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Background: Cervical cancer (CC) is one of the most deadly cancers in women, its current treatments still result in poor outcomes and developing the novel targets and therapeutic strategies are urgently needed. Qiu's Cervical Prescription (QCP) is one of the traditional Chinese medicines used in the treatment of cervical cancer in China. Although its curative effect is remarkable, the internal mechanism of its treatment is still poorly understood. Recent studies have shown that LncRNA ATB might be used as a new proliferation marker for cancer diagnosis and prognosis. This study aimed to investigate the possible mechanism of action of QCP in the treatment of cervical cancer., Methods: The functional assays of migration and invasion in vitro using transwell assays and wound healing assays was performed to confirm the pro-carcinogenic effect of LncRNA ATB, and the changes of migration and invasion of HeLa cells were observed after treatment with QCP containing drug serum. The changes in tumor volume, general condition of transplanted tumor-bearing mice and expression of LncRNA ATB pathway-related proteins were detected by qPCR, Western blotting and HE staining after treatment with the QCP., Results: We induced LncRNA ATB knockdown and overexpression in cervical cancer cell lines and detected the biological behavior changes in vitro. Furthermore, we established murine models using stable LncRNA ATB-shRNA HeLa cells or overexpression LncRNA ATB cells or normal Hela cells with QCP to evaluate how suppression of LncRNA ATB affects tumor growth., Conclusion: We showed that potential mechanism of QCP in the treatment of cervical cancer may be through inhibition of the LncRNA ATB/miR-126/TGFβ1 signaling axis. In conclusion, QCP may be a promising approach for the treatment of CC., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier GmbH. All rights reserved.)

Background: Cervical cancer is the fourth most common malignancy in women, of which cervical squamous cell carcinoma (CESC) is the main pathological type of cervical cancer. B-cell translocation gene 2 (BTG2) protein has been recognized as a tumor suppressor in several cancer types. However, BTG2 expression and molecular function in CESC are unknown., Methods: In this study, we first assessed the expression of BTG2 in tumor tissue specimens from CESC patients using immunohistochemical staining and real-time quantitative PCR, and explored the relationship between BTG2 expression status and clinical manifestations. Next, we constructed BTG2 knockdown and overexpression CESC cell lines to observe the effects of BTG2 on CESC proliferation and metastasis at the cellular level. Finally, we employed a nude mouse xenograft tumor model in an in vivo experiment to observe the effect of BTG2 on tumorigenesis in vivo., Results: The results showed that the expression of BTG2 protein was lower in CESC tissues than in normal tissues, and high BTG2 expression was associated with better survival in CESC patients versus CESC patients. The results of cellular assays confirm that overexpression of BTG2 inhibits the proliferation, migration and metastasis of CESC cells. Nude mouse xenograft tumor model showed that overexpression of BTG2 inhibited tumor growth in vivo, and conversely knockdown of BTG2 promoted tumor growth., Conclusion: In summary, our data suggest that BTG2 acts as a tumor suppressor in CESC and inhibits the growth and metastasis of CESC. BTG2 may serve as a potential prognostic marker in CESC and is expected to provide a therapeutic strategy for patients with CESC., Competing Interests: Declaration of Competing Interest The authors declare that they have no conflict of interest., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Glioblastoma (GBM) is the most malignant primary brain tumor. The 5-year survival rate of the patients is poor, and they are prone to relapse and the treatment is limited. Therefore, the search for biological targets is one of the key measures for the treatment and prognosis of GBM. Ubiquitin-specific peptidase 18 (USP18) plays a regulatory role in tumorigenesis. In this study, we found that USP18 was up-regulated in GBM, promoted the growth and proliferation of glioblastoma stem cells (GSCs), affected the epithelial-mesenchymal transition (EMT), and was associated with poor clinical prognosis of patients. Finally, our findings reveal a critical role for USP18 in GBM malignancy, targeting USP18 may open new avenues for GBM treatment., Competing Interests: Declaration of Competing Interest The authors declare that they have no conflict of interest., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Background: The incidence and death rate of cervical cancer rank fourth among female malignant tumors worldwide. A growing number of researches are devoted to exploring more effective treatment methods and cancer stem cells (CSCs) are thought to be a potential therapeutic target in cervical cancer. In our study, we focused on the expression and function of UCHL1 in cervical squamous cell carcinoma (CESC)., Methods: We detected and the expression of UCHL1 in 134 CESC patients through immunohistochemistry and further confirm UCHL1 was a prognostic factor by univariate and multivariate analysis. Then, according to TCGA database for CESC, we found that UCHL1 expression correlated with the markers associated with CSCs (CD133, ABCG2 and SOX2). Therefore, we used western blot and spheroid formation assays to future evaluate the function of UCHL1 on cancer stemness in C-33A and SiHa cell lines. At the same time, we detected the cell proliferation, migration and invasion change by CCK-8 assay, scratch assay and transwell assay, when UCHL1 was knockdown or overexpressed. Finally, xenograft models were used to examine the effect of UCHL1 in vivo., Results: We found the expression of UCHL1 in mRNA and protein was higher in tumor than in paired normal tissue and was a prognostic factor in CESC. The UCHL1 high expression group showed a shorter survival in the overall survival. According to TCGA database, the expression of UCHL1 was correlated with CD133, ABCG2 and SOX2. The results of sphere-forming ability and CSCs related markers expression were showed UCHL1 promoted cancer stemness in CESC. Similarly, CCK-8 assay, scratch assay and transwell assay were applied to demonstrate that overexpression of UCHL1 promoted the proliferation, migration and invasion in SiHa, but when UCHL1 was knockdown in C-33A, the function of UCHL1 displayed the opposite result. Finally, knockdown UCHL1 inhibited CESC tumor propagation in xenograft models., Conclusion: Our results suggest that UCHL1 is a prognostic factor and correlated with cancer stemness, proliferation, migration and invasion of CESC, which may provide a novel therapeutic strategy for CESC treatment., Competing Interests: Declaration of Competing Interest The authors declare that they have no conflict of interest., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Ferroptosis is an iron-dependent form of RCD correlates with the accumulation of markers of lipid peroxidation. Bulks of studies focusing on revealing ferroptosis and its regulators involved in oncogenic pathways. Connection between iron metabolism and abnormal iron metabolism in CSCs synergistically making ferroptosis a target process of great potential in combating with CSCs to improve therapeutic effectiveness and reverse resistance. Ferroptosis inducers could specifically induce CSCs death in tumors, predisposing ferroptosis to a target in killing CSCs to overcome cancer resistances. By ferroptosis induction and other cell death pathways in CSCs, cancer therapeutic outcome would be improved., Competing Interests: Conflict of interest The authors declare that they have no conflict of interest., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Background: As most common primary tumor in adult's brain, the glioblastoma (GBM) still ends up with poor survival period. Little progress has been made in recent decades in terms of improving prognosis. There's still an urgent need for novel targets and strategies to overcome such malignancy., Methods: Both the Cancer Genome Atlas and Gene Expression Omnibus databases were used to analyze expression differences and correlations. The immunohistochemistry and survival analysis were used to verify expression differences. Tumorigenesis was assessed using cholecystokinin and the orthotopic xenograft model. Metastasis was determined by the transwell assay and the tail vein xenograft model., Results: Inhibin subunit beta B (INHBB) was upregulated in GBM and predicted poor survival. It promoted tumor growth, invasion and stemness in GBM. INHBB expression correlated with the epidermal growth factor receptor (EGFR) expression and downstream AKT and ERK expression levels. The increased tumor progression induced by INHBB could be inhibited by afatinib., Conclusion: This study revealed INHBB as a tumor progression and independent prognostic factor in GBM, which could be a potential upper stream molecular of EGFR/ERK/AKT signaling., Competing Interests: Declaration of Competing Interest All authors declare no conflict of interest., (Copyright © 2023. Published by Elsevier GmbH.)

Osteosarcoma (OS) is one of the most common primary bone malignancy. Combining chemotherapy and surgical treatment significantly improved clinical outcomes for osteosarcoma patients. Osteosarcoma stem cells (OSCs) are often more malignant than differentiated cancer cells and are a key determinant of responses to chemotherapy and radiation therapy, therefore, the removal of OSCs could be an effective therapeutic strategy. Myxoprotein 1 (MUC1) is aberrantly overexpressed in many human cancers and it promotes cancer stemness through activation of pluripotency networks. In this study, we observed elevated MUC1 in osteosarcoma and a depressed prognosis in patients with high MUC1 expression profiles. Our observations also revealed that MUC1 promoted OS stemness and tumor metastasis both in vivo and in vitro. These data led us to hypothesize that MUC1 may be a therapeutic target for patients with OS., Competing Interests: Conflict of interest The authors declare that they have no conflict of interest., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Background: PRKCH is a member of the PKC family with the potential to regulate cell proliferation and differentiation. Glioma is the most common primary tumor of the central nervous system, with a high recurrence rate and poor prognosis. Recent studies have demonstrated that PRKCH can promote the proliferation of glioma cells. The purpose of this study was to investigate the promoting effect and possible mechanism of PRKCH on glioma development., Methods: Tumor tissue and paracancerous tissue were collected from 160 glioma patients treated at the General Hospital of Northern Theater Command. The expression level of PRKCH was detected by immunohistochemistry and immunoblotting. Univariate/multivariate analysis and log-rank analysis, as well as prognosis and survival analysis, were performed using SPSS26 software. The PRKCH overexpression model was constructed in vitro to study the effect of PRKCH expression on the characteristics of glioma stem cells., Results: The expression of PRKCH in glioma tissues was higher than that in adjacent tissues. PRKCH expression level is an independent prognostic factor in glioma patients, promoting poor prognosis and shorter survival in glioma patients. Furthermore, overexpression of PRKCH in glioma stem cells significantly increased stem cell properties and enhanced cell viability. Downregulation of PRKCH significantly inhibited the progression of glioma stem cells., Conclusion: PRKCH promotes the development of gliomas and may be a therapeutic target for gliomas., Competing Interests: Conflict of interest The authors declare that they have no conflict of interest., (Copyright © 2022 Elsevier GmbH. All rights reserved.)

Background: Glioblastoma (GBM) is the most common primary malignant brain tumor. It has a poor 5-year survival rate, a high recurrence rate, and few therapeutic options. Exploring the molecular processes underlying the formation and progression of GBM, as well as identifying novel therapeutic targets, is critical for improving GBM therapy and prognosis., Methods: We extracted primary GSCs (glioblastoma stem cells) from patient-derived samples. Different levels of CSNK1D were evaluated through immunohistochemistry, western blot and real-time PCR assays. A Transwell assay was used to detect invasive ability of cell lines. Tumorsphere formation assay was performed to detect cancer stemness properties. Orthotopic xenograft models were used to evaluate the effect of CSNK1D on GSC tumorigenesis., Results: We found the expression levels of CSNK1D was elevated in GBM tissues compared with normal brain. CSNK1D expression had an increased tendency among WHO grades (G2-G4), and was higher in IDH wildtype group than in mutation group. The prognosis of the CSNK1D high expression group was significantly worse than that of the low expression group. Cox multivariate analysis showed that CSNK1D was also an independent prognostic factor in GBM patients. In primary GBM cells, we observed increased levels of CSNK1D in GSCs compared to non-stem tumor cells (NSTCs). In addition, the change of stemness markers expression and proliferation of GSCs were in coordinate with CSNK1D overexpression or knockdown. Furthermore, CSNK1D could affect the epithelial-mesenchymal transition (EMT) markers and MMPs expression in GSCs. Finally, disruption of CSNK1D expression impairs GSC survival and GBM tumor propagation in orthotopic xenograft models., Conclusion: Our results suggest that CSNK1D correlated with GBM prognosis and might influence the stemness and invasiveness of GSCs, which represented a potential therapeutic target in GBM patients., Competing Interests: Conflict of interest The authors declare that they have no conflict of interest., (Copyright © 2022 Elsevier GmbH. All rights reserved.)

Background: Triple-negative breast cancer (TNBC) is a special kind of breast cancer with strong ability of invasion and metastasis. UCHL1 belongs to the ubiquitin carboxy-terminal hydrolase family and is found to be increased in a variety of malignancies, but its expression in TNBC is unknown., Methods: First, we analyzed the expression of UCHL1 in 128 TNBC specimens and paired adjacent normal tissues from 17 TNBC patients undergoing curative resection by immunohistochemistry. Then, the relationship between UCHL1 and cancer stemness was investigated by cell flow cytometry, spheroid formation assays and western blot. Moreover, cell scratch assay and Transwell assays were performed to explore whether UCHL1 promotes the migration and invasion of TNBC cells. Finally, we constructed a xenografts model of TNBC cell lines to observe the effect of UCHL1 on tumorigenesis in vivo., Results: UCHL1 was overexpressed in TNBC tissues and associated with poor prognosis. UCHL1 promoted stem cancer cells properties, including the percentage of CD44 + /CD24 - cells, sphere-forming ability and CSCs related markers. Furthermore, Scratch assay and Transwell assay proved that UCHL1 enhanced the migration and invasion of TNBC cells. The experimental results of xenografts model in nude mice showed that UCHL1 promoted tumorigenesis of TNBC in vivo., Conclusion: UCHL1 may play a role in the malignant progression of TNBC by maintaining the stemness and promoting cell invasion and is expected to become a potential therapeutic target for TNBC patients., Competing Interests: Conflict of interest The authors declare that they have no conflict of interest., (Copyright © 2022 Elsevier GmbH. All rights reserved.)

Gliomas are common brain tumors with poor prognosis. F-box protein39 (FBXO39) is found to be increased in a variety of malignancies, but its expression in gliomas is unknown. Here, we report that FBXO39 as an oncogene is upregulated in glioma and associated with poor prognosis. The degree of FBXO39 positive expression is doubtlessly concomitant with the grade of glioma. The data analyses show that patients with high FBXO39 expression have poor overall survival. What's more, FBXO39 accelerates the invasion and migration abilities of glioma cells and promotes glioma stem cell growth and stemness. In summary, these results suggest that FBXO39 is expected to become a new biological target for judging the prognosis and treatment of glioma., Competing Interests: Conflict of interest The authors declare that they have no conflict of interest., (Copyright © 2022 Elsevier GmbH. All rights reserved.)

Objective: In the mouse model, manipulations of assisted reproductive technology (ART) can lead to enlarged placentas and influence the expression of amino acid transporters in placentas during mid-to late-gestation. However, it is uncertain whether those abnormal changes presented in ART mouse placentas also occur in human ART placentas., Methods: We choose the placenta tissue of pregnant woman by ART in term birth (ART group) and by natural pregnancy in term birth (control group) to compare the birth weight of the baby, placental weight and ratio of the fetal/placental weight of these two groups. We then detect the mRNA and protein expression of placental amino acid transporter genes (SNAT1, SNAT2, SNAT4, LAT1 and LAT2) in these two groups by real-time quantitative PCR, Western blot and immunofluorescence staining. Additionally, the PI3K-AKT-mTOR signaling activity was also analyzed., Results: There were no statistical differences in new birth weight between the ART group and the control group. Compared with the control group, the placenta weight of baby was significantly higher in ART group and ratio of the fetal/placental weight was significantly lower in ART group. We found that the mRNA and protein expression of A system of amino acid transporter SNAT1, SNAT2 and SNAT4 in placenta were significantly down-regulated in ART group compared with placentas from natural pregnancies. Additionally, there were no statistical differences of the mRNA and protein expression of L system of amino acid transporter LAT1 between these two groups, but amino acid transporter LAT2 in placenta was significantly down-regulated in ART group. Furthermore, the PI3K-AKT-mTOR signaling activity was inhibited in ART group., Conclusions: ART leads to the expressions of amino acid transporter genes SNAT1, SNAT2, SNAT4 and LAT2 significantly down-regulated in placenta accompanied by the PI3K-AKT-mTOR signaling inhibition, which suggests that ART may affect the function of placenta amino acid transporter during the late pregnancy, leading to enlarged placentas and probably low birth weight., (Copyright © 2022 Elsevier GmbH. All rights reserved.)

Background: Cancer/testis antigen (CTA) is a class of antigen molecules mainly expressed in the germinal epithelium of testis and some tumor tissues. FBXO39, also known as F-box protein 39, is a crucial CTA molecule. F-box protein 39 (FBXO39) is overexpressed in cervical squamous cell carcinomas (CESCs), however its function in cancer development and clinical significance are still unknown., Methods: We used paraffin-embedded tumor tissues from 124 patients and fresh-harvested and paired adjacent normal esophageal tissues from 15 CESC patients who underwent primary surgical resection in Xijing Hospital between 2015 and 2020. The expression level of FBXO39 was evaluated through immunohistochemistry, Western Blot and q-PCR. Prognostic and survival analyses were conducted using univariate/multivariate analysis and log-rank analysis with SPSS 23.0. CCK-8, wound-healing and Transwell assays were applied to demonstrate that FBXO39 promoted the proliferation, migration and invasion. Finally, we constructed a xenografts model of the C-33A cell lines to observe the effect of FBXO39 on tumorigenesis in vivo., Results: Immunohistochemical results showed that FBXO39 was highly expressed in cancer tissues than in corresponding non-cancer tissues. Similarly, we proved this result at protein and mRNA level by Western-Blotting and q-PCR. Prognostic and OS analyses showed that the FBXO39 expression level was an individual prognostic factor in CESC patients. CCK-8, wound-healing and Transwell assays proved that the overexpression of FBXO39 in Si-Ha cells promoted the proliferation, migration and invasion of the cells. Knocking down FBXO39 in C-33A cells inhibited the proliferation, migration and invasion of cells. The experimental results of xenografts model in nude mice showed that the knockdown of FBXO39 in C-33A cells slowed down the growth of tumor., Conclusion: FBXO39 is a poor prognostic factor of cervical squamous cell carcinoma, which may provide a novel therapeutic target for CESC., (Copyright © 2022 Elsevier GmbH. All rights reserved.)

Esophageal squamous cell carcinoma (ESCC) is one of the most intractable challenges among human diseases with poor prognosis and shortness of effective therapeutic options. Cancer stem cells (CSCs), a tumor sub-population, are considered the cause of tumor growth, differentiation, metastasis and therapeutic resistance, etc. In this review, we discuss the known methods for isolation and verification of ESCC CSCs, the biomarkers of ESCC CSCs and their significance in diagnosis and prognosis. Then we review the ESCC CSC signaling pathway and therapeutic resistance. In pace with the detailed studies of ESCC CSCs increasing, treatment strategies of ESCC based on CSCs are becoming more promising., Competing Interests: Conflict of interest The authors declare that they have no conflict of interest., (Copyright © 2022. Published by Elsevier GmbH.)

Objective: Breast cancer (BC) is the most commonly diagnosed cancer among females and has a poor prognosis, breast invasive ductal carcinoma is the most common histological type. The occurrence and development of BC is closely related to aberrant glucose metabolism. In the hyperglycemic environment caused by abnormal glucose metabolism, hypoxia-inducible factor-1 alpha (HIF-1α) enables tumor cells to absorb large amounts of glucose and enhance glycolysis by inducing the expression of glucose transporter type1 (GLUT1) and glycolysis genes, thus promoting tumor cell proliferation and metastasis. Mitochondrial Sirtuin5 (SIRT5) plays a role in the rewiring of glucose metabolism during the progression of cancers. Thus, we aimed to elucidate whether SIRT5 promotes BC proliferation and metastasis by facilitating aerobic glycolysis in BC., Methods: The expression of SIRT5 in breast carcinoma tissue and cells was evaluated using immunohistochemical staining, western blot and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis to confirm the biological role of SIRT5 in breast carcinoma. We established a stable cell line with SIRT5 knockdown using lentiviral transduction in T47D cells to reduce SIRT5 expression and then evaluated the effect of SIRT5 on cells cultured in the presence of high glucose (4500 mg/L) and normal glucose (2000 mg/L) concentrations. Cell proliferation was detected using the CCK-8 assay, the cell cycle and cell apoptosis were measured using flow cytometry and Annexin V staining, and cell migration was tested by performing Celigo scratch and Transwell assays. The expression of PKM2, HK2, mTOR and HIF-1α, which play roles in aerobic glycolysis, was investigated using western blot., Results: SIRT5 was overexpressed in BC tissues compared with paired normal tissues. Prognostic and OS analyses showed that the SIRT5 expression level was an individual prognostic factor for patients with BC. SIRT5 knockdown inhibited proliferation and metastasis and slightly increased apoptosis in T47D cells under high-glucose conditions. Furthermore, the downregulation of HK2 and HIF-1α caused by SIRT5 knockdown was a high glucose-dependent process, while the downregulation of PKM2 was mediated by a high glucose-independent process., Conclusions: SIRT5 is an independent prognostic factor for BC and contributes to cell proliferation and metastasis in a high glucose-dependent manner to some degree, which might be mediated by promoting aerobic glycolysis., (Copyright © 2022 Elsevier GmbH. All rights reserved.)

Background: Esophageal squamous cell carcinoma (ESCC) is a multifactorial disease and the sixth leading cause of death from cancer worldwide. Patients with ESCC usually have a short survival period due to the late stage at diagnosis. Incidence rates of ESCC remain high among the elderly. With recent advances, it has been demonstrated that ESCC tumors display a unique genetic profile. This study aimed to examine the possible function of OTX1 in ESCC., Methods: We collected paraffin-embedded tumor tissues from 107 patients originally diagnosed with ESCC at Xijing Hospital and fresh-harvested and paired adjacent normal esophageal tissues from 15 ESCC patients undergoing curative resection. The expression level of OTX1 was evaluated through immunohistochemistry and western blot. Prognostic and survival analyses were conducted using univariate/multivariate analysis and log-rank analysis with SPSS 23.0. Cell models and xenograft models were used to examine the overexpression of OTX1 in vivo and in vitro., Results: OTX1 was overexpressed in ESCC tissues compared with normal esophageal tissues. Both the mRNA expression level and protein level of OTX1 were higher than they were in paired normal tissue. Prognostic and OS analyses showed that the OTX1 expression level was an individual prognostic factor in ESCC patients. Cell viability was significantly promoted when OTX1 was overexpressed in ESCC cell, Furthermore, downregulating OTX1 in EC109 cell significantly attenuated the cell proliferation migration and invasion. Flow cytometric detection showed that cells overexpressing OTX1 were predominantly in the S and G2&M phases. In the xenograft model, both tumor size and weight in the OTX1 overexpression group were significantly larger than those in the control group., Conclusion: OTX1 is an independent prognostic factor of ESCC and contributes to tumorigenesis both in vivo and in vitro., (Copyright © 2022 Elsevier GmbH. All rights reserved.)

Background: The main pathological change causing carotid artery stenosis is atherosclerosis, and studies suggest that tumor necrosis factor-stimulated gene-6 (TSG-6) has an anti-atherogenic effect and may be a new target for the diagnosis of carotid artery stenosis disease. We hypothesized that serum TSG-6 levels might also be associated with carotid artery stenosis. The aim of this study was to evaluate the diagnostic significance and potential predictive value of serum TSG-6 levels in patients with severe carotid artery stenosis and symptomatic stenosis., Methods: Serum TSG-6 levels were measured in 96 patients with carotid stenosis and 40 sex and age matched control healthy subjects. The expression of TSG-6 in carotid plaques (4 severe stenoses, 4 moderate stenoses, and 4 mild stenoses) and 4 superficial temporal artery vascular tissues of 12 patients with carotid stenosis who underwent endarterectomy at our hospital were detected by Western blot. Histological analysis of carotid plaque and superficial temporal artery tissues was also performed., Results: Compared with controls, serum TSG-6 levels were higher in patients with carotid stenosis, TSG-6 expression was increased in tissues with moderate and severe stenosis, and TSG-6 expression was significantly higher in the fibrous cap component of the plaque than in the non-fibrous cap component. Serum TSG-6 levels were higher in patients with symptomatic stenosis than in patients with asymptomatic stenosis. Tissue TSG-6 staining levels and serum TSG-6 levels were positively correlated (r = 0.694, p < 0.05) and tissue TSG-6 staining levels were positively correlated with macrophage staining levels (r = 0.932, p < 0.05). Logistic regression analysis showed that serum TSG-6 was an independent factor for the presence of severe carotid stenosis and symptomatic stenosis in patients (p < 0.001). Serum TSG-6 levels were more diagnostically efficient than other indices in identifying severe and symptomatic carotid stenosis (p < 0.05), especially in identifying symptomatic stenosis (p < 0.01). We further significantly increased the diagnostic power of symptomatic stenosis using a combined model of serum TSG-6 and homocysteine (p < 0.05)., Conclusions: Serum TSG-6 may serve as a new non-invasive and easily measured biomarker to better screen people with severe and symptomatic carotid stenosis in clinical practice., (Copyright © 2022 Elsevier GmbH. All rights reserved.)