Innovative targets of the lncRNA-miR-mRNA network in response to low-dose aspirin in breast cancer patients

Alipour, Sadaf; Khalighfard, Solmaz; Khori, Vahid; Amiriani, Taghi; Tajaldini, Mahboubeh; Dehghan, Mohammad Hossein; Sadani, Somayeh; Omranipour, Ramesh; Vahabzadeh, Gelareh; Eslami, Bita; Alizadeh, Ali Mohammad

doi:10.1038/s41598-022-16398-7

Cited by 6 publications

(6 citation statements)

References 63 publications

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“…Depending on their functions and pattern of expression, they can be divided into tumor suppressors and oncogene classes 11 . In addition, growing exploratory evidence supports the idea that LncRNAs function as competitive endogenous RNAs (ceRNAs), which compete for microRNA (miRNA) binding to their upregulated target genes 12 . The ceRNA theory can critically help to understand and identify the function of lncRNA 13 .…”

Section: Introductionmentioning

confidence: 99%

Targeting long non-coding RNA MALAT1 reverses cancerous phenotypes of breast cancer cells through microRNA-561-3p/TOP2A axis

Hajibabaei

Nafisi

Azimi

et al. 2023

Sci Rep

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Non-coding RNAs, including Inc-RNA and miRNA, have been reported to regulate gene expression and are associated with cancer progression. MicroRNA-561-3p (miR-561-3p), as a tumor suppressor, has been reported to play a role in preventing cancer cell progression, and MALAT1 (Lnc-RNA) have also been demonstrated to promote malignancy in various cancers, such as breast cancer (BC). In this study, we aimed to determine the correlation between miR-561-3p and MALAT1 and their roles in breast cancer progression. The expression of MALAT1, mir-561-3p, and topoisomerase alpha 2 (TOP2A) as a target of miR-561-3p was determined in BC clinical samples and cell lines via qRT-PCR. The binding site between MALAT1, miR-561-3p, and TOP2A was investigated by performing the dual luciferase reporter assay. MALAT1 was knocked down by siRNA, and cell proliferation, apoptotic assays, and cell cycle arrest were evaluated. MALAT1 and TOP2A were significantly upregulated, while mir-561-3p expression was downregulated in BC samples and cell lines. MALAT1 knockdown significantly increased miR-561-3p expression, which was meaningfully inverted by co-transfection with the miR 561-3p inhibitor. Furthermore, the knockdown of MALAT1 by siRNA inhibited proliferation, induced apoptosis, and arrested the cell cycle at the G1 phase in BC cells. Notably, the mechanistic investigation revealed that MALAT1 predominantly acted as a competing endogenous RNA in BC by regulating the miR-561-3p/TOP2A axis. Based on our results, MALAT1 upregulation in BC may function as a tumor promoter in BC via directly sponging miRNA 561-3p, and MALAT1 knockdown serves a vital antitumor role in BC cell progression through the miR-561-3p/TOP2A axis.

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Section: Introductionmentioning

confidence: 99%

Targeting long non-coding RNA MALAT1 reverses cancerous phenotypes of breast cancer cells through microRNA-561-3p/TOP2A axis

Hajibabaei

Nafisi

Azimi

et al. 2023

Sci Rep

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“…Peripheral blood cells of invasive BC patients produced high levels of IL-1β, leading to metastasis [ 69 ]. In sera and plasma of BC patients, ELISA findings showed that IL-β expressions were significantly increased compared to those in the control group [ 70 , 71 ]. Remarkably, IL-1β is secreted via not only the inflammasome pathway [ 143 ], but also NF-κB [ 115 , 116 ] which is activated via extracellular ATP [ 147 ] and the purinergic receptor P2X7R [ 148 ].…”

Section: Discussionmentioning

confidence: 99%

“…In patients with invasive BC, IL-1β production by peripheral blood cells was associated with lymphatic metastasis [ 69 ]. Enzyme-linked immunosorbent assay (ELISA) findings showed that IL-β expressions were significantly increased in the sera and plasma of BC patients compared to the control group [ 70 , 71 ] and were related to tumor size, clinical stage, histological grade, and lymph node metastasis [ 70 ]. In addition, patients with metastatic BC exhibited an increased production of IL-1β compared to patients with early BC [ 72 ].…”

Section: Introductionmentioning

confidence: 99%

Thymoquinone, a Novel Multi-Strike Inhibitor of Pro-Tumorigenic Breast Cancer (BC) Markers: CALR, NLRP3 Pathway and sPD-L1 in PBMCs of HR+ and TNBC Patients

Elgohary,

Eissa,

El Tayebi

2023

IJMS

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Breast cancer (BC) is not only a mass of malignant cells but also a systemic inflammatory disease. BC pro-tumorigenic inflammation has been shown to promote immune evasion and provoke BC progression. The NOD-like receptor (NLR) family pyrin domain-containing protein 3 (NLRP3) inflammasome is activated when pattern recognition receptors (PRRs) sense danger signals such as calreticulin (CALR) from damaged/dying cells, leading to the secretion of interleukin-1β (IL-1β). CALR is a novel BC biological marker, and its high levels are associated with advanced tumors. NLRP3 expression is strongly correlated with an elevated proliferative index Ki67, BC progression, metastasis, and recurrence in patients with hormone receptor-positive (HR+) and triple-negative BC (TNBC). Tumor-associated macrophages (TAMs) secrete high levels of IL-1β promoting endocrine resistance in HR+ BC. Recently, an immunosuppressive soluble form of programmed death ligand 1 (sPD-L1) has been identified as a novel prognostic biomarker in triple-negative breast cancer (TNBC) patients. Interestingly, IL-1β induces sPD-L1 release. BC Patients with elevated IL-1β and sPD-L1 levels show significantly short progression-free survival. For the first time, this study aims to investigate the inhibitory impact of thymoquinone (TQ) on CALR, the NLRP3 pathway and sPD-L1 in HR+ and TNBC. Blood samples were collected from 45 patients with BC. The effect of differing TQ concentrations for different durations on the expression of CALR, NLRP3 complex components and IL-1β as well as the protein levels of sPD-L1 and IL-1β were investigated in the peripheral blood mononuclear cells (PBMCs) and TAMs of TNBC and HR+ BC patients, respectively. The findings showed that TQ significantly downregulated the expression of CALR, NLRP3 components and IL-1β together with the protein levels of secreted IL-1β and sPD-L1. The current findings demonstrated novel immunomodulatory effects of TQ, highlighting its potential role not only as an excellent adjuvant but also as a possible immunotherapeutic agent in HR+ and TNBC patients.

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“…The qRT-PCR reactions were performed with an ABI StepOne Plus System (Applied Biosystems; Thermo Fisher Scientific, Inc.). The expression level of the genes was calculated according to the 2−ΔΔCT method 54 .…”

Section: Methodsmentioning

confidence: 99%

Low-frequency magnetic fields potentiate plasma-modified magneto-electric nanoparticle drug loading for anticancer activity in vitro and in vivo

Mahdikia,

Saadati,

Alizadeh

et al. 2023

Sci Rep

Self Cite

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A multiferroic nanostructure of manganese ferrite barium-titanate called magneto-electric nanoparticles (MENs) was synthesized by a co-precipitation method. FTIR, Raman spectroscopy, TEM, and X-ray diffraction confirmed the presence of spinel core and perovskite shell phases with average crystallite sizes of 70–90 nm. Magnetic, optical, and magnetoelectrical properties of MENs were investigated using VSM, UV-Vis spectrophotometry, DLS, and EIS spectroscopy techniques. After pre-activation by low-pressure argon (Ar) plasma, the MENs were functionalized by a highly hydrophilic acrylic acid and Oxygen (AAc+O2) mixture to produce COOH and C=O-rich surfaces. The loading and release of doxorubicin hydrochloride (DOX) on MENs were investigated using UV-vis and fluorescence spectrophotometry under alternating low-frequency magnetic fields. Plasma treatment enabled drug-loading control by changing the particles’ roughness as physical adsorption and creating functional groups for chemical absorption. This led to reduced metabolic activity and cell adherences associated with elevated expression of pro-apoptotic genes (BCL-2, caspase 3) in 4T1 breast cancer cells in vitro exposed to alternating current magnetic field (ACMF) compared to MENs-DOX without field exposure. ACMF-potentiated anticancer effects of MENs were validated in vivo in tumor-bearing Balb/C mice. Altogether, our results suggest potentiated drug loading of MENs showing superior anticancer activity in vitro and in vivo when combined with ACMF.

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Innovative targets of the lncRNA-miR-mRNA network in response to low-dose aspirin in breast cancer patients

Cited by 6 publications

References 63 publications

Targeting long non-coding RNA MALAT1 reverses cancerous phenotypes of breast cancer cells through microRNA-561-3p/TOP2A axis

Targeting long non-coding RNA MALAT1 reverses cancerous phenotypes of breast cancer cells through microRNA-561-3p/TOP2A axis

Thymoquinone, a Novel Multi-Strike Inhibitor of Pro-Tumorigenic Breast Cancer (BC) Markers: CALR, NLRP3 Pathway and sPD-L1 in PBMCs of HR+ and TNBC Patients

Low-frequency magnetic fields potentiate plasma-modified magneto-electric nanoparticle drug loading for anticancer activity in vitro and in vivo

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