Biochimica et biophysica acta. General subjects · 2026
Primase subunit 2 regulates the proliferation and apoptosis of gastric cancer cells via MCM7/CDK4 and Bax/Bcl-2 pathways.
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Liu Bingbing, Wang Xiansheng, Wang Yue, Zhang Tingyu, Guo Rongliang, Chen Xiaodan, Zhang Zhiwei
Аннотация
BACKGROUND: PRIM2 (DNA primase subunit 2), a key regulator of DNA replication initiation, is aberrantly expressed in multiple cancer types and contributes to tumor progression.
OBJECTIVE: This study aimed to investigate the expression of PRIM2 in GC and its effects on cell proliferation and apoptosis, particularly through the MCM7/CDK4 and Bax/Bcl-2 pathways.
METHODS: PRIM2 expression in gastric cancer (GC) and adjacent normal tissues was analyzed using TCGA data, and Kaplan-Meier analysis evaluated its prognostic value. PRIM2 was knocked down or overexpressed in GC cell lines. Western blot measured PRIM2, MCM7, CDK4, Bax, and Bcl-2. Cell proliferation and apoptosis were assessed by CCK-8, colony formation, and flow cytometry. RNA-seq with GO/KEGG analyses and a nude mouse xenograft model examined pathways and in vivo growth.
RESULTS: PRIM2 was highly expressed in GC tissues and cell lines, and its elevated expression was significantly correlated with poor 5-year progression-free survival (PFS) and overall survival (OS) in GC patients. PRIM2 knockdown significantly inhibited proliferation of AGS and HGC-27 cells, whereas PRIM2 overexpression promoted proliferation. Apoptosis was increased upon PRIM2 knockdown. Transcriptomic analysis revealed that PRIM2 knockdown primarily affected the MCM7/CDK4 and Bax/Bcl-2 pathways, which was further confirmed by Western blot. In vivo, PRIM2 knockdown markedly suppressed tumor growth in the xenograft model.
CONCLUSION: PRIM2 regulates GC cells proliferation and apoptosis by the MCM7/CDK4 and Bax/Bcl-2 pathways. Future studies should further investigate the interactions between PRIM2 and other downstream pathways, as well as elucidate its specific mechanisms of action in tumor tissues.
OBJECTIVE: This study aimed to investigate the expression of PRIM2 in GC and its effects on cell proliferation and apoptosis, particularly through the MCM7/CDK4 and Bax/Bcl-2 pathways.
METHODS: PRIM2 expression in gastric cancer (GC) and adjacent normal tissues was analyzed using TCGA data, and Kaplan-Meier analysis evaluated its prognostic value. PRIM2 was knocked down or overexpressed in GC cell lines. Western blot measured PRIM2, MCM7, CDK4, Bax, and Bcl-2. Cell proliferation and apoptosis were assessed by CCK-8, colony formation, and flow cytometry. RNA-seq with GO/KEGG analyses and a nude mouse xenograft model examined pathways and in vivo growth.
RESULTS: PRIM2 was highly expressed in GC tissues and cell lines, and its elevated expression was significantly correlated with poor 5-year progression-free survival (PFS) and overall survival (OS) in GC patients. PRIM2 knockdown significantly inhibited proliferation of AGS and HGC-27 cells, whereas PRIM2 overexpression promoted proliferation. Apoptosis was increased upon PRIM2 knockdown. Transcriptomic analysis revealed that PRIM2 knockdown primarily affected the MCM7/CDK4 and Bax/Bcl-2 pathways, which was further confirmed by Western blot. In vivo, PRIM2 knockdown markedly suppressed tumor growth in the xenograft model.
CONCLUSION: PRIM2 regulates GC cells proliferation and apoptosis by the MCM7/CDK4 and Bax/Bcl-2 pathways. Future studies should further investigate the interactions between PRIM2 and other downstream pathways, as well as elucidate its specific mechanisms of action in tumor tissues.
Предметные рубрики MeSH
HumansStomach NeoplasmsCell ProliferationApoptosisMinichromosome Maintenance Complex Component 7AnimalsProto-Oncogene Proteins c-bcl-2Mice, NudeCyclin-Dependent Kinase 4Micebcl-2-Associated X ProteinCell Line, TumorFemaleSignal TransductionDNA PrimaseGene Expression Regulation, NeoplasticMaleMice, Inbred BALB C