miR-410-3p is induced by vemurafenib via ER stress and contributes to resistance to BRAF inhibitor in melanoma

Grzywa, Tomasz M.; Klicka, Klaudia; Paskal, Wiktor; Dudkiewicz, Julia; Wejman, Jarosław; Pyźlak, Michał; Włodarski, Paweł

doi:10.1371/journal.pone.0234707

Cited by 18 publications

(19 citation statements)

References 53 publications

(82 reference statements)

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“…Significantly, Tan et al ( Tan et al, 2018 ) found that miR-146a induces cisplatin resistance in lung cancer cells by binding to CHOP 3′UTR to inhibit CHOP ( Figure 1 ). Furthermore, another study indicated ( Grzywa et al, 2020 ) that vemurafenib promotes the expression of miR-410-3p by inducing 12 transcription factors downstream of ERS in melanoma. The overexpression of miR-410-3p results in the transformation of melanoma cells into an invasive phenotype, thereby causing their resistance to vemurafenib ( Grzywa et al, 2020 ).…”

Section: Intrinsic Drug-induced Ers and Drug Resistance In Solid Tumorsmentioning

confidence: 99%

The Road of Solid Tumor Survival: From Drug-Induced Endoplasmic Reticulum Stress to Drug Resistance

Cao

Tang

Huang

et al. 2021

Front. Mol. Biosci.

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Endoplasmic reticulum stress (ERS), which refers to a series of adaptive responses to the disruption of endoplasmic reticulum (ER) homeostasis, occurs when cells are treated by drugs or undergo microenvironmental changes that cause the accumulation of unfolded/misfolded proteins. ERS is one of the key responses during the drug treatment of solid tumors. Drugs induce ERS by reactive oxygen species (ROS) accumulation and Ca2+ overload. The unfolded protein response (UPR) is one of ERS. Studies have indicated that the mechanism of ERS-mediated drug resistance is primarily associated with UPR, which has three main sensors (PERK, IRE1α, and ATF6). ERS-mediated drug resistance in solid tumor cells is both intrinsic and extrinsic. Intrinsic ERS in the solid tumor cells, the signal pathway of UPR-mediated drug resistance, includes apoptosis inhibition signal pathway, protective autophagy signal pathway, ABC transporter signal pathway, Wnt/β-Catenin signal pathway, and noncoding RNA. Among them, apoptosis inhibition is one of the major causes of drug resistance. Drugs activate ERS and its downstream antiapoptotic proteins, which leads to drug resistance. Protective autophagy promotes the survival of solid tumor cells by devouring the damaged organelles and other materials and providing new energy for the cells. ERS induces protective autophagy by promoting the expression of autophagy-related genes, such as Beclin-1 and ATG5–ATG12. ABC transporters pump drugs out of the cell, which reduces the drug-induced apoptosis effect and leads to drug resistance. In addition, the Wnt/β-catenin signal pathway is also involved in the drug resistance of solid tumor cells. Furthermore, noncoding RNA regulates the ERS-mediated survival and death of solid tumor cells. Extrinsic ERS in the solid tumor cells, such as ERS in immune cells of the tumor microenvironment (TME), also plays a crucial role in drug resistance by triggering immunosuppression. In immune system cells, ERS in dendritic cells (DCs) and myeloid-derived suppressor cells (MDSCs) influences the antitumor function of normal T cells, which results in immunosuppression. Meanwhile, ERS in T cells can also cause impaired functioning and apoptosis, leading to immunosuppression. In this review, we highlight the core molecular mechanism of drug-induced ERS involved in drug resistance, thereby providing a new strategy for solid tumor treatment.

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Section: Intrinsic Drug-induced Ers and Drug Resistance In Solid Tumorsmentioning

confidence: 99%

The Road of Solid Tumor Survival: From Drug-Induced Endoplasmic Reticulum Stress to Drug Resistance

Cao

Tang

Huang

et al. 2021

Front. Mol. Biosci.

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“…Recent studies showed miRNAs may serve as diagnostic and prognostic biomarkers in different cancers (Rapado-Gonzalez et al 2019 ; Delangle et al 2019 ; Butz and Patocs 2019 ; Bhat et al 2019 ). Importantly, miRNAs can be detected in formalin-fixed tissues (FFPE), therefore, they may be potentially an extension of conventional histopathological diagnosis (Klopfleisch et al 2011 ; Grzywa et al 2020 ). Numerous studies evaluating miRNA expression in PC led to inconclusive results possibly due to the highly heterogeneous structure of the tumor (Yadav et al 2018 ; Grzywa et al 2017 ).…”

Section: Introductionmentioning

confidence: 99%

miR-96-5p, miR-134-5p, miR-181b-5p and miR-200b-3p heterogenous expression in sites of prostate cancer versus benign prostate hyperplasia—archival samples study

Pełka

Klicka

Grzywa

et al. 2020

Histochem Cell Biol

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MicroRNAs are involved in various pathologies including cancer. The aim of the study was to assess the level of expression of miR-96-5p, -134-5p, -181b-5p, -200b-3p in FFPE samples of prostate cancer, adjacent cancer-free tissue, and benign prostatic hyperplasia. Samples of 23 FFPE prostate cancer and 22 benign prostatic hyperplasias were dissected and HE stained. Compartments of tumor tissue and adjacent healthy glandular tissue were isolated from each sample using Laser Capture Microdissection. Total RNA was isolated from dissected tissues. Expression of miR-96-5p, miR-134-5p, 181b-5p, and miR-200b-3p was determined by real-time RT-qPCR method. The expression of miR-200b-3p was significantly higher in cancerous prostate: both in adenocarcinomatous glands and in the adjacent, apparently unaffected glands compared to BPH samples. The expression of miR-181b-5p was lower in in both prostate cancer tissues and adjacent tissue compared to BPH samples. Expression of miR-96-5p and miR-134-5p was lower in prostate cancer tissues compared to BPH. Levels of miR-96-5p, miR-134-5p, and 181b-5p negatively correlated with the Gleason score. Given further studies, miR-96-5p, miR-134-5p and especially miR-200b-3p and miR-181b-5p may differentiate BPH and PC.

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“…Epigenetic regulation of ER stress is also of importance when considering disease therapy. An accumulating body of evidence demonstrates the regulation of ER stress by ncRNAs mediators such as miRNAs, lncRNAs, and circRNAs [ 280 , 281 , 282 , 283 ]. Various interactions between ncRNAs and ER stress mediators have already been identified in different types of cancers [ 284 , 285 ].…”

Section: Discussionmentioning

confidence: 99%

The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis

Aghaei

Dastghaib

Aftabi

et al. 2020

Life

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Cellular protein homeostasis in the lungs is constantly disrupted by recurrent exposure to various external and internal stressors, which may cause considerable protein secretion pressure on the endoplasmic reticulum (ER), resulting in the survival and differentiation of these cell types to meet the increased functional demands. Cells are able to induce a highly conserved adaptive mechanism, known as the unfolded protein response (UPR), to manage such stresses. UPR dysregulation and ER stress are involved in numerous human illnesses, such as metabolic syndrome, fibrotic diseases, and neurodegeneration, and cancer. Therefore, effective and specific compounds targeting the UPR pathway are being considered as potential therapies. This review focuses on the impact of both external and internal stressors on the ER in idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) and discusses the role of the UPR signaling pathway activation in the control of cellular damage and specifically highlights the potential involvement of non-coding RNAs in COPD. Summaries of pathogenic mechanisms associated with the ER stress/UPR axis contributing to IPF and COPD, and promising pharmacological intervention strategies, are also presented.

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miR-410-3p is induced by vemurafenib via ER stress and contributes to resistance to BRAF inhibitor in melanoma

Cited by 18 publications

References 53 publications

The Road of Solid Tumor Survival: From Drug-Induced Endoplasmic Reticulum Stress to Drug Resistance

The Road of Solid Tumor Survival: From Drug-Induced Endoplasmic Reticulum Stress to Drug Resistance

miR-96-5p, miR-134-5p, miR-181b-5p and miR-200b-3p heterogenous expression in sites of prostate cancer versus benign prostate hyperplasia—archival samples study

The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis

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