Lung cancer is one of the most common malignant neoplasms worldwide. CD24 is a marker of tumor stem cells that plays an important role in tumorigenesis. Hsp70 is an important molecular chaperone. However, the co-expression and interaction of CD24 and Hsp70, as well as the significance for the prognosis of lung cancer are still unclear. The expression levels of CD24 and Hsp70 were detected by immunohistochemistry and their correlation was analyzed. The expression levels of CD24 mRNA and protein were examined using qRT-PCR and western blotting in SPCA1, A549, H1975, and H1650 cell lines. A CD24-overexpressing cell model was established. The interaction betwee n CD24 and Hsp70 was verified by co-immunoprecipitation and western blotting. CD24 and Hsp70 expression were significantly higher in lung cancer tissues than in adjacent tissues (CD24: P = 0.008; Hsp70: P < 0.001). CD24 protein expression showed a positive correlation with lymph node metastasis, TNM stage, and vascular cancer thrombus. Hsp70 protein expression showed a positive correlation with differentiation, lymph node metastasis, and TNM stage. CD24 and Hsp70 high expression were also correlated with poor survival. The positive co-expression rate of CD24 and Hsp70 in lung cancer tissues was 52.7% (49/93). CD24 and Hsp70 expression in lung cancer were positively correlated (r = 0.368, P < 0.001), and co-immunoprecipitation was verified that both endogenous and exogenous CD24 co-precipitated with Hsp70 directly or indirectly. When Hsp70 inhibitor 17-AAG was added to A549 cells, Hsp70 and CD24 protein expression were significantly decreased. The present study demonstrated that CD24 and Hsp70 were highly expressed in lung cancer tissues, and associated with invasion, metastasis, and poor survival. Hsp70 may regulate CD24 expression. Co-expression of CD24 and Hsp70 may be a prognostic biomarker for lung cancer.

Jagged canonical Notch ligand 1 (JAG1) regulates the progression of many cancers by the Notch signaling pathway, but its role in breast cancer (BC) remains unclear. In this research, JAG1 protein expression in BC tissues was detected by immunohistochemistry. The association between JAG1 and clinical significance was analyzed. The effect of JAG1 on malignant behaviors of BC cells was demonstrated by in vitro experiments. JAG1 expression in BC tissues was higher than that in para-carcinoma tissues. High JAG1 expression was significantly linked to advanced lymph node metastasis, distant metastasis, and the TNM stage. JAG1 was an independent prognostic factor for BC patients. JAG1 knockdown inhibited the proliferation, motility, migration, and invasion of BC cells, and weakened adhesion and penetration abilities to the blood–brain barrier, whereas JAG1 overexpression had the opposite effects. JAG1 has the potential to be a prognostic marker and therapeutic target for BC patients.

Background Alterations in genes encoding chromatin regulatory proteins are prevalent in cancers and may confer oncogenic properties and molecular changes linked to therapy resistance. However, the impact of copy number alterations (CNAs) of the SWItch/Sucrose NonFermentable (SWI/SNF) complex on the oncogenic and immunologic properties has not been systematically explored across human cancer types. Methods We comprehensively analyzed the genomic, transcriptomic and clinical data of The Cancer Genome Atlas (TCGA) dataset across 33 solid cancers. Results CNAs of the SWI/SNF components were identified in more than 25% of all queried cancers, and tumors harboring SWI/SNF CNAs demonstrated a worse overall survival (OS) than others in several cancer types. Mechanistically, the SCNA events in the SWI/SNF complex are correlated with dysregulated genomic features and oncogenic pathways, including the cell cycle, DNA damage and repair. Notably, the SWI/SNF CNAs were associated with homologous recombination deficiency (HRD) and improved clinical outcomes of platinum-treated ovarian cancer. Furthermore, we observed distinct immune infiltrating patterns and immunophenotypes associated with SWI/SNF CNAs in different cancer types. Conclusion The CNA events of the SWI/SNF components are a key process linked to oncogenesis, immune infiltration and therapeutic responsiveness across human cancers.

Jagged canonical Notch ligand 1 (JAG1) regulates the progression of many cancers by the Notch signaling pathway, but its role in breast cancer (BC) remains unclear. In this research, JAG1 protein expression in BC tissues was detected by immunohistochemistry. The association between JAG1 and clinical significance was analyzed. The effect of JAG1 on malignant behaviors of BC cells was demonstrated by in vitro experiments. JAG1 expression in BC tissues was higher than that in para-carcinoma tissues. High JAG1 expression was significantly linked to advanced lymph node metastasis, distant metastasis, and the TNM stage. JAG1 was an independent prognostic factors for BC patients. JAG1 knockdown inhibited the proliferation, motility, migration, and invasion of BC cells, and weakened adhesion and penetration abilities to the blood–brain barrier, whereas JAG1 overexpression had the opposite effects. JAG1 has the potential to be a prognostic marker and therapeutic target for BC patients.