Long non-coding RNAs as novel prognostic biomarkers for breast cancer in Egyptian women

El-Helkan, Basma; Emam, Manal A.; Mohanad, Marwa; Fathy, Shadia A.; Zekri, Abdel‐Rahman N.; Ahmed, Ola

doi:10.1038/s41598-022-23938-8

Cited by 6 publications

(14 citation statements)

References 56 publications

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“…Dysregulation and deficiency, or mutations of LncRNAs, have been reported in complex diseases 7 – 9 , including BC cancer 10 . Depending on their functions and pattern of expression, they can be divided into tumor suppressors and oncogene classes 11 .…”

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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“…Furthermore, UCA1 concentrations were measured to be even more elevated in the blood samples of patients in advanced stages, and women with lymph node and distant organ metastatic disease [ 4 , 5 ]. Nonetheless, one study found that UCA1 levels were not significantly correlated with clinicopathological characteristics, whereas another study proposed that UCA1 expression was reduced in left-sided MBC tumors, suggesting a potential correlation between UCA1 levels and laterality in MBC patients [ 2 , 30 ]. Almost all studies identified overexpressed UCA1 levels in BC tissues compared to the healthy ones, while additionally revealing the remarkable association of high UCA1 levels with short overall survival and advanced clinical stage disease [ 31 , 32 , 34 , 35 , 37 , 38 , 40 , 41 ].…”

Section: Discussionmentioning

confidence: 99%

“…Of note, El-Helkan et al found the UCA1 expression to be markedly upregulated in the plasma of non-metastatic BC (NMBC) patients, while also discovering the considerable downregulation of UCA1 in left breast tumors of metastatic BC patients (MBC), indicating its significant association with laterality in MBC [ 2 ].…”

Section: The Role Of Uca1 In Bc Oncogenesis Proliferation and Invasionmentioning

confidence: 99%

“…Mammography and breast examination represent the two main screening methods for BC. Histopathological examination of tumor biopsies represents the gold standard for diagnosis [ 2 ]. The latest research proves that about 70% of all cases are estrogen receptor-positive (ER+), whereas triple-negative BC (TNBC), lacking estrogen receptors, progesterone receptors (PR), and the human epidermal growth factor receptor 2 (Her2), constitute 10–20% of BC cases [ 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

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The Role of Urothelial Cancer-Associated 1 in Gynecological Cancers

Nousiopoulou,

Vrettou,

Damaskos

et al. 2024

CIMB

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Gynecological cancers (GC) represent some of the most frequently diagnosed malignancies in women worldwide. Long-non-coding RNAs (lncRNAs) are regulatory RNAs increasingly being recognized for their role in tumor progression and metastasis in various cancers. Urothelial cancer-associated 1 (UCA1) is a lncRNA, first found deregulated in bladder cancer, and many studies have exposed its oncogenic effects in more tumors since. However, the role of UCA1 in gynecological malignancies is still unclear. This review aims to analyze and define the role of UCA1 in GC, in order to identify its potential use as a diagnostic, prognostic, or therapeutic biomarker of GC. By employing the search terms “UCA1”, “breast cancer”, “endometrial cancer”, “ovarian cancer”, “cervical cancer”, “vaginal cancer”, and “vulvar cancer” in the PubMed database for the literature review, we identified a total of sixty-three relevant research articles published between 2014 and 2024. Although there were some opposing results, UCA1 was predominantly found to be upregulated in most of the breast, endometrial, ovarian, cervical, and vulvar cancer cells, tissue samples, and mouse xenograft models. UCA1 overexpression mainly accounts for enhanced tumor proliferation and increased drug resistance, while also being associated with some clinicopathological features, such as a high histological grade or poor prognosis. Nonetheless, no reviews were identified about the involvement of UCA1 in vaginal carcinogenesis. Therefore, further clinical trials are required to explore the role of UCA1 in these malignancies and, additionally, examine its possible application as a target for upcoming treatments, or as a novel biomarker for GC diagnosis and prognosis.

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“…Since the deregulation of gene expression is an important event in carcinogenesis, it has been suggested that a signi cant proportion of cancer risk may be attributed to transcribed LncRNAs from cancer-related loci 6 . Dysregulation and de ciency, or mutations of LncRNAs, have been reported in complex diseases [7][8][9] , including BC cancer 10 . Depending on their functions and pattern of expression, they can be divided into tumor suppressors and oncogene classes 11 .…”

Section: Introductionmentioning

confidence: 99%

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

Hajibabaei

Nafissi

Azimi

et al. 2022

Preprint

View full text Add to dashboard Cite

Non-coding RNAs, including Inc-RNA and miRNA, had been reported to regulate gene expression and were 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) has also been demonstrated to promote malignancy in various cancer, 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, 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.

show abstract

Long non-coding RNAs as novel prognostic biomarkers for breast cancer in Egyptian women

Cited by 6 publications

References 56 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

The Role of Urothelial Cancer-Associated 1 in Gynecological Cancers

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

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