SIGNIFICANCE: These findings identify Rab7 as a substrate for TBK1 for regulation of innate immune signaling, thereby providing important insight for strategies aimed at manipulating the immune response to enhance therapeutic efficacy in TNBC.
In a previous work, we showed that in TNBC miR-210 is expressed in tumor cells and also in the tumor microenvironment (TME), particularly in inflammatory CD45-LCA positive cells.
In a previous work, we showed that in TNBC miR-210 is expressed in tumor cells and also in the tumor microenvironment (TME), particularly in inflammatory CD45-LCA positive cells.
Our research group as well as others previously identified ANCCA/ATAD2 as a putative oncogene and a poor prognosis factor in many types of cancer including triple‑negative breast cancer (TNBC).
Crosslinking of CD32A<sup>131R</sup> -CR on T cells by cetuximab or panitumumab and CD16<sup>158F</sup> -CR T cells by cetuximab induced elimination of triple negative breast cancer (TNBC) MDA-MB-468 cells, and the secretion of interferon gamma and tumor necrosis factor alpha.
For the first time, we report the close association between NCAPD2 and cancer and demonstrate that NCAPD2 plays an important role in TNBC progression and acts as an independent poor prognostic factor and a potential therapeutic target for TNBC.
Importantly, knockdown of combined p27 and FOXE3 reversed the DTX-induced cell growth inhibition observed upon FOXE3 knockdown, indicating that the FOXE3's effects on TNBC progression were mediated mainly through transcriptional regulation of the p27 signaling.
miR-122-5p promotes aggression and epithelial-mesenchymal transition in triple-negative breast cancer by suppressing charged multivesicular body protein 3 through mitogen-activated protein kinase signaling.
We identified a four-biomarker signature based on miR-221, miR-1305, miR-4708, and RMDN2 expression levels that allowed for the subdivision of TNBC into high- or low-risk groups (Hazard Ratio - HR=0.32; 95% Confidence Interval - CI = 0.11-0.91; p=0.03) and are also statistically associated with survival outcome in subgroups of postmenopausal status (HR=0.19; 95%CI = 0.04-0.90; p=0.016), node negative status (HR=0.12; 95%CI = 0.01-1.04; p=0.026), and tumors larger than 2cm (HR=0.21; 95%CI = 0.05-0.81; p=0.021).
The expression of VEGFA, VEGF receptor (VEGFR), matrix metalloproteinase (MMP)-2, MMP-9, Delta-like ligand 4 (DLL4) and Integrin-5 was significantly reduced in TNBC tumor tissues.
Bio-Field Array: The Influence of Junction Mediating and Regulatory Protein Expression on Cytoskeletal Filament Behavior During Apoptosis in Triple-Negative Breast Cancer.
Additionally, the expression of semaphorin 3A (Sema3A) and nerve growth factor receptor (NGFR) p75 in TNBC tissue was significantly upregulated in response to electroacupuncture.
Serum levels of sPD-1 and sPD-L1 could be used as noninvasive biomarkers for evaluating the malignancy of TNBC before NAC and for predicting the NAC response in TNBC patients.