microRNA triggered drug release in triplenegativebreast cancer (TNBC) therapy

سال انتشار: 1402
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 145

نسخه کامل این مقاله ارائه نشده است و در دسترس نمی باشد

استخراج به نرم افزارهای پژوهشی:

لینک ثابت به این مقاله:

شناسه ملی سند علمی:

CGC01_213

تاریخ نمایه سازی: 29 آبان 1402

چکیده مقاله:

Background: Triple-negative breast cancer (TNBC) accountsfor ۱۰-۱۵% of all breast cancer and is the most aggressive malignanttumor, with poor prognosis, and high mortality, whichmakes it unresponsive to current therapies.Materials and Methods: In this review, we queried PubMed,Scopus, and Web of Science databases in miRNA relation withTNBC prognosis and drug resistance. The articles that addressedthese domains were included; data were qualitativelysummarized.Results: Many therapeutic strategies are used for the TNBC,including surgery, radiation therapy, chemotherapy, targetingangiogenesis vascular endothelial growth factor, an inhibitorof immune checkpoint programmed cell death ligand ۱ (PDL۱),poly (ADP-ribose) polymerase inhibitors and secretions ofexosomes. Considering that chemotherapy-resistant drugs, themost common of which include doxorubicin, paclitaxel, docetaxel,and epirubicin, are one of the factors in failure of TNBCtreatment, it was found that non-coding RNAs such as longnon-coding RNAs (lncRNAs) and circular RNAs (circRNAs)and microRNAs (miRNAs) are involved in these resistances.miRNAs regulation plays important roles in TNBC, includingtumor progression, poor prognosis, stimulated proliferation, invasion,migration, apoptosis, cell cycle progression, DNA repair,rapid relapse, low overall survival rates, positive lymphnodes, autophagy, epithelial-mesenchymal transition (EMT),metastasis, and particularly drug sensitivity and resistance. Accordingly,miR-۳۰۲b/SNHG۱۰ axis, miR-۱۲۰۵/DNAJB۱axis,and miR-۱۰۱ regulated doxorubicin, docetaxel, and paclitaxelresistance in TNBC, respectively. So, microRNA-containingnanoparticles are more efficient than singular release. Sincesignaling pathways including WNT, TGF-β۱/SMAD۳, NF-κB,EGFR/PI۳K/Akt, PI۳K/Akt/mTOR and Notch play an importantrole in recurrence of TNBC. The regulation of signalingpathways by tumor suppressor miRNAs was also identified.Conclusion: Overcoming TNBC therapy resistance is a significantchallenge. We investigate the role and therapeutic functionof miRNAs in TNBC drug resistance. miRNA linked to TNBCcan be targeted in future as a novel anticancer target of TNBC,offering a promising technique for susceptibility to inhibitionof drug.

نویسندگان

Fatemeh Nejatifar

Assistant professor، hematology and medical oncology department, Guilan University of Medical Sciences,Rasht,Iran

Sogand Vahidi

Medical Biology Research Center, Kermanshah University ofMedical Sciences, Kermanshah, Iran

Bahar Jamaldar

Medical student, Guilan university of medical sciences,Rasht,Iran

Hannaneh Bakhshesh

Medical student, Guilan university of medical sciences,Rasht,Iran

Mahshid Taslimi

Medical student, Guilan university of medical sciences,Rasht,Iran