HNRNPA2B1 stabilizes NFATC3 levels to potentiate its combined actions with FOSL1 to mediate vasculogenic mimicry in GBM cells.

Background: Vasculogenic mimicry (VM) is an enigmatic physiological feature that influences blood supply within glioblastoma (GBM) tumors for their sustained growth. Previous studies identify NFATC3, FOSL1 and HNRNPA2B1 as significant mediators of VEGFR2, a key player in vasculogenesis, and their molecular relationships may be crucial for VM in GBM.

Aims: The aim of this study was to understand how NFATC3, FOSL1 and HNRNPA2B1 collectively influence VM in GBM.

EP300 restores the glycolytic activity and anti-tumor function of CD8 cytotoxic T cells in nasopharyngeal carcinoma.

Competition for glucose may metabolically limit T cells during cancer progression. This study shows that culturing in the condition medium (CM) of NPC c6661 cells restricted glycolytic and immune activities of CD8 T cells. These cells also exhibited limited tumor-eliminating effects in mouse xenograft tumor models.

Modification of Metal-Organic Framework Nanoparticles Using Dental Pulp Mesenchymal Stem Cell Membranes to Target Oral Squamous Cell Carcinoma.

Engineering a targetable nanoparticle to tumor cell is a challenge issue for clinical application. Our results demonstrated that the chemokine CXCL8 secreted by oral squamous cell carcinoma (OSCC) could act as a chemoattractant to attract dental pulp mesenchymal stem cell (DPSC), which expressed the CXCL8 binding receptor, CXCR2, to the OSCC. Therefore, to create OSCC targetable nanoparticles, we used DPSC membranes to modify nanoparticles of metal-organic framework nanoparticles (MOFs) resulting in a novel MOF@DPSCM nanoparticle.

Bone mesenchymal stem cells are recruited via CXCL8-CXCR2 and promote EMT through TGF-β signal pathways in oral squamous carcinoma.

Objectives: Bone mesenchymal stem cells (BMSCs) play critical roles in tumour microenvironment. However, molecular mechanisms of how BMSCs to be recruited and effect subsequent tumour progression are poorly understood in oral squamous cell carcinoma (OSCC).

Materials And Methods: The distribution of CXCL8 was detected by immunohistochemical staining in OSCC tissues.

Osteopromotive carbon dots promote bone regeneration through the PERK-eIF2α-ATF4 pathway.

Bone defects are still an unsolved clinical issue that must be overcome. Carbon dots have shown very promising effects in biological therapy. In the current study, we explored their effects on osteogenesis.

Chemotherapy Modulates Endocrine Therapy-Related Resistance Mutations in Metastatic Breast Cancer.

Purpose: Accumulation of PIK3CA, ESR1, and GATA3 mutations results in resistance to endocrine therapy in breast cancer patients; however, the response of these genes to chemotherapy is unclear. Therefore, we sought to evaluate the genetic response of circulating tumor DNA (ctDNA) to chemotherapy in metastatic breast cancer patients.

Methods: The mutation frequency of 1021 genes was examined prior to chemotherapy in ctDNA of 44 estrogen receptor-positive metastatic breast cancer patients.