The Long Non-Coding RNA XIST: A New Cornerstone in Carcinogenesis

Samir, A.; Salama, Esraa A.; Hm, El-Tayebi

doi:10.4172/1747-0862.1000356

Cited by 4 publications

(3 citation statements)

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“…lncRNAs represent ideal candidates as novel BC immune biomarkers due to their stability and their massive involvement in BC carcinogenesis (24,25,(36)(37)(38). A mounting body of evidence highlighted different contributing roles of the lncRNA XIST either as an oncogene or as a tumor suppressor gene in diverse cancers (39)(40)(41)(42)(43). Nonetheless, limited evidence displayed lncRNA XIST involvement as a tumor suppressor lncRNA in BC (28,29) in addition to the absence of concerns regarding lncRNA TSIX, the negative regulator of lncRNA XIST in BC.…”

Section: Discussionmentioning

confidence: 99%

XIST and TSIX: Novel Cancer Immune Biomarkers in PD-L1-Overexpressing Breast Cancer Patients

2020

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Escaping antitumor immunity is a hallmark in cancer progression. Programmed cell death protein 1 (PD-1) is an immune checkpoint receptor responsible for the maintenance of immune tolerance; PD-1 ligand (PD-L1) is overexpressed in tumor cells, simplifying their escape from the immune system through T-cell function suppression. Notwithstanding that cancer antigen (CA)125, carcinoembryonic antigen (CEA), CA15-3, and alpha-fetoprotein (AFP) are among conventional breast cancer diagnostic biomarkers, their lack of sensitivity and specificity resides among their major limitations. Furthermore, human epidermal growth factor receptor (HER)2 and interleukin (IL)-6-demonstrated as breast cancer immune biomarkers-still possess limitations, for instance, technical detection problems and stability problems, which necessitate the discovery of novel, stable non-invasive cancer immune biomarkers. XIST and TSIX are two long non-coding (lnc)RNAs possessing a role in X chromosome inactivation (XCI) as well as in breast cancer (BC). In the present study, they were investigated as stable non-invasive breast cancer immune biomarkers. The study demonstrated that PD-L1 was overexpressed in the different molecular subtypes of breast cancer patients as well as in MDA-MB-231 cells. Furthermore, lncRNAs XIST and TSIX were markedly increased in the tissues, lymph nodes, and different body fluids of breast cancer patients compared to controls. In addition, XIST and TSIX were differentially expressed in subtypes of BC patients, and their levels were correlated to PD-L1 expression level. In conclusion, this correlative study has shed light on the role of both lncRNAs XIST and TSIX as potential non-invasive BC immune biomarkers reflecting the evaded immune system of the patient and overcoming the instability problem of common BC biomarkers.

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Section: Discussionmentioning

confidence: 99%

XIST and TSIX: Novel Cancer Immune Biomarkers in PD-L1-Overexpressing Breast Cancer Patients

2020

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“…274). LncRNA XIST has been extensively studied by our research group (Refs 275, 276). LncRNA XIST acted as a tumour suppressor where it was downregulated in BC tissues (Ref.…”

Section: Non-coding Rna and Inflammasomes In Breast Cancermentioning

confidence: 99%

“…LncRNA XIST acted as a tumour suppressor where it was downregulated in BC tissues (Ref. 275) and was able to suppress PD-L1 expression in MDA-MB231 cells (Refs 275, 276). In addition, PD-L1-overexpressing BC patients as well as TNBC cell lines showed an inverse correlation with low levels of XIST, where XIST was described as non-invasive cancer immune biomarker for anti-PD-L1 personalised therapy (Ref.…”

Section: Non-coding Rna and Inflammasomes In Breast Cancermentioning

confidence: 99%

Inflammasomes in breast cancer: the ignition spark of progression and resistance?

Elgohary

Tayebi

2023

Expert Rev. Mol. Med.

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Inflammation and immune evasion are major key players in breast cancer (BC) progression. Recently, the FDA approved the use of anti-programmed death-ligand 1 antibody (anti-PD-L1) and phosphoinositide 3-kinase (PI3K) inhibitors against aggressive BC. Despite the paradigm shift in BC treatments, patients still suffer from resistance, recurrence and serious immune-related adverse events. These obstacles require unravelling of the hidden molecular contributors for such therapy failure hence yielding therapeutics that are at least as efficient yet safer. Inflammasome pathway is activated when the pattern recognition receptor senses danger signals (danger-associated molecular patterns) from damagedRdying cells or pathogen-associated molecular patterns found in microbes, leading to secretion of the active pro-inflammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18). It has been shown throughout numerous studies that inflammasome pathway enhanced invasion, metastasis, provoked BC progression and therapy resistance. Additionally, inflammasomes upregulated the proliferative index ki67 and enhanced PD-L1 expression leading to immunotherapy resistance. IL-1β contributed to significant decrease in oestrogen receptor levels and promoted BC chemo-resistance. High levels of IL-18 in sera of BC patients were associated with worst prognosis. Stimulation of purinergic receptors and modulation of adipokines in obese subjects activated inflammasomes that evoked radiotherapy resistance and BC progression. The micro RNA miR-223-3p attenuated the inflammasome over-expression leading to lowered tumour volume and lessened angiogenesis in BC. This review sheds the light on the molecular pathways of inflammasomes and their impacts in distinct BC subtypes. In addition, it highlights novel strategies in treatment and prevention of BC.

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