Triple-negative breast cancer (TNBC) is a subtype of breast cancer (BC) with the most aggressive phenotype and poor overall survival. Using bioinformatics tools, we identified LINC00908 encoding a 60-aa polypeptide and differentially expressed in TNBC tissues. We named this endogenously expressed polypeptide ASRPS (a small regulatory peptide of STAT3). ASRPS expression was down-regulated in TNBCs and associated with poor overall survival. We showed that LINC00908 was directly regulated by ERα, which was responsible for the differential down-regulation of LINC00908 in TNBCs. ASRPS directly bound to STAT3 through the coiled coil domain (CCD) and down-regulated STAT3 phosphorylation, which led to reduced expression of VEGF. In human endothelial cells, a mouse xenograft breast cancer model, and a mouse spontaneous BC model, ASRPS expression reduced angiogenesis. In a mouse xenograft breast cancer model, down-regulation of ASRPS promoted tumor growth, and ASRPS acted as an antitumor peptide. We presented strong evidence that LINC00908-encoded polypeptide ASRPS represented a TNBC-specific target for treatment.

/pdf/lncrna-encoded-polypeptide-asrps-inhibits-triple-negative-26bdznunfp.pdf

LncRNA-encoded polypeptide ASRPS inhibits triple-negative breast cancer angiogenesis.

Micro-RNA: The darkhorse of cancer.

MicroRNA biogenesis, gene silencing mechanisms and role in breast, ovarian and prostate cancer.

Nanoparticle Drug Delivery Systems and Their Applications as Targeted Therapies for Triple Negative Breast Cancer

Increasing evidence has confirmed the vital roles of circular RNAs (CircRNAs) in the drug resistance of breast cancer (BC). Herein, we intended to study the effect of circular RNA FAT atypical cadherin 1 (circFAT1) on BC oxaliplatin (OX) resistance and find out the potential molecular mechanism in it. In this study, mRNA and protein levels of genes were measured by RT-qPCR and western blotting, respectively. Luciferase reporter assay confirmed the relationship between microRNA-525-5p (miR-525-5p) and circFAT1 or spindle and kinetochore-associated complex subunit 1 (SKA1). CCK-8, transwell, and flow cytometry experiments were utilized to investigate the chemosensitivity, migration, invasion, and apoptosis of BC cells. Gene Set Enrichment Analysis (GSEA) was applied to discover possible pathways related to SKA1. It was uncovered that circFAT1 was overexpressed in OX-resistant BC tissues and cells. Functional experiments showed that circFAT1 depletion reduced the level of chemoresistance-related genes. Moreover, circFAT1 knockdown remarkably facilitated apoptosis and decreased OX (half-maximal inhibitory concentration) IC50 value, migration, and invasion in OX-resistant BC cells. It was identified that miR-525-5p directly targeted circFAT1 and SKA1. Besides, rescue assays exhibited that circFAT1 promoted OX resistance in BC cells via the miR-525-5p/SKA1 regulatory network. Furthermore, GSEA and western blotting identified that SKA1 activated the Notch and Wnt pathway in OX-resistant BC cells. In conclusion, our results demonstrated that circFAT1 conferred OX resistance in BC by regulating the miR-525-5p/SKA1 via the Notch and Wnt pathway, providing a potential therapeutic target for patients with OX-resistant BC.

Circular RNA FAT atypical cadherin 1 (circFAT1)/microRNA-525-5p/spindle and kinetochore-associated complex subunit 1 (SKA1) axis regulates oxaliplatin resistance in breast cancer by activating the notch and Wnt signaling pathway.

https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/1878-0261.13180

Autophagy inhibits cancer stemness in triple‐negative breast cancer via miR‐181a‐mediated regulation of ATG5 and/or ATG2B

Checkpoint kinase 1 (Chk1) expression is enhanced in most cancers owing to oncogenic activation and constant replicative stress. Chk1 inactivation is a promising cancer therapy, as its inactivation leads to genomic instability, chromosomal catastrophe, and cancer cell death. Herein, we observed that miR-320c, downregulated in triple-negative breast cancer (TNBC) patients, can target Chk1. In addition, downregulated miR-320c expression was associated with poor overall survival in TNBC patients. As Chk1 was associated with the DNA damage response (DDR), we investigated the effect of miR-320c on DDR in TNBC cells. To induce DNA damage, we used platinum-based drugs, especially oxaliplatin, which is most effective with miR-320c. We observed that overexpression of miR-320c in TNBC regulated the oxaliplatin responsiveness by mediating DNA damage repair through the negative regulation of Chk1 in vitro. Furthermore, using a xenograft model, a combination of miR-320c mimic and oxaliplatin effectively inhibited tumor progression. These investigations indicate the potential of miR-320c as a marker of oxaliplatin responsiveness and a therapeutic target to increase the efficacy of chemotherapy in TNBC.

/pdf/inhibition-of-chk1-by-mir-320c-increases-oxaliplatin-3f8d8hxps5.pdf

Inhibition of Chk1 by miR-320c increases oxaliplatin responsiveness in triple-negative breast cancer

Abstract Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer; however, specific prognostic biomarkers have not yet been developed. In this study, we identified dysregulated microRNAs (miRNAs) in TNBC by profiling miRNA and mRNA expression. In patients with TNBC, miR-371b-5p expression was reduced, and miR-371b-5p overexpression significantly mitigated TNBC cell growth, migration, and invasion. In addition, we found that expression of cold shock domain-containing protein E1 (CSDE1), a direct target gene of miR-371b-5p, was upregulated in TNBC cells, and inhibition of CSDE1 expression alleviated TNBC cell growth by regulating RAC1 transcription. Mechanistically, CSDE1, phosphorylated C-terminal domain (p-CTD) of RNA polymerase II (RNAPII), and CDK7 form a complex, and downregulation of CSDE1 leads to weak interaction between RNAPII p-CTD and CDK7, resulting in a decrease in RNAPII p-CTD expression to reduce RAC1 transcript levels in CSDE1-deficient TNBC cells. Our data demonstrate that miR-371b-5p is a tumor-suppressive miRNA that regulates the CSDE1/Rac1 axis and could be a potential prognostic biomarker for TNBC. 

/pdf/reduced-mir-371b-5p-expression-drives-tumor-progression-via-8d98t1y2.pdf

Reduced miR-371b-5p expression drives tumor progression via CSDE1/RAC1 regulation in triple-negative breast cancer

miR-374a-5p promotes tumor progression by targeting ARRB1 in triple negative breast cancer.

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Autophagy inhibits cancer stemness in triple‐negative breast cancer via miR‐181a‐mediated regulation of ATG5 and/or ATG2B

Inhibition of Chk1 by miR-320c increases oxaliplatin responsiveness in triple-negative breast cancer

Reduced miR-371b-5p expression drives tumor progression via CSDE1/RAC1 regulation in triple-negative breast cancer

miR-374a-5p promotes tumor progression by targeting ARRB1 in triple negative breast cancer.