Open Access Journal of Gynecology (OAJG)

ISSN: 2474-9230

Review Article

Novel Ways of Targeting Triple Negative Breast Cancer (TNBC) with the Latest Research-will it Improve Prognoses

Authors: Kulvinder Kochar Kaur*, Allahbadia GN and Singh M

DOI: 10.23880/oajg-16000185

Abstract

Breast Cancer, is the commonest malignancy that gets diagnosed in women, leading to the greatest cancer associated deaths all over the world. Triple negative breast cancer (TNBC) refers to the absence of estrogen, progesterone and HER2 receptors, possesses an aggressive clinical nature, having the high metastases rates. Thus here in this review we have tried to study the mechanism responsible for the high metastases rates by studying the role of Haematopoietic protein tyrosine phosphatases (HePTP) which had a crucial role in metastases of TNBC through activation of Wnt/β-catenin signaling. Further we examined, how certain regional anesthetics like ropivacaine and levobupivacaine had a protective effect in BC, roles of some novel therapies like those combining embelin (EMB)/TRAIL-HA(hyaluronic acid)/ poly(1,6- hexanediol )-diacrylate –β-5-hydroxyamylamine(PBAE)-polyethylamine (PEI) as cytotoxix and proapoptotic agents against TNBC, how regulation of miR 122-5p that causes aggression via epithelial mesenchymal transition(EMT) in TIMC via suppression of charged multivesicular body protein 3(CHMP3)through MAPK signaling might help in controlling TNBC. Further combining thiosemicarbazone compound 4 with cisplatin increased p53 phosphorylation, along with Bax level induction, as well as a decreased Bcl2 protein amounts ,increased PARP cleavage and modulated miR expression levels in TNBCs with special overexpression of miR-125a-5p ,and miR-181a-5p and thus role of miR control utilization by other way by thiosemicarbazone compound 4 targeting TNBC apoptosis might be utilized. Moreover how combining Src inhibitor dasatinib, with the PARP inhibitor veliparib, and the DNA damaging drug carboplatin in TNBC might prove effective in TNBC. Further role of DDB2 in causing resistance to PARP, combination of PARP with metabolic inhibitors is discussed. Additionally liposomes modified by fructose and RGD had >potential for forming a targeted TNBC therapy, particularly the covalently modified Fru-RGD–Lip, marking them as good liposomes having multiple functions. Thus novel therapies for TNBC which might help in developing novel therapies further for controlling TNBC has been emphasized.

Keywords: TNBC; mIR 122-5p; miR-125a-5p and miR-181a-5p; Thiosemicarbazone Compound 4; HePTP; Dasatinib

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