Objective:Gastric cancer(GC)is a globally common cancer characterized by high incidence and mortality worldwide.Advances in the molecular understanding of GC provide promising targets for GC diagnosis and therapy.Long...Objective:Gastric cancer(GC)is a globally common cancer characterized by high incidence and mortality worldwide.Advances in the molecular understanding of GC provide promising targets for GC diagnosis and therapy.Long non-coding RNAs(lncRNAs)and their downstream regulators are regarded to be implicated in the progression of multiple types of malignancies.Studies have shown that the lncRNA small nucleolar RNA host gene 4(SNHG4)serves as a tumor promoter in various malignancies,while its function in GC has yet to be characterized.Therefore,our study aimed to explore the role and underlying mechanism of SNHG4 in GC.Methods:We used qRT-PCR to analyze SNHG4 expression in GC tissues and cells.Kaplan-Meier analysis was used to assess the correlation between SNHG4 expression and the survival rate of GC patients.Cellular function experiments such as CCK-8,BrdU,colony formation,flow cytometry analysis,and transwell were performed to explore the effects of SNHG4 on GC cell proliferation,apoptosis,cell cycle,migration,and invasion.We also established xenograft mouse models to explore the effect of SNHG4 on GC tumor growth.Mechanically,dual luciferase reporter assay was used to verify the interaction between SNHG4 and miR-409-3p and between miR-409-3p and cAMP responsive element binding protein 1(CREB1).Results:The results indicated that SNHG4 was overexpressed in GC tissues and cell lines,and was linked with poor survival rate of GC patients.SNHG4 promoted GC cell proliferation,migration,and invasion while inhibiting cell apoptosis and cell cycle arrest in vitro.The in vivo experiment indicated that SNHG4 facilitated GC tumor growth.Furthermore,SNHG4 was demonstrated to bind to miR-409-3p.Moreover,CREB1 was directly targeted by miR-409-3p.Rescue assays demonstrated that miR-409-3p deficiency reversed the suppressive impact of SNHG4 knockdown on GC cell malignancy.Additionally,miR-409-3p was also revealed to inhibit GC cell proliferation,migration,and invasion by targeting CREB1.Conclusion:In conclusion,we verified that the SNHG4 promoted GC growth and metastasis by binding to miR-409-3p to upregulate CREB1,which may deepen the understanding of the underlying mechanism in GC development.展开更多
To investigate the histological,immunohistochemical,and molecular characteristics of sclerosing epithelioid fibrosarcoma(SEF),a rare intracranial lesion,we analyzed the clinical,pathological,and molecular features of ...To investigate the histological,immunohistochemical,and molecular characteristics of sclerosing epithelioid fibrosarcoma(SEF),a rare intracranial lesion,we analyzed the clinical,pathological,and molecular features of a group of cases involving both intracranial(case 1)and extracranial(cases 2,3,and 4)soft tissue tumors.These tumors were located in the bilateral parietal sinuses(one of four cases;25%),thoracic vertebrae(1 of 4 cases;25%),mediastinum(1 of 4 cases;25%),and parathyroid soft tissue(1 of 4 cases;25%).Microscopically,tumor cells were observed in both sparse and dense areas,arranged in sheets,cords,and a fusiform braided pattern,all within a dense sclerotic matrix.All four patients exhibited strong and diffuse positivity for MUC4.Cases 1 and 2 harbored an EWSR1–CREB3L1 fusion;case 3 had a CPSF6–ITPR2 fusion;and case 4 exhibited multiple fusion genes,including FUS–CREB3L2,KDM5A–ERC1,AKAP8L–BRD4,and ATF2–CHN1.Methylation analysis indicated that all cases clustered within the SEF spectrum.Copy number variation analysis revealed deletions in chromosomal arms 11p and 22q across all cases.The morphologies of intracranial and extracranial SEF were found to be similar.Although MUC4 serves as a reliable marker for diagnosing SEF,its molecular findings remain nonspecific.Methylation clustering and aneuploidy score assessment should be considered as additional tools to assist in diagnosis and prognostic monitoring.展开更多
文摘Objective:Gastric cancer(GC)is a globally common cancer characterized by high incidence and mortality worldwide.Advances in the molecular understanding of GC provide promising targets for GC diagnosis and therapy.Long non-coding RNAs(lncRNAs)and their downstream regulators are regarded to be implicated in the progression of multiple types of malignancies.Studies have shown that the lncRNA small nucleolar RNA host gene 4(SNHG4)serves as a tumor promoter in various malignancies,while its function in GC has yet to be characterized.Therefore,our study aimed to explore the role and underlying mechanism of SNHG4 in GC.Methods:We used qRT-PCR to analyze SNHG4 expression in GC tissues and cells.Kaplan-Meier analysis was used to assess the correlation between SNHG4 expression and the survival rate of GC patients.Cellular function experiments such as CCK-8,BrdU,colony formation,flow cytometry analysis,and transwell were performed to explore the effects of SNHG4 on GC cell proliferation,apoptosis,cell cycle,migration,and invasion.We also established xenograft mouse models to explore the effect of SNHG4 on GC tumor growth.Mechanically,dual luciferase reporter assay was used to verify the interaction between SNHG4 and miR-409-3p and between miR-409-3p and cAMP responsive element binding protein 1(CREB1).Results:The results indicated that SNHG4 was overexpressed in GC tissues and cell lines,and was linked with poor survival rate of GC patients.SNHG4 promoted GC cell proliferation,migration,and invasion while inhibiting cell apoptosis and cell cycle arrest in vitro.The in vivo experiment indicated that SNHG4 facilitated GC tumor growth.Furthermore,SNHG4 was demonstrated to bind to miR-409-3p.Moreover,CREB1 was directly targeted by miR-409-3p.Rescue assays demonstrated that miR-409-3p deficiency reversed the suppressive impact of SNHG4 knockdown on GC cell malignancy.Additionally,miR-409-3p was also revealed to inhibit GC cell proliferation,migration,and invasion by targeting CREB1.Conclusion:In conclusion,we verified that the SNHG4 promoted GC growth and metastasis by binding to miR-409-3p to upregulate CREB1,which may deepen the understanding of the underlying mechanism in GC development.
基金supported by grants from the National Natural Science Foundation of China(No.82273082)Chongqing Technical Innovation and Application Development Key Project(No.cstc2021jscx-cylhX0005)。
文摘To investigate the histological,immunohistochemical,and molecular characteristics of sclerosing epithelioid fibrosarcoma(SEF),a rare intracranial lesion,we analyzed the clinical,pathological,and molecular features of a group of cases involving both intracranial(case 1)and extracranial(cases 2,3,and 4)soft tissue tumors.These tumors were located in the bilateral parietal sinuses(one of four cases;25%),thoracic vertebrae(1 of 4 cases;25%),mediastinum(1 of 4 cases;25%),and parathyroid soft tissue(1 of 4 cases;25%).Microscopically,tumor cells were observed in both sparse and dense areas,arranged in sheets,cords,and a fusiform braided pattern,all within a dense sclerotic matrix.All four patients exhibited strong and diffuse positivity for MUC4.Cases 1 and 2 harbored an EWSR1–CREB3L1 fusion;case 3 had a CPSF6–ITPR2 fusion;and case 4 exhibited multiple fusion genes,including FUS–CREB3L2,KDM5A–ERC1,AKAP8L–BRD4,and ATF2–CHN1.Methylation analysis indicated that all cases clustered within the SEF spectrum.Copy number variation analysis revealed deletions in chromosomal arms 11p and 22q across all cases.The morphologies of intracranial and extracranial SEF were found to be similar.Although MUC4 serves as a reliable marker for diagnosing SEF,its molecular findings remain nonspecific.Methylation clustering and aneuploidy score assessment should be considered as additional tools to assist in diagnosis and prognostic monitoring.
