Editorial
Copyright ©The Author(s) 2025.
World J Gastrointest Oncol. Feb 15, 2025; 17(2): 100546
Published online Feb 15, 2025. doi: 10.4251/wjgo.v17.i2.100546
Table 2 Recent findings of the experimental studies in gastrointestinal cancers related to protein tyrosine phosphatase nonreceptor 2
Ref.
Organ
Methods
Findings related to PPTN2
Spalinger et al[14]ColonCC, IFPPTN2 dysfunction in T cells drives the secretion of IFN-γ and IL-17. PPTN2 dysfunction promotes IL-18, IL-1β secretion and increased inflammasome assembly. Protects from CRC development
Manguso et al[15]ColonAELoss of PTPN2 enhances Tim-3+ CD8+ T cell differentiation promoting anti-tumor immunity
Tang et al[1]
ColonTCGA, GTEx data analysisPositive correlation with CD8+ cells. Knockdown inhibits proliferation of cancer cells and leads to abundance of PD-L1
Huang et al[26]PancreasCC, WBSilencing PTPN2 attenuates the proliferation of cancer cells. PTPN2 regulates the level of tyrosine phosphorylation of KRAS. PTPN2 knockdown was consistent with that of knockdown of KRAS
Kuang et al[25]PancreasTCGA, GTEx data analysisPTPN2 mRNA expression upregulated and related to JAK-STAT pathway. Down-regulation diminishes tumor burden
Zhang et al[18]PancreasHuman tumor tissue, IHC, RT-PCR, IF, WB, CC, AEKnockdown promotes the migration and invasion abilities. PTPN2 inhibited metastasis, and presented a novel PTPN2/p-STAT3/MMP-1 axis in progression
Grohmann et al[28]HCCAEPTPN2 deletion in hepatocytes promoted T cell recruitment. PTPN2 deletion promotes STAT-3 dependent HCC
Tang et al[1]HCCTCGA, GTEx data analysis Terminal differentiation-induced lncRNA preserved STAT3 phosphorylation via direct interacting with PTPN2. The activation of STAT3 downstream target genes and promote HCC cell growth, migration, and infiltration