Clinical significance of aberrant microRNAs expression in predicting disease relapse/refractoriness to treatment in diffuse large B-cell lymphoma: A meta-analysis

Ting, Choo-Yuen; Liew, Su May; Price, Amy; Gan, Gin Gin; Ong, Diana Bee-Lan; Tan, Soo‐Yong; Bee, Ping Chong

doi:10.1016/j.critrevonc.2019.102818

Cited by 17 publications

(13 citation statements)

References 78 publications

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“…Data sharing is the future of science and the utilization of these large patient datasets could potentially identify new determinants of drug resistance, biomarkers, and refinements in patient risk stratification with the incorporation of altered non-coding transcripts. Aberrant ncRNA expression has been shown to serve as prognostic indicators to predict treatment response or disease relapse for various malignancies [ 158 , 159 , 160 , 161 ]. Additionally, due to high cell-type specific expression patterns, ncRNA signatures may act as non-invasive biomarkers for diagnosis and prediction of treatment outcomes [ 16 ].…”

Section: Emerging Perspectivesmentioning

confidence: 99%

Non-Coding RNA Signatures of B-Cell Acute Lymphoblastic Leukemia

Rodriguez

Paculova

Kogut

et al. 2021

IJMS

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Non-coding RNAs (ncRNAs) comprise a diverse class of non-protein coding transcripts that regulate critical cellular processes associated with cancer. Advances in RNA-sequencing (RNA-Seq) have led to the characterization of non-coding RNA expression across different types of human cancers. Through comprehensive RNA-Seq profiling, a growing number of studies demonstrate that ncRNAs, including long non-coding RNA (lncRNAs) and microRNAs (miRNA), play central roles in progenitor B-cell acute lymphoblastic leukemia (B-ALL) pathogenesis. Furthermore, due to their central roles in cellular homeostasis and their potential as biomarkers, the study of ncRNAs continues to provide new insight into the molecular mechanisms of B-ALL. This article reviews the ncRNA signatures reported for all B-ALL subtypes, focusing on technological developments in transcriptome profiling and recently discovered examples of ncRNAs with biologic and therapeutic relevance in B-ALL.

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Section: Emerging Perspectivesmentioning

confidence: 99%

Non-Coding RNA Signatures of B-Cell Acute Lymphoblastic Leukemia

Rodriguez

Paculova

Kogut

et al. 2021

IJMS

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“…In recent years, research on the relationship between DLBCL and miRNAs has made great advances. For example, Ting et al (29) systematically analyzed a large number of studies and found that miR-155, miR-334, miR-21, miR-146b-5p and miR-17/92 clusters have certain value in predicting the chemotherapy response in DLBCL. In previous research, UCA1 was revealed to competitively bind with several miRNAs (13,30).…”

Section: Mir-331-3p Expression --------------------------------------mentioning

confidence: 99%

Knockdown of UCA1 restrains cell proliferation and metastasis of diffuse large B‑cell lymphoma by counteracting miR‑331‑3p expression

Zhang

Shang

et al. 2020

Oncol Lett

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Long non-coding RNA urothelial cancer associated 1 (UCA1) has been reported to act as a carcinogen in bladder cancer, while its role in diffuse large B-cell lymphoma (DLBCL) remains unclear. The present study was designed to explore the expression pattern and role of UCA1 in DLBCL. The expression pattern of UCA1 and microRNA (miR)-331-3p in DLBCL tissues and cell lines were detected by RT-qPCR. Dual luciferase reporter assay was performed to explore the relationship between UCA1 and miR-331-3p. Cell proliferation was explored by MTT assay. Cell migration and invasion abilities were assessed by Transwell assay. In the present study, it was revealed that the expression of UCA1 was significantly upregulated, while miR-331-3p was downregulated in DLBCL tissues and cell lines. Moreover, UCA1 was revealed to competitively bind with miR-331-3p in DLBCL. Functionally, knockdown of UCA1 was revealed to suppress cell proliferation, migration and invasion in DLBCL cells. Furthermore, upregulation of miR-331-3p prevented cell proliferation, migration and invasion in DLBC cells. In conclusion, the present findings firstly demonstrated that UCA1 silencing restrained DLBCL cell proliferation and metastases viability by suppressing miR-331-3p expression. It is suggested that UCA1 could be a possible medicinal target and biomarker for DLBCL.

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“…MicroRNAs (miRs), a cargo of EVs, are also essential for DLBCL development (13). Aberrant expression of miRs has been shown to have a profound impact on treatment outcomes and chemoresistance in DLBCL (14). Therefore, it was hypothesized that TNFAIP3 may be regulated by a miR shuttled in DLBCL cell-derived EVs, thus modulating the sensitivity of DLBCL to rituximab.…”

Section: Introductionmentioning

confidence: 99%

Potential of the tumor‑derived extracellular vesicles carrying the miR‑125b‑5p target TNFAIP3 in reducing the sensitivity of diffuse large B cell lymphoma to rituximab

Zhang

Zhou

et al. 2021

Int J Oncol

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Diffuse large B-cell lymphoma (DLBCL) is the most common and aggressive form of non-Hodgkin's lymphoma. Extracellular vesicles (EVs) derived from cancer cells are known to modify the tumor microenvironment. The aim of the present study was to investigate the role of miR-125b-3p carried by EVs in DLBCL in vitro and in vivo. TNFAIP3 expression in patient lesions was measured and the upstream miR that regulates TNFAIP3 was predicted using the starBase database. EVs were isolated from DLBCL cells and identified. DLBCL cells were transfected with pcDNA to overexpress TNFAIP3 or inhibit miR-125b-5p expression, incubated with EVs, and treated with rituximab to compare cell growth and TNFAIP3/CD20 expression. DLBCL model mice were administered EVs, conditioned medium, and rituximab to observe changes in tumor size, volume, and weight. TNFAIP3 was downregulated in patients with DLBCL and its levels further decreased in patients with drug-resistant DLBCL. Overexpression of TNFAIP3 in DLBCL cells enhanced the inhibitory effect of rituximab and increased CD20 expression. miR-125b-5p targeted TNFAIP3. Inhibition of miR-125b-5p enhanced the inhibitory effect of rituximab in DLBCL cells. The EV-carried miR-125b-5p reduced the sensitivity of DLBCL cells to rituximab, which was averted by overexpression of TNFAIP3. EVs reduced the sensitivity of DLBCL model mice to rituximab via the miR-125b-5p/TNFAIP3 axis. The study findings indicate that the tumor-derived EVs carrying miR-125b-5p can enter DLBCL cells and target TNFAIP3, thus reducing the sensitivity of DLBCL to rituximab, which may provide a novel therapeutic approach for DLBCL.

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Clinical significance of aberrant microRNAs expression in predicting disease relapse/refractoriness to treatment in diffuse large B-cell lymphoma: A meta-analysis

Cited by 17 publications

References 78 publications

Non-Coding RNA Signatures of B-Cell Acute Lymphoblastic Leukemia

Non-Coding RNA Signatures of B-Cell Acute Lymphoblastic Leukemia

Knockdown of UCA1 restrains cell proliferation and metastasis of diffuse large B‑cell lymphoma by counteracting miR‑331‑3p expression

Potential of the tumor‑derived extracellular vesicles carrying the miR‑125b‑5p target TNFAIP3 in reducing the sensitivity of diffuse large B cell lymphoma to rituximab

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