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Review
. 2021 Jul 23;9(8):876.
doi: 10.3390/biomedicines9080876.

TNBC: Potential Targeting of Multiple Receptors for a Therapeutic Breakthrough, Nanomedicine, and Immunotherapy

Desh Deepak Singh  1 , Dharmendra Kumar Yadav  2
Affiliations
Review

TNBC: Potential Targeting of Multiple Receptors for a Therapeutic Breakthrough, Nanomedicine, and Immunotherapy

Desh Deepak Singh et al. Biomedicines. .

Abstract

Triple-negative breast cancer (TNBC) is a heterogeneous, recurring cancer associated with a high rate of metastasis, poor prognosis, and lack of therapeutic targets. Although target-based therapeutic options are approved for other cancers, only limited therapeutic options are available for TNBC. Cell signaling and receptor-specific targets are reportedly effective in patients with TNBC under specific clinical conditions. However, most of these cancers are unresponsive, and there is a requirement for more effective treatment modalities. Further, there is a lack of effective biomarkers that can distinguish TNBC from other BC subtypes. ER, PR, and HER2 help identify TNBC and are widely used to identify patients who are most likely to respond to diverse therapeutic strategies. In this review, we discuss the possible treatment options for TNBC based on its inherent subtype receptors and pathways, such as p53 signaling, AKT signaling, cell cycle regulation, DNA damage, and programmed cell death, which play essential roles at multiple stages of TNBC development. We focus on poly-ADP ribose polymerase 1, androgen receptor, vascular endothelial growth factor receptor, and epidermal growth factor receptor as well as the application of nanomedicine and immunotherapy in TNBC and discuss their potential applications in drug development for TNBC.

Keywords: clinical trial; signaling pathway; therapeutic target; triple-negative breast cancer.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Molecular classification of breast cancer.
Figure 2
Figure 2
Classification of triple-negative breast cancer.
Figure 3
Figure 3
Representation of TNBC-associated molecular targets and their small molecule inhibitors. The arrows represent excitatory regulation, Reversible arrows represent reversible effect of regulation and the headed line arrows represent inhibitory effects.
Figure 4
Figure 4
Expression of PARP via Caspase predicts good chemotherapy response and poor survival for patients with TNBC.
Figure 5
Figure 5
The mechanism of PARP inhibitors is synthetic lethality in homologous recombination DNA repair (HRR) deficient cells. The molecular mode of action of poly (ADP ribose) polymerase inhibitors in chemosensitization and radiosensitization.
Figure 6
Figure 6
Immunotherapy agents in triple-negative breast cancer.
See this image and copyright information in PMC

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