Long non‑coding RNA regulation of TRAIL in breast cancer: A tangle of non‑coding threads (Review)

Javed, Zeeshan; Khan, Khushbukhat; Iqbal, Masood; Ahmad, Touqeer; Raza, Qamar; Sadia, Haleema; Raza, Shahid; Salehi, Bahare; Sharifi‐Rad, Javad; Cho, William C.

doi:10.3892/ol.2020.11896

Cited by 5 publications

(6 citation statements)

References 144 publications

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“…In breast cancer, multiple lncRNAs played an important role in the regulation of TRAIL, like HOTAIR, NEAT1, BCAR4 and DSCAM-AS1 [ 18 ]. In hepatocellular carcinoma, the well-established tumor suppressive lncRNA of CASC2 could serve as a sponge of miR-24 and miR-221, and thus modulate TRAIL-induced tumor cell apoptosis [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA AC079630.4 expression associated with the progression and prognosis in lung cancer

Wang

Wen

2021

Aging

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Mounting evidence has demonstrated the important role of long non-coding RNAs (lncRNAs) in the development and progression of lung cancer. In this study, we combined the methods of bioinformatics analysis and experimental validation, and aim to investigate the clinical significance and underlying mechanism of the novel lncRNA AC079630.4 in lung cancer. Finally, we found that AC079630.4 was significantly down-regulated in lung cancer tissues, including in its subtypes. Samples with low AC079630.4 expression had a more advanced pathological stage and a worse prognosis than those with high expression. In functional prediction, the KEGG pathway of apoptosis and the TRAIL signaling pathway were enriched in the samples with high AC079630.4 expression. In experimental validation, AC079630.4 over-expression could significantly inhibit the proliferation and clonality, and up-regulated the receptors of TRAIL (TRAIL-R1 and TRAIL-R2) in lung cancer cells. In conclusion, we adopted the methods of bioinformatics analysis and experimental validation, and identified a novel lncRNA of AC079630.4 as a tumor suppressor in lung cancer.

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Section: Discussionmentioning

confidence: 99%

LncRNA AC079630.4 expression associated with the progression and prognosis in lung cancer

Wang

Wen

2021

Aging

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“…Subsequent processes include the activation of pro-caspases 8 and 10, followed by activation of caspase 3. The activation of caspase 3, in turn, leads to the activation of either the external pathway (mediated by caspase 8) or the internal pathway (release of cytochrome c and activation of caspase 9) [63].…”

Section: Trailmentioning

confidence: 99%

“…TRAIL induces apoptosis in triple-negative breast cancer cells with a mesenchymal but not an epithelial phenotype [65]. However, the effectiveness of the apoptotic action of TRAIL depends on many internal and external causes [63,66], and there is evidence that the effect of death receptors on apoptosis and cancer cell survival is ambiguous [66].…”

Section: Trailmentioning

confidence: 99%

Long Noncoding RNA GAS5 in Breast Cancer: Epigenetic Mechanisms and Biological Functions

Филиппова

Фридман

Burdennyy

et al. 2021

IJMS

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Long noncoding RNAs (lncRNAs) have been identified as contributors to the development and progression of cancer through various functions and mechanisms. LncRNA GAS5 is downregulated in multiple cancers and acts as a tumor suppressor in breast cancer. GAS5 interacts with various proteins (e.g., E2F1, EZH2, and YAP), DNA (e.g., the insulin receptor promoter), and various microRNAs (miRNAs). In breast cancer, GAS5 binds with miR-21, miR-222, miR-221-3p, miR-196a-5p, and miR-378a-5p that indicates the presence of several elements for miRNA binding (MREs) in GAS5. Mediated by the listed miRNAs, GAS5 is involved in the upregulation of a number of mRNAs of suppressor proteins such as PTEN, PDCD4, DKK2, FOXO1, and SUFU. Furthermore, the aberrant promoter methylation is involved in the regulation of GAS5 gene expression in triple-negative breast cancer and some other carcinomas. GAS5 can stimulate apoptosis in breast cancer via diverse pathways, including cell death receptors and mitochondrial signaling pathways. GAS5 is also a key player in the regulation of some crucial signal pathways in breast cancer, such as PI3K/AKT/mTOR, Wnt/β-catenin, and NF-κB signaling. Through epigenetic and other mechanisms, GAS5 can increase sensitivity to multiple drugs and improve prognosis. GAS5 is thus a promising target in the treatment of breast cancer patients.

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“…Certain malignant cells are resistant to TRAIL-induced cell death [ 67 ]. Many investigators pay special attention to treatment strategies based on the regulation of TRAIL-related processes [ 68 ]. Several metabolic inhibitors of the mitochondria, such as complex I inhibitor (rotenone (ROT)), complex III inhibitor (antimycin A (AM)), and mitochondrial uncoupling agent (carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP)) have been reported to increase mROS levels, and subsequently stimulated TRAIL-induced apoptosis in human leukemia cells (Jurkat cells) [ 69 ].…”

Section: Chemical Compoundsmentioning

confidence: 99%

Pathological and Pharmacological Roles of Mitochondrial Reactive Oxygen Species in Malignant Neoplasms: Therapies Involving Chemical Compounds, Natural Products, and Photosensitizers

et al. 2020

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Oxidative stress plays an important role in cellular processes. Consequently, oxidative stress also affects etiology, progression, and response to therapeutics in various pathological conditions including malignant tumors. Oxidative stress and associated outcomes are often brought about by excessive generation of reactive oxygen species (ROS). Accumulation of ROS occurs due to dysregulation of homeostasis in an otherwise strictly controlled physiological condition. In fact, intracellular ROS levels are closely associated with the pathological status and outcome of numerous diseases. Notably, mitochondria are recognized as the critical regulator and primary source of ROS. Damage to mitochondria increases mitochondrial ROS (mROS) production, which leads to an increased level of total intracellular ROS. However, intracellular ROS level may not always reflect mROS levels, as ROS is not only produced by mitochondria but also by other organelles such as endoplasmic reticulum and peroxisomes. Thus, an evaluation of mROS would help us to recognize the biological and pathological characteristics and predictive markers of malignant tumors and develop efficient treatment strategies. In this review, we describe the pathological significance of mROS in malignant neoplasms. In particular, we show the association of mROS-related signaling in the molecular mechanisms of chemically synthesized and natural chemotherapeutic agents and photodynamic therapy.

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Long non‑coding RNA regulation of TRAIL in breast cancer: A tangle of non‑coding threads (Review)

Cited by 5 publications

References 144 publications

LncRNA AC079630.4 expression associated with the progression and prognosis in lung cancer

LncRNA AC079630.4 expression associated with the progression and prognosis in lung cancer

Long Noncoding RNA GAS5 in Breast Cancer: Epigenetic Mechanisms and Biological Functions

Pathological and Pharmacological Roles of Mitochondrial Reactive Oxygen Species in Malignant Neoplasms: Therapies Involving Chemical Compounds, Natural Products, and Photosensitizers

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