Exosomal transfer of long non-coding RNA SBF2-AS1 enhances chemoresistance to temozolomide in glioblastoma

Zhang, Zhuoran; Yin, Jianxing; Lu, Chenfei; Wei, Yutian; Zeng, Ailiang; You, Yongping

doi:10.1186/s13046-019-1139-6

Cited by 213 publications

(207 citation statements)

References 68 publications

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“…Exosomes released by cancer cells of the central nervous system (CNS) (e.g., brain tumor) or non-CNS (e.g., cancer that spreads from the periphery to the brain) can contribute to reduced cognition by modulating the cellular mechanism that perturbs brain function. Certain cancers (e.g., glioblastoma [78,93] and medulloblastoma [76,94]) arising from the CNS have been shown to express exosomes that could affect cellular integrity. For example, glioblastoma was shown to remodel the tumor microenvironment and lead to chemotherapy resistance (e.g., temozolomide) through the intracellular transfer of oncogenic long non-coding RNA SBF2-AS1 by exosomes [93].…”

Section: Cancer Exosomes and Cognitive Impairmentmentioning

confidence: 99%

“…Certain cancers (e.g., glioblastoma [78,93] and medulloblastoma [76,94]) arising from the CNS have been shown to express exosomes that could affect cellular integrity. For example, glioblastoma was shown to remodel the tumor microenvironment and lead to chemotherapy resistance (e.g., temozolomide) through the intracellular transfer of oncogenic long non-coding RNA SBF2-AS1 by exosomes [93]. In addition to the ability to achieve chemoresistance, glioblastoma secretion of pro-permeability factor (e.g., Semaphorin3A) through exosomes has been associated with the loss of endothelial barrier integrity, resulting in debilitating cognitive deficits [78].…”

Section: Cancer Exosomes and Cognitive Impairmentmentioning

confidence: 99%

“…Although the precise mechanisms underlying CRCI remain to be established, several studies suggest there is a link between exosomes and CRCI. Exosome biogenesis, its cargo content, function, and activity may be influenced by cancer [97], cancer therapies [93,102], genetics [54,111], age [71], existing comorbidities [112,113], lifestyle [114,115], and environmental [116] factors. Differences in exosomal content (e.g., miRNAs and proteins) and release may exert protective or damaging effects that could alter the brain and CNS function, and cause declining cognitive health in cancer survivors.…”

Section: Potential Implication Of Exosomes In Crci Researchmentioning

confidence: 99%

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Role of Exosomes in Cancer-Related Cognitive Impairment

Koh

Tan

Toh

et al. 2020

IJMS

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A decline in cognitive function following cancer treatment is one of the most commonly reported post-treatment symptoms among patients with cancer and those in remission, and include memory, processing speed, and executive function. A clear understanding of cognitive impairment as a result of cancer and its therapy can be obtained by delineating structural and functional changes using brain imaging studies and neurocognitive assessments. There is also a need to determine the underlying mechanisms and pathways that impact the brain and affect cognitive functioning in cancer survivors. Exosomes are small cell-derived vesicles formed by the inward budding of multivesicular bodies, and are released into the extracellular environment via an exocytic pathway. Growing evidence suggests that exosomes contribute to various physiological and pathological conditions, including neurological processes such as synaptic plasticity, neuronal stress response, cell-to-cell communication, and neurogenesis. In this review, we summarize the relationship between exosomes and cancer-related cognitive impairment. Unraveling exosomes' actions and effects on the microenvironment of the brain, which impacts cognitive functioning, is critical for the development of exosome-based therapeutics for cancer-related cognitive impairment.Int. J. Mol. Sci. 2020, 21, 2755 2 of 16 attention, learning, and executive function [10]. CRCI adversely affects cancer patients and survivors, causing distress and reduced quality of life, and impacts many facets of their daily lives [11]. CRCI is complicated by many factors including the direct effects of cancer, genetic predisposition (e.g., carrier of apolipoprotein E type epsilon 4 allele [12] and brain-derived neurotrophic factor Met allele [13]), comorbidities independent of the actual disease, and/or treatments or combinations of treatments administered for the disease [14].Efforts to better understand cancer-and cancer-therapy-associated cognitive impairment have relied on methods ranging from cognitive functioning assessment to imaging technologies on brain structure and function (e.g., magnetic resonance imaging scan). However, these approaches may be limited to help us understand the etiology and pathophysiology of cognitive dysfunction. The emerging application of the use of liquid biopsies (e.g., plasma and cerebrospinal fluid) as a strategy for biomarker discovery to detect, assess and monitor CRCI is fast-expanding and evolving [15,16]. In published literature, studies have revealed that genetics and neurobiological and immunological mechanisms may be involved in the biogenesis and development of CRCI. Preclinical studies have also provided insights into the pathophysiological mechanisms underlying CRCI, including neurotoxicity and inflammatory factors, which were shown to be responsible for CRCI [17]. Nevertheless, the underlying mechanisms of CRCI have yet to be established. While the role of exosomes in cancer has been well-documented [18][19][20], the role of cancer exosomes and their ability ...

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Section: Cancer Exosomes and Cognitive Impairmentmentioning

confidence: 99%

Section: Cancer Exosomes and Cognitive Impairmentmentioning

confidence: 99%

Section: Potential Implication Of Exosomes In Crci Researchmentioning

confidence: 99%

See 1 more Smart Citation

Role of Exosomes in Cancer-Related Cognitive Impairment

Koh

Tan

Toh

et al. 2020

IJMS

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“…tested and identified miR‐151a loss pathway was key element of temozolomide‐resistant glioblastoma multiforme, and miR‐151a also provided a potential avenue for therapy‐refractory GBMs (Table ). Moreover, exosomal long‐noncoding RNA (lncRNA) SBF2‐AS1 (lncSBF2‐AS1), could also increase temozolomide tolerance to glioblastoma mainly via exerting reconstructive action to tumor microenvironment (Table ) . Qu et al .…”

Section: Exosome and Tumor Developmentmentioning

confidence: 99%

“…Moreover, exosomal long-noncoding RNA (lncRNA) SBF2-AS1 (lncSBF2-AS1), could also increase temozolomide tolerance to glioblastoma mainly via exerting reconstructive action to tumor microenvironment ( Table 1). 8 Qu et al 9 reported an identified lncARSR which increased the expression of AXL and c-MET, was transmitted to renal epithelial cell carcinoma cells, increased sunitinib tolerance (Table 1). Exosomal RNA also represents a novel strategy in enhancing chemosensitivity in cancer, not only for increased therapy tolerance.…”

Section: Therapy Resistancementioning

confidence: 99%

The cancer exosomes: Clinical implications, applications and challenges

Tang

Hou

et al. 2019

Intl Journal of Cancer

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The exosome is a small functional vesicle enriched in selected proteins, lipids and nucleic acids, displaying distinct molecular heterogeneity. Exosomes released can transform the extracellular matrix microenvironments, transmit signals and molecules to recipient cells and trigger changes in their pathophysiological functions. Tumor‐derived exosomes mediate the interactions of tumor cells and microenvironment significantly, and they stimulate tumor growth and development through specific signaling pathways related to metastasis, therapeutic resistance and immunosuppression. Exosome biogenesis from tumors often represents abundant biological information, and novel and efficient isolation and detection methods of exosomes provide a promising approach for tumor diagnosis and prognosis estimation. Moreover, exosome can even be developed as therapeutic agents for multiple disease models based on effective material transport characteristics and biofilm specificity. This review reports the clinical implications and challenges of exosomes in cancer progression, therapy resistance, metastasis and immune escape, and underlying cancerogenic pathological phenotypes including fibrosis and viral infection.

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Small but Fierce: Tracking the Role of Extracellular Vesicles in Glioblastoma Progression and Therapeutic Resistance

Schweiger

Tannous

2020

Adv. Biosys.

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(30%), mouse double minute 2 (MDM2) amplifications (<10%) and/ or overexpression (50%), p16INK4a deletions (30-40%), and loss of heterozygosity on chromosome 10 in 50-80% of all cases. [3] Around 5-10% of all GBMs harbor isocitrate dehydrogenase (IDH) mutations with a better prognosis compared to tumors carrying the wildtype form known to exhibit a much more aggressive clinical behavior, particularly in adults. [4,5] It is now appreciated that IDH-wildtype and IDH-mutant gliomas represent distinct clinical and genetic entities, and efforts have been made to restrict the term "glioblastoma" to tumors without IDH mutations. [6,7] The standard-of-care treatment consists of maximal surgical resection of the tumor in combination with radiation and temozolomide (TMZ) chemotherapy. However, GBM is insidious and treatments have not been effective in preventing eventual disease progression as recurrence remains inevitable. [8-11] Transcriptomic, genomic, and epigenomic characterization have unveiled the highly heterogeneous nature of GBM with complex interactions among different cells within as well as cells surrounding the tumor. [3,12-17] Comprehensive longitudinal analyses of the tumor transcriptome have uncovered intricate intertumoral heterogeneity and classified GBM into three distinct subtypes: classical (CL), proneural (PN), and mesenchymal (MES). [18] In addition to this intertumoral heterogeneity, single-cell RNA sequencing demonstrated the presence of numerous transcriptome subtypes within the same tumor. [14] Further, single-cell lineage tracking and expression analysis of specimens from The Cancer Genome Atlas (TCGA) revealed that malignant cells in GBM exist in four main cellular states: neural-progenitor-like, oligodendrocyte-progenitor-like, astrocyte-like, and mesenchymal-like. [19] The number and frequency of cells in each defined state varies between patients and is influenced by mutations in the neurofibromin 1 (NF1) locus and copy number amplifications of EGFR, cyclin dependent kinase 4 (CDK4), and platelet-derived growth factor receptor alpha (PDGFRA) loci. The intricate combination of inter-as well as intratumoral heterogeneity plays a key role in rendering conventional and experimental targeted therapy approaches ultimately ineffective. [20-22] The majority of glioma cells lack the capacity to recapitulate a phenocopy of the original tumor and only a small subpopulation of neural stem-like cells within the tumor, called glioma stem cells (GSCs) or tumor initiating cells, have that ability upon xenotransplantation in immunocompromised mice. [23-25] Evidence suggests that these GSCs act as a driving Glioblastoma is the most common and aggressive brain tumor in adults. Most patients die within a year and long-term survival remains rare, owing to a combination of rapid progression/degeneration, lack of successful treatments, and high recurrence rates. Extracellular vesicles are cell-derived membranous structures involved in numerous physiological and pathological processes. In the context of cancer, th...

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Exosomal transfer of long non-coding RNA SBF2-AS1 enhances chemoresistance to temozolomide in glioblastoma

Cited by 213 publications

References 68 publications

Role of Exosomes in Cancer-Related Cognitive Impairment

Role of Exosomes in Cancer-Related Cognitive Impairment

The cancer exosomes: Clinical implications, applications and challenges

Small but Fierce: Tracking the Role of Extracellular Vesicles in Glioblastoma Progression and Therapeutic Resistance

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