microRNA-181a-5p impedes the proliferation, migration, and invasion of retinoblastoma cells by targeting the NRAS proto-oncogene

Ouyang, Ming; Liu, Guiqin; Xiong, Cheng; Rao, Jing

doi:10.1016/j.clinsp.2022.100026

Cited by 13 publications

(5 citation statements)

References 20 publications

(23 reference statements)

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“…Through their interaction with various cellular proteins, E6 and E7 activate Fas, MAPK, Akt, PI3K, and Wnt signaling pathways, which modulate cellular proliferation, migration, invasion, and apoptosis, as well as epithelial–mesenchymal transition (EMT) and metastasis [ 6 , 7 , 8 , 9 , 10 , 11 ], cellular processes that modulate CC progression [ 12 , 13 , 14 ]. The dysregulation in the function of proteins, signaling pathways, and cellular processes, result from altered gene expression [ 15 , 16 ]. Viral oncoproteins, the accumulation of genetic and epigenetic alterations, and post-translational modifications lead to the inactivation of tumor suppressor genes, activation of oncogenes, and increase or decrease the expression of microRNAs (miRNAs) [ 17 , 18 ].…”

Section: Introductionmentioning

confidence: 99%

miR-23b-3p, miR-124-3p and miR-218-5p Synergistic or Additive Effects on Cellular Processes That Modulate Cervical Cancer Progression? A Molecular Balance That Needs Attention

Romero-López

Jiménez‐Wences

Rosa

et al. 2022

IJMS

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In cervical cancer (CC), miR-23b-3p, miR-124-3p, and miR-218-5p have been found to act as tumor suppressors by regulating cellular processes related to progression and metastasis. The objective of the present review is to provide an update on the experimental evidence about the role of miR-23b-3p, miR-124-3p, and miR-218-5p in the regulation of CC progression. Additionally, we present the results of a bioinformatic analysis that suggest that these miRNAs have a somewhat redundant role in the same cellular processes that may result in a synergistic effect to promote CC progression. The results indicate that specific and common target genes for miR-23b-3p, miR-124-3p, and miR-218-5p regulate proliferation, migration, apoptosis, and angiogenesis, all processes that are related to CC maintenance and progression. Furthermore, several target genes may regulate cancer-related signaling pathways. We found that a total of 271 proteins encoded by the target mRNAs of miR-23b-3p, miR-124-3p, or miR-218-5p interact to regulate the cellular processes previously mentioned, and some of these proteins are regulated by HPV-16 E7. Taken together, information analysis indicates that miR-23b-3p, miR-124-3p, and miR-218-5p may potentiate their effects to modulate the cellular processes related to the progression and maintenance of CC with and without HPV-16 involvement.

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Section: Introductionmentioning

confidence: 99%

miR-23b-3p, miR-124-3p and miR-218-5p Synergistic or Additive Effects on Cellular Processes That Modulate Cervical Cancer Progression? A Molecular Balance That Needs Attention

Romero-López

Jiménez‐Wences

Rosa

et al. 2022

IJMS

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“…Furthermore, we identified chemotherapy resistance pathway genes, such as ABCB1 (MDR1) [ 41 ] and CTSL (cathepsin L) [ 42 ], as EMT targets in Rb tumors. Likewise, the miR-181a-5p clusters located on chromosome 1 are known to repress E2F transcription factors [ 43 ], G1/S cell cycle regulators [ 44 ], and proto-oncogenes [ 45 ]. We found that miR-181a-5p negatively controls EMT and chemoresistance through the regulation of SNAI2 and CTSL transcripts in vitro.…”

Section: Discussionmentioning

confidence: 99%

Enhanced Epithelial-to-Mesenchymal Transition and Chemoresistance in Advanced Retinoblastoma Tumors Is Driven by miR-181a

Babu

Bisht²,

Mallipatna³

et al. 2022

Cancers

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Advanced retinoblastoma (Rb) tumors display high metastatic spread to distant tissues, causing a potent threat to vision and life. Through transcriptomic profiling, we discovered key upregulated genes that belonged to the epithelial–mesenchymal transition (EMT) and chemotherapy resistance pathways in advanced Rb tumors. Through in vitro models, we further showed that Rb null tumor cells under prolonged chemo drug exposure, acquires a metastasis-like phenotype through the EMT program mediated by ZEB1 and SNAI2 and these cells further acquires chemotherapeutic resistance through cathepsin-L- and MDR1-mediated drug efflux mechanisms. Using a miRNA microarray, we identified miR-181a-5p as being significantly reduced in advanced Rb tumors, which was associated with an altered EMT and drug-resistance genes. We showed that enhancing miR-181a-5p levels in Rb null chemo-resistant sublines reduced the ZEB1 and SNAI2 levels and halted the mesenchymal transition switch, further reducing the drug resistance. We thus identified miR-181a-5p as a therapeutically exploitable target for EMT-triggered drug-resistant cancers that halted their invasion and migration and sensitized them to low-dose chemotherapy drugs.

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“…Furthermore, we have identified chemotherapy resistance pathway genes like ABCB1 (MDR1) (Krech et al, 2012) and CTSL (Cathepsin L)(Zheng et al, 2009) as EMT targets in Rb tumors. Likewise, the miR-181a-5p clusters located on chromosome 1 are known to repress E2F transcription factors (Lin et al, 2018), G1/S cell cycle regulators (Shen et al, 2018) and proto-oncogenes (Ouyang et al, 2022). We have found that miR-181a-5p negatively controls EMT and chemoresistance through regulation of SNAI2 and CTSL transcripts invitro.…”

Section: Discussionmentioning

confidence: 99%

Enhanced epithelial to mesenchymal transition and chemoresistance in advanced Retinoblastoma tumors is driven by miR-181a

Babu

Bisht

Mallipatna

et al. 2022

Preprint

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Advanced retinoblastoma (Rb) tumors can infiltrate distant tissues and cause a potent threat to vision and life. Through transcriptomic profiling, we discovered key epithelial to mesenchymal transition (EMT) and chemotherapy resistance genes at higher expression levels in advanced Rb tumors. Rb-/- tumor cells acquire metastasis-like phenotype through the EMT program that critically contributes to chemoresistance. We demonstrate that prolonged chemo-drug exposure in Rb cells elicits an EMT program through ZEB1 and SNAI2 that further acquires therapeutic resistance through cathepsin L and MDR1 mediated drug efflux mechanisms. Further, 16 significantly differentially expressed miRNAs were identified in patient tumors, of which miR-181a-5p was significantly reduced in advanced Rb tumors and associated with altered EMT and drug resistance genes. Enhancing miR-181a-5p levels in Rb-/- cells and Rb-/- chemo-resistant sublines controls EMT transcription factors ZEB1 and SNAI2 and halts the transition switch, thereby reversing drug resistance. We thus identify miR-181a-5p as a potential therapeutic target for EMT triggered drug-resistant cancers that can halt their invasion and sensitize them to low dose chemotherapy drugs.

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microRNA-181a-5p impedes the proliferation, migration, and invasion of retinoblastoma cells by targeting the NRAS proto-oncogene

Cited by 13 publications

References 20 publications

miR-23b-3p, miR-124-3p and miR-218-5p Synergistic or Additive Effects on Cellular Processes That Modulate Cervical Cancer Progression? A Molecular Balance That Needs Attention

miR-23b-3p, miR-124-3p and miR-218-5p Synergistic or Additive Effects on Cellular Processes That Modulate Cervical Cancer Progression? A Molecular Balance That Needs Attention

Enhanced Epithelial-to-Mesenchymal Transition and Chemoresistance in Advanced Retinoblastoma Tumors Is Driven by miR-181a

Enhanced epithelial to mesenchymal transition and chemoresistance in advanced Retinoblastoma tumors is driven by miR-181a

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