferation and invasion in colon cancer cell lines HCT8 and HCT116 through PI3K/AKT/mTOR signaling pathway,and potentially be transformed as a novel therapeutic agent for colon cancer.