Long noncoding RNAs and exosomal lncRNAs: classification, and mechanisms in breast cancer metastasis and drug resistance

Yousefi, Hassan; Maheronnaghsh, Maryam; Molaei, Fatemeh; Mashouri, Ladan; Aref, Amir Reza; Momeny, Majid; Alahari, Suresh K.

doi:10.1038/s41388-019-1040-y

Cited by 169 publications

(135 citation statements)

References 141 publications

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“…Intriguingly, the expression of some lncRNAs is deregulated in cancers, and these lncRNAs exert oncogenic or tumor-suppressive functions via various mechanisms, such as regulating the transcription or translation of target genes and modulating signal transduction [9,10]. Furthermore, some lncRNAs are involved in breast cancer progression via controlling some processes of breast cancer pathophysiologies, such as invasion and metastasis, and drug resistance (reviewed in [11]). Thus, lncRNAs may be promising biomarkers and therapeutic targets of cancers, including breast cancer.…”

Section: Lncrnasmentioning

confidence: 99%

“…LncRNAs play key roles in various biological process and diseases, including cancers [6][7][8][9][10]. In breast cancer, some lncRNAs exert oncogenic or tumor-suppressive functions to control breast cancer pathophysiology, such as invasion and metastasis, and drug resistance; these findings are summarized in a recent review article [11]. In terms of endocrine therapy, selective estrogen receptor modulators (SERMs), selective estrogen receptor degraders or downregulators (SERDs), and aromatase inhibitors, are mainly used as drugs to suppress estrogen signaling.…”

Section: Introductionmentioning

confidence: 99%

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Long Noncoding RNAs Involved in the Endocrine Therapy Resistance of Breast Cancer

Takeiwa

Ikeda

Mitobe

et al. 2020

Cancers

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Long noncoding RNAs (lncRNAs) are defined as RNAs longer than 200 nucleotides that do not encode proteins. Recent studies have demonstrated that numerous lncRNAs are expressed in humans and play key roles in the development of various types of cancers. Intriguingly, some lncRNAs have been demonstrated to be involved in endocrine therapy resistance for breast cancer through their own mechanisms, suggesting that lncRNAs could be promising new biomarkers and therapeutic targets of breast cancer. Here, we summarize the functions and mechanisms of lncRNAs related to the endocrine therapy resistance of breast cancer.

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Section: Lncrnasmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNAs Involved in the Endocrine Therapy Resistance of Breast Cancer

Takeiwa

Ikeda

Mitobe

et al. 2020

Cancers

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“…Latest studies depict that lncRNA expression is vastly regulated by exosomes present in lung tumor microenvironment, that create an immunosuppressive tumor promoting status [39,40]. To investigate this hypothesis, we quantified PCAT-1 expression in exosomes, extracted from serum of LC patients ( Supplementary Figure 3).…”

Section: Exosomal Pcat-1 Promotes Tumor Growth and Guides Lymph Node mentioning

confidence: 99%

Exosomal lncRNA PCAT-1 promotes Kras-associated chemoresistance via immunosuppressive miR-182/miR-217 signaling and p27/CDK6 regulation

et al. 2020

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Immunosuppressive chemoresistance is a major burden in lung cancer. Recent data reveal that long noncoding RNAs (lncRNAs) present in the lung tumor microenvironment are implicated in chemoresistant-related immune deregulation, and metastasis but their exact pathogenic role is still unknown. In this study, we investigate the role of lncRNA PCAT-1 in chemoresistant immunosuppression and its involvement in tumor stroma remodeling. Findings reveal PCAT-1 to regulate Kras-related lung chemoresistance through increased expression of the immunosuppressive micrornas miR-182/miR217 in lung tissues, thus promoting a pre-metastatic niche formation and a subsequent increase in lung metastatic burden. Elevated expression of PCAT-1 negative regulates p27/CDK6 expression by inducing G 0 /G 1 cell cycle arrest through AMPK augmentation, contributing to a tumor-promoting status. Furthermore, PCAT-1 triggered fibroblast differentiation followed by CAF/myofibroblast secretion in TME triggering a CD133/SOX2-related stem cell phenotype. Subsequent PCAT-1 knockdown impaired CAF-mediated stromal activation, and reversed chemoresistance and tumor growth in vivo. Overall, these findings demonstrate the versatile roles of PCAT-1 in sustaining lung immunosuppressive neoplasia through tumor microenvironment remodeling and provide new opportunities for effective metastasis inhibition, especially in chemoresistant tumors.

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“…EMT is triggered by a genetic phenotype shift from epithelial-like to mesenchymal-like in response to pleiotropic signal; cells acquire the migratory and invasive properties by modifying adhesion molecules [3][4][5]. During this process, EMT specific transcription factors (EMT-TFs), in company with other regulatory factors like histone modifier and non-coding RNA, modify the gene expression through different states along EMT [6][7][8][9][10][11]. With the transcriptional activation of EMT-TFs, the expression of adherent junction components and tight junction components are negative-regulated, followed by the alteration in cadherin intermediate filament composition and cellular adhesion status [1, 3,8,9].…”

Section: Introductionmentioning

confidence: 99%

(20S)G-Rh2 Inhibits NF-κB Regulated Epithelial-Mesenchymal Transition by Targeting Annexin A2

Wang

et al. 2020

Biomolecules

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(1) Background: Epithelial-mesenchymal transition (EMT) is an essential step for cancer metastasis; targeting EMT is an important path for cancer treatment and drug development. NF-κB, an important transcription factor, has been shown to be responsible for cancer metastasis by enhancing the EMT process. Our previous studies showed that (20S)Ginsenoside Rh2 (G-Rh2) inhibits NF-κB activity by targeting Anxa2, but it is still not known whether this targeted inhibition of NF-κB can inhibit the EMT process. (2) Methods: In vivo (20S)G-Rh2-Anxa2 interaction was assessed by cellular thermal shift assay. Protein interaction was determined by immuno-precipitation analysis. NF-κB activity was determined by dual luciferase reporter assay. Gene expression was determined by RT-PCR and immuno-blot. EMT was evaluated by wound healing and Transwell assay and EMT regulating gene expression. (3) Results: Anxa2 interacted with the NF-κB p50 subunit, promoted NF-κB activation, then accelerated mesenchymal-like gene expression and enhanced cell motility; all these cellular processes were inhibited by (20S)G-Rh2. In contrast, these (20S)G-Rh2 effect were completely eliminated by overexpression of Anxa2-K301A, an (20S)G-Rh2-binding-deficient mutant of Anxa2. (4) Conclusion: (20S)G-Rh2 inhibited NF-κB activation and related EMT by targeting Anxa2 in MDA-MB-231 cells.

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Long noncoding RNAs and exosomal lncRNAs: classification, and mechanisms in breast cancer metastasis and drug resistance

Cited by 169 publications

References 141 publications

Long Noncoding RNAs Involved in the Endocrine Therapy Resistance of Breast Cancer

Long Noncoding RNAs Involved in the Endocrine Therapy Resistance of Breast Cancer

Exosomal lncRNA PCAT-1 promotes Kras-associated chemoresistance via immunosuppressive miR-182/miR-217 signaling and p27/CDK6 regulation

(20S)G-Rh2 Inhibits NF-κB Regulated Epithelial-Mesenchymal Transition by Targeting Annexin A2

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