Investigator
Second Affiliated Hospital Of Harbin Medical University
Circular RNA circRNA_101996 promoted cervical cancer development by regulating miR‐1236‐3p/TRIM37 axis
AbstractCircular RNAs (circRNAs) appear to be significant modulators in various physiological processes. Recently, it is found that circRNA_101996 exerts important roles in various cancers. Our previous studies showed that circRNA_101996 promoted cervical cancer growth and metastasis by regulating miR‐8075/TPX2. However, the potential regulatory role of circRNA_101996 in cervical cancer still needs further investigation. Our results in this study suggested that circRNA_101996 was over‐expressed in cervical cancer patients. circRNA_101996 up‐regulation remarkably assisted cell proliferation, cell cycle progression, and cell migration in cervical cancer, while circRNA_101996 knockdown exerted the inverse effects. The molecular investigations indicated that circRNA_101996 could increase the expression level of miR‐1236‐3p, tripartite motif‐containing 37 (TRIM37), through binding to miR‐1236‐3p and reducing its expression. Moreover, in vivo results demonstrated that circRNA_101996 shRNA can function as a tumor suppressor through down‐regulating TRIM37 in cervical cancer. In conclusion, our data indicated that circRNA_101996/miR‐1236‐3p/TRIM37 axis accelerated cervical cancer development, providing novel insights into cervical cancer diagnosis and treatment.
Tumor‐Associated Macrophage‐Derived CXCL1 Promotes Endometrial Cancer Progression Through the CXCR2/NF‐κB Pathway
ABSTRACT Advanced‐stage and metastatic endometrial cancer (EC) are characterized by markedly poor survival outcomes, necessitating a deeper understanding of the mechanisms driving disease advancement. Tumor‐associated macrophages (TAMs), particularly the M2 subtype, are instrumental in remodeling the tumor microenvironment and promoting EC proliferation, migration, and metastasis. However, the specific mediators responsible for TAM‐driven EC progression remain inadequately elucidated. In this study, we investigated the role of the C–X–C motif chemokine ligand 1 (CXCL1) and its receptor, chemokine receptor 2 (CXCR2), in TAM‐induced EC progression. CXCR2, as the primary receptor for CXCL1, activates the NF‐κB signaling pathway upon binding, thereby mediating the epithelial–mesenchymal transition process in EC cells and enhancing metastatic potential. This mechanism can be effectively inhibited by silencing CXCR2 or by employing the NF‐κB inhibitor BAY 11‐7082. Neutralizing CXCL1 markedly diminished the proliferative and migratory burdens imposed by TAMs on EC in subcutaneous xenograft EC models. Additionally, in EC tissue samples, CXCL1 and CXCR2 expression, as well as the extent of macrophage infiltration, exhibited a significant positive relationship with disease progression, suggesting an unfavorable prognosis. In conclusion, targeting the CXCL1/CXCR2 axis is a potential therapeutic approach for EC treatment.
